PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 6125449-0 1982 Difference in calcium dependency of insulin, glucagon and somatostatin secretion in response to glibenclamide in perfused rat pancreas. Glyburide 96-109 somatostatin Rattus norvegicus 58-70 6125449-1 1982 The extracellular calcium requirements for insulin, glucagon and somatostatin release induced by 1 microgram/ml of glibenclamide have been compared in the perfused, isolated rat pancreas. Glyburide 115-128 somatostatin Rattus norvegicus 65-77 6125449-3 1982 In contrast, glibenclamide evoked somatostatin release at 2.6 but not at 0.25 mmol/l of calcium. Glyburide 13-26 somatostatin Rattus norvegicus 34-46 6285503-7 1982 Furthermore, a significant decrease in both antithrombin III levels and basal and venostasis-stimulated plasminogen activator levels were seen in glibenclamide patients. Glyburide 146-159 serpin family C member 1 Homo sapiens 44-60 7029541-2 1981 Identification of the Golgi apparatus by immunofluorescence required the prior degranulation of B cells with glibenclamide to reduce the insulin immunostaining due to secretory granules. Glyburide 109-122 insulin Homo sapiens 137-144 6803519-5 1982 Glibenclamide and gliquidone reduced fasting blood glucose values (p less than 0.001), diurnal urine glucose concentrations (p less than 0.001, resp. p less than 0.01) and HbA1 concentrations (p less than 0.02 resp. p less than 0.05) compared to the values in the diet period. Glyburide 0-13 hemoglobin subunit alpha 1 Homo sapiens 172-176 6800910-16 1982 These finding suggest that the hypoglycemic effect of glibenclamide treatment in the short term is mainly, if not entirely, due to augmented endogenous insulin secretion. Glyburide 54-67 insulin Homo sapiens 152-159 6805141-5 1981 In general the improvement of the glucose tolerance was not associated with an increased secretion of insulin, so that an extrapancreatic effect of glibenclamide (improvement of the peripheral insulin sensitivity?) Glyburide 148-161 insulin Homo sapiens 193-200 7029541-4 1981 With the electron microscope, the insulin immunoreactive sites revealed by the protein A/gold technique were localized in the cisternae and vesicles of the Golgi apparatus of glibenclamide-treated and control B cells and over maturing and mature secretory granules. Glyburide 175-188 insulin Homo sapiens 34-41 6790327-3 1981 The enkephalin analogue D-ala2, MePhe4, Met(0)-ol (DAMME), 8.3 X 10(-8) mol/l, augmented insulin release stimulated by glucose (5 or 7 mmol/l) by 76% and 47% respectively; increased insulin release stimulated by alpha-ketoisocaproate (7.5 mmol/l) by 23%; and enhanced insulin release in the presence of glibenclamide (10 microgram/ml) plus glucose (3.3 mmol/l) by 38%. Glyburide 303-316 proenkephalin Rattus norvegicus 4-14 106617-0 1979 Increased insulin sensitivity and cellular insulin binding in obese diabetics following treatment with glibenclamide. Glyburide 103-116 insulin Homo sapiens 10-17 6776759-0 1980 Stimulation of residual insulin secretion by glibenclamide in insulin dependent diabetics. Glyburide 45-58 insulin Homo sapiens 24-31 6776759-3 1980 It is suggested that glibenclamide might be a useful adjunct to insulin therapy in insulin-requiring diabetics who still secrete C-peptide. Glyburide 21-34 insulin Homo sapiens 83-90 6777211-0 1980 The effect of glibenclamide on the glucose and insulin profile in maturity onset diabetics following both acute and long term treatment. Glyburide 14-27 insulin Homo sapiens 47-54 6778077-0 1980 Effects of glucagon and pentagastrin on glibenclamide-induced insulin release. Glyburide 40-53 insulin Homo sapiens 62-69 6778077-6 1980 Glucagon in contrast to pentagastrin thus positively modulates the insulin secretory pathway stimulated by the sulphonylurea drug glibenclamide. Glyburide 130-143 insulin Homo sapiens 67-74 118458-1 1979 The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. Glyburide 30-43 somatostatin Rattus norvegicus 86-98 118458-4 1979 A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Glyburide 43-56 somatostatin Rattus norvegicus 76-88 118458-5 1979 Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. Glyburide 108-121 somatostatin Rattus norvegicus 130-142 115730-0 1979 The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics. Glyburide 14-27 insulin Homo sapiens 45-52 115730-1 1979 Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. Glyburide 0-13 insulin Homo sapiens 45-52 116478-2 1979 Gastrin appears in perfusates of extirpated cat legs after administration of tolbutamide or glibenclamide (5-50 mg/kg or 5-500 microgram/kg perfused tissue respectively) to the perfusion medium. Glyburide 92-105 LOC105260099 Felis catus 0-7 111449-1 1979 The effect of two second generation sulphonylureas, gliquidone and glibenclamide, on insulin secretion has been studied in the basal state and in combination with glucose infusions in normal controls, patients with mild maturity-onset diabetes, and subjects with normal glucose tolerance but low insulin response. Glyburide 67-80 insulin Homo sapiens 85-92 111449-2 1979 When injected intravenously, gliquidone caused rapid elevation of plasma insulin, peaking at 5 min in all groups, while glibenclamide induced a slow rise in insulin. Glyburide 120-133 insulin Homo sapiens 157-164 111449-4 1979 In all groups, 25 micrograms/kg glibenclamide and 200 micrograms/kg gliquidone were equipotent in generating an insulin response at the basal state. Glyburide 32-45 insulin Homo sapiens 112-119 111449-7 1979 Addition of sulphonylurea induced a left shift in the dose-response relationships in controls and low insulin responders; under these conditions the effect of glibenclamide was more pronounced than that of gliquidone. Glyburide 159-172 insulin Homo sapiens 102-109 376293-3 1979 As with pertussis vaccine, pretreatment of rats with IAP was effective in enhancing insulin release from pancreas during perfusion or from islets during incubation in response to secretagogues such as glucose and glibenclamide. Glyburide 213-226 Cd47 molecule Rattus norvegicus 53-56 6772676-1 1980 We have studied the effects of the oral sulfonylurea agent glyburide to modulate insulin receptors on nontransformed human fibroblasts in tissue culture. Glyburide 59-68 insulin Homo sapiens 81-88 6772676-4 1980 When the process of insulin-induced receptor loss (or down regulation) was studied in the presence of glyburide, the drug exerted a marked inhibitory effect on this regulatory process. Glyburide 102-111 insulin Homo sapiens 20-27 6772676-5 1980 Thus, glyburide inhibited insulin-induced receptor loss in a dose-dependent fashion, and the maximally effective drug concentration (1 microgram/ml) inhibited 34% of the receptor loss. Glyburide 6-15 insulin Homo sapiens 26-33 6103639-2 1980 A sulphonylurea, glibenclamide, markedly enhanced the effect of arginine on somatostatin release and inhibited its effect on glucagon release. Glyburide 17-30 somatostatin Rattus norvegicus 76-88 6776763-0 1980 Diurnal pattern of plasma insulin and blood glucose during glibenclamide and glipizide therapy in elderly diabetics. Glyburide 59-72 insulin Homo sapiens 26-33 6776763-1 1980 The effect of a single and a split dose of glibenclamide and glipizide on the diurnal levels of blood glucose and plasma insulin were compared in 15 insulin-independent diabetics. Glyburide 43-56 insulin Homo sapiens 121-128 6778079-4 1980 Glipizide and glibenclamide were more potent inducers of insulin release and blood glucose reduction than tolbutamide and chlorpropamide. Glyburide 14-27 insulin Homo sapiens 57-64 106617-0 1979 Increased insulin sensitivity and cellular insulin binding in obese diabetics following treatment with glibenclamide. Glyburide 103-116 insulin Homo sapiens 43-50 109337-2 1979 Antiserum against glibenclamide was obtained from rabbits immunized with an antigen prepared by conjugating the diazonium salt of N(p-amino-benzamidoethyl)-benzenesulfonyl-N"-cyclohexylurea to bovine serum albumin through the diazocoupling. Glyburide 18-31 albumin Oryctolagus cuniculus 200-213 106617-1 1979 The aim of the present study was to examine the effect of glibenclamide on the insulin receptors, the insulin sensitivity and the insulin secretion in obese non-ketotic diabetics. Glyburide 58-71 insulin Homo sapiens 79-86 106617-6 1979 In the group treated with glibenclamide and diet the insulin secretory pattern was unchanged, too (p greater than 0.1). Glyburide 26-39 insulin Homo sapiens 53-60 106617-10 1979 After 1 year we found a significantly (P less than 0.005) higher cellular insulin binding in the glibenclamide treated patients compared to the patients who got diet alone. Glyburide 97-110 insulin Homo sapiens 74-81 106617-11 1979 We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors. Glyburide 241-254 insulin Homo sapiens 44-51 106617-11 1979 We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors. Glyburide 241-254 insulin Homo sapiens 160-167 106617-11 1979 We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors. Glyburide 241-254 insulin Homo sapiens 160-167 106617-11 1979 We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors. Glyburide 241-254 insulin Homo sapiens 160-167 106617-11 1979 We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors. Glyburide 241-254 insulin Homo sapiens 160-167 105351-2 1979 A study was made of the effect of administration of maninyl (glybenclamide) into the stomach in a dose of 10 mg/kg of body weight for 7 days on the blood glucose level, insulin and zinc content in the pancreatic islands, and on the "dithizone" diabetes development. Glyburide 61-74 insulin Oryctolagus cuniculus 169-176 101402-3 1978 There was no significant difference between serum insulin concentrations on the two doses, however, serum insulin/blood glucose ratio was higher during the larger dose of glibenclamide. Glyburide 171-184 insulin Homo sapiens 106-113 97083-4 1978 The addition of treatment with 5 mg/day glibenclamide to the regular human growth hormone injections resulted in an increased growth rate in four children while one patient developed hypoglycemic symptoms. Glyburide 40-53 growth hormone 1 Homo sapiens 75-89 97083-5 1978 The results show that STH-deficient children may benefit from combined treatment with human growth hormone plus glibenclamide. Glyburide 112-125 saitohin Homo sapiens 22-25 415745-0 1978 [Insulin and pro-insulin secretion following intravenous administration of tolbutamide, glisoxepide and glibenclamide]. Glyburide 104-117 insulin Homo sapiens 1-8 415745-4 1978 The maximum level of insulin follows the injection of tolbutamide with a value of 70.5 micronU/ml after 2 min, of glisoxepide after 5 min (67.0 micronU/ml) and of glibenclamide after 20 min (32.3 micronU/ml). Glyburide 163-176 insulin Homo sapiens 21-28 413023-1 1978 Eleven insulin-dependent ketosis-prone diabetics were given glibenclamide (5 mg/day) in addition to their usual insulin treatment for a period of 1 or 6 mo. Glyburide 60-73 insulin Homo sapiens 7-14 199621-6 1977 Tolbutamide and glyburide, two other sulfonylurea compounds, also enhanced vasopressin-stimulated water flow and inhibited vasopressin-stimulated prostaglandin E biosynthesis. Glyburide 16-25 arginine vasopressin Homo sapiens 75-86 199621-6 1977 Tolbutamide and glyburide, two other sulfonylurea compounds, also enhanced vasopressin-stimulated water flow and inhibited vasopressin-stimulated prostaglandin E biosynthesis. Glyburide 16-25 arginine vasopressin Homo sapiens 123-134 415444-3 1977 Then lycanol or daonil were used for treatment, serum GOT, GPT, and ceruloplasmin were changes towards normalization, while ceruloplasmin returned to normal values. Glyburide 16-22 ceruloplasmin Rattus norvegicus 68-81 415444-3 1977 Then lycanol or daonil were used for treatment, serum GOT, GPT, and ceruloplasmin were changes towards normalization, while ceruloplasmin returned to normal values. Glyburide 16-22 ceruloplasmin Rattus norvegicus 124-137 411723-1 1977 The blood glucose and plasma insulin response to the two hypoglycaemic agents, chlorpropamide (Diabenese) and glibenclamide (Daonil) was determined in normal subjects under strict metabolic control in a double blind study. Glyburide 110-123 insulin Homo sapiens 29-36 411723-5 1977 Chlorpropamide was capable of lowering blood glucose without raising plasma insulin levels, whereas glibenclamide produced a prolonged and marked increase in plasma insulin levels only to be associated with a short-lived hypoglycaemic response. Glyburide 100-113 insulin Homo sapiens 165-172 411723-6 1977 The latter suggested that a degree of insulin resistance had been produced secondary to the early profound lowering of the blood glucose following glibenclamide. Glyburide 147-160 insulin Homo sapiens 38-45 410692-0 1977 Potentiation of glibenclamide-induced insulin release by calcium infusion. Glyburide 16-29 insulin Homo sapiens 38-45 410692-1 1977 The effect of calcium on glibenclamide-induced insulin release was studied in 14 diabetic patients. Glyburide 25-38 insulin Homo sapiens 47-54 410692-5 1977 It is concluded that calcium may temporarily improve carbohydrate tolerance in diabetic patients by potentiating the glibenclamide-stimulated insulin secretion. Glyburide 117-130 insulin Homo sapiens 142-149 4214480-0 1974 Influence of glyburide on the antidiuretic response induced by 1-deamino-8-D-arginine vasopressin (DDAVP) in patients with pituitary diabetes insipidus. Glyburide 13-22 arginine vasopressin Homo sapiens 86-97 829387-0 1976 [Blood sugar and serum insulin levels with reference to the glibenclamide concentration in suicidal glibenclamide poisoning. Glyburide 60-73 insulin Homo sapiens 23-30 829387-0 1976 [Blood sugar and serum insulin levels with reference to the glibenclamide concentration in suicidal glibenclamide poisoning. Glyburide 100-113 insulin Homo sapiens 23-30 817889-0 1975 Inhibition of the antidiuretic effect of 1-deamino-8d-arginine vasopressin (DDAVP) by glibenclamide in water-loaded healthy subjects. Glyburide 86-99 arginine vasopressin Homo sapiens 63-74 817889-4 1975 These findings are consistent with the hypothesis that glibenclamide competitively inhibits the peripheral action of vasopressin. Glyburide 55-68 arginine vasopressin Homo sapiens 117-128 811925-1 1975 The effects of tolbutamide, glibenclamide, arginine and arginine in combination with glibenclamide upon insulin, glucagon and glucose serum levels have been studied in healthy young men. Glyburide 85-98 insulin Homo sapiens 104-111 805520-2 1975 Diabetics controlled on diet therapy showed no change in disaccharidase activity while two diabetics controlled on insulin or insulin-producing drug, glibenclamide, showed a fall in disaccharidase values toward normal. Glyburide 150-163 insulin Homo sapiens 126-133 804684-0 1975 [Daily curves of blood sugar and serum insulin after treatment with various combinations of glibenclamide and phenformin]. Glyburide 92-105 insulin Homo sapiens 39-46 403065-0 1977 [Attempted suicide using glibenclamide:course of glucose, insulin, glibenclamide and C-peptide blood levels]. Glyburide 25-38 insulin Homo sapiens 85-94 404205-6 1977 Serum insulin concentration was higher on glibenclamide than with either biguanide. Glyburide 42-55 insulin Homo sapiens 6-13 12072-1 1976 Sustained, 60-minute perfusion of glibenclamide (0.5, 1.5 and 10 mug/ml) elicits a one-phase insulin release profile, formed by a rapid secretion peak followed by a second peak with lower insulin levels than the former. Glyburide 34-47 insulin Homo sapiens 93-100 12072-1 1976 Sustained, 60-minute perfusion of glibenclamide (0.5, 1.5 and 10 mug/ml) elicits a one-phase insulin release profile, formed by a rapid secretion peak followed by a second peak with lower insulin levels than the former. Glyburide 34-47 insulin Homo sapiens 188-195 12072-7 1976 Both theophylline and phentolamine modify and increase the glibenclamide-induced insulin release pattern. Glyburide 59-72 insulin Homo sapiens 81-88 12072-8 1976 Propranolol and imidazole inhibit glibenclamide-induced insulin release. Glyburide 34-47 insulin Homo sapiens 56-63 12072-12 1976 Glibenclamide and glucose induce secretion of insulin originating in the same compartment. Glyburide 0-13 insulin Homo sapiens 46-53 814956-4 1976 Treatment with glibenclamide increased insulin secretion but phenformin had no significant effect. Glyburide 15-28 insulin Homo sapiens 39-46 4213806-0 1973 [Effects of the association of phenformin and glibenclamide on insulin secretion in anesthetized dogs]. Glyburide 46-59 insulin Canis lupus familiaris 63-70 4218049-0 1974 Inhibition of the diuretic action of glibenclamide by clofibrate, carbamazepine and 1-deamino-8-d-arginine-vasopressin (DDAVP) in patients with pituitary diabetes insipidus. Glyburide 37-50 arginine vasopressin Homo sapiens 107-118 4201174-1 1973 Inhibitory effects of a membrane probe on the islet uptake and insulin-releasing action of glibenclamide. Glyburide 91-104 insulin Homo sapiens 63-70 4353086-10 1973 The sulphonylureas, tolbutamide and glibenclamide, agents that increase insulin release, also increased the protein kinase activity; however, leucine, arginine and xylitol, which also stimulate insulin release, were without effect on the kinase activity. Glyburide 36-49 insulin Homo sapiens 72-79 4197367-0 1973 [Plasma insulin and glucose levels in diabetics treated with glibenclamide and chlorporpamide]. Glyburide 61-74 insulin Homo sapiens 8-15 4198966-2 1972 Increase of the effect of insulin due to tolbutamide, glibornuride, and glibenclamide in vitro]. Glyburide 72-85 insulin Homo sapiens 26-33 4622788-0 1972 Profile of insulin release due to intrapancreatic glyburide infusion. Glyburide 50-59 insulin Homo sapiens 11-18 5005528-0 1971 [Is the increase of hypoglycemic reactions during glibenclamide therapy due to a substance-specific stronger stimulation of the insulin secretion? Glyburide 50-63 insulin Homo sapiens 128-135 5005530-0 1971 [Behavior of serum insulin in the double intravenous glucose tolerance test in diabetics before and during glibenclamide therapy]. Glyburide 107-120 insulin Homo sapiens 19-26 4107054-0 1970 [In-vitro changes of the serum binding capacity for 131 I-insulin under tolbutamide and glybenclamide in normal persons, in juvenile and senile diabetes, as well as in insulin resistance]. Glyburide 89-102 insulin Homo sapiens 59-66 5533294-0 1970 Plasma insulin and metabolic study on diabetes treated with glibenclamide. Glyburide 60-73 insulin Homo sapiens 7-14 5526611-1 1970 A clinical and metabolic study of 32 patients treated with glibenclamide for a period of about one year confirmed that the drug is a potent stimulator of insulin release in maturity onset diabetes, and glibenclamide continued to have this action after a period of eight months. Glyburide 59-72 insulin Homo sapiens 154-161 5434298-0 1970 Effects of glycodiazin and glybenclamide upon insulin secretion in vitro. Glyburide 27-40 insulin Homo sapiens 46-53 34052309-0 2021 Inhibition of NLRP3 inflammasome by glibenclamide attenuated dopaminergic neurodegeneration and motor deficits in paraquat and maneb-induced mouse Parkinson"s disease model. Glyburide 36-49 NLR family, pyrin domain containing 3 Mus musculus 14-19 5440469-0 1970 [Blood sugar and plasma insulin levels in children following the oral administration of glybenclamide (HB 419)]. Glyburide 88-101 insulin Homo sapiens 24-31 33028147-1 2021 Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (KATP) channel. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 46-49 33028147-1 2021 Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (KATP) channel. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 99-103 33028147-1 2021 Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (KATP) channel. Glyburide 0-13 transient receptor potential cation channel subfamily M member 4 Homo sapiens 133-145 33028147-1 2021 Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (KATP) channel. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 147-151 33028147-1 2021 Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (KATP) channel. Glyburide 0-13 transient receptor potential cation channel subfamily M member 4 Homo sapiens 152-157 33652124-6 2021 Our results have shown that glibenclamide and glimepiride decrease 1.2B4 cells viability with accompanied increase in intracellular Ca2+ concentration and increased expression of apoptosis-related CASP-3 and TP53. Glyburide 28-41 caspase 3 Homo sapiens 197-203 33652124-6 2021 Our results have shown that glibenclamide and glimepiride decrease 1.2B4 cells viability with accompanied increase in intracellular Ca2+ concentration and increased expression of apoptosis-related CASP-3 and TP53. Glyburide 28-41 tumor protein p53 Homo sapiens 208-212 33652124-8 2021 Interestingly, 50 muM glimepiride increased expression of CAPN-1, CAPN-2 and CAPN-10 whereas 50 muM glibenclamide solely upregulated CAPN-2 expression. Glyburide 100-113 calpain 2 Homo sapiens 133-139 33652124-9 2021 We have shown that 10 muM and 50 muM glibenclamide and glimepiride increased the activity of CASP-3, but decreased total calpain activity. Glyburide 37-50 caspase 3 Homo sapiens 93-99 33652124-9 2021 We have shown that 10 muM and 50 muM glibenclamide and glimepiride increased the activity of CASP-3, but decreased total calpain activity. Glyburide 37-50 calpain 1 Homo sapiens 121-128 34052309-4 2021 This study was designed to investigate whether glibenclamide, an inhibitor of NLRP3 inflammasome, could offer a reliable protective strategy for PD in a mouse PD model induced by paraquat and maneb. Glyburide 47-60 NLR family, pyrin domain containing 3 Mus musculus 78-83 34052309-5 2021 We found that glibenclamide exerted potent neuroprotection against paraquat and maneb-induced upregulation of alpha-synuclein, dopaminergic neurodegeneration and motor impairment in brain of mice. Glyburide 14-27 synuclein, alpha Mus musculus 110-125 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 17-30 NLR family, pyrin domain containing 3 Mus musculus 49-54 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 17-30 NLR family, pyrin domain containing 3 Mus musculus 115-120 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 17-30 caspase 1 Mus musculus 132-141 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 17-30 interleukin 1 beta Mus musculus 153-170 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 174-187 NLR family, pyrin domain containing 3 Mus musculus 49-54 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 174-187 NLR family, pyrin domain containing 3 Mus musculus 115-120 34052309-6 2021 Mechanistically, glibenclamide treatment blocked NLRP3 inflammasome activation evidenced by reduced expressions of NLRP3, activated caspase-1 and mature interleukin-1beta in glibenclamide co-treated mice compared with those in paraquat and maneb group mice. Glyburide 174-187 interleukin 1 beta Mus musculus 153-170 34052309-8 2021 Finally, the increased superoxide production, lipid peroxidation, protein levels of NADPH oxidase 2 (NOX2) and inducible nitric oxide synthase (iNOS) induced by paraquat and maneb were all attenuated by glibenclamide. Glyburide 203-216 cytochrome b-245, beta polypeptide Mus musculus 84-99 34052309-8 2021 Finally, the increased superoxide production, lipid peroxidation, protein levels of NADPH oxidase 2 (NOX2) and inducible nitric oxide synthase (iNOS) induced by paraquat and maneb were all attenuated by glibenclamide. Glyburide 203-216 nitric oxide synthase 2, inducible Mus musculus 111-142 34052309-8 2021 Finally, the increased superoxide production, lipid peroxidation, protein levels of NADPH oxidase 2 (NOX2) and inducible nitric oxide synthase (iNOS) induced by paraquat and maneb were all attenuated by glibenclamide. Glyburide 203-216 nitric oxide synthase 2, inducible Mus musculus 144-148 34052309-9 2021 Overall, our findings demonstrated that glibenclamide protected dopaminergic neurons in a mouse PD model induced by combined exposures of paraquat and maneb through suppression of NLRP3 inflammasome activation, microglial M1 polarization and oxidative stress. Glyburide 40-53 NLR family, pyrin domain containing 3 Mus musculus 180-185 34037304-0 2021 Glyburide attenuates B(a)p and LPS-induced inflammation-related lung tumorigenesis in mice. Glyburide 0-9 prohibitin 2 Mus musculus 21-26 34037304-1 2021 Glyburide (Gly) could inhibit NLRP3 inflammasome, as well as could be treated with Type 2 diabetes as a common medication. Glyburide 0-9 NLR family, pyrin domain containing 3 Mus musculus 30-35 34037304-1 2021 Glyburide (Gly) could inhibit NLRP3 inflammasome, as well as could be treated with Type 2 diabetes as a common medication. Glyburide 0-3 NLR family, pyrin domain containing 3 Mus musculus 30-35 34037304-7 2021 While the incidence and mean tumor count of mice in B(a)P/LPS+Gly group were decreased compared with B(a)p/LPS group. Glyburide 62-65 prohibitin 2 Mus musculus 52-57 34037304-7 2021 While the incidence and mean tumor count of mice in B(a)P/LPS+Gly group were decreased compared with B(a)p/LPS group. Glyburide 62-65 prohibitin 2 Mus musculus 101-106 34037304-9 2021 The B(a)p/LPS increased the expression of NLRP3, IL-1beta, and Cleaved-IL-1beta protein significantly than Vehicle, whereas decreased in B(a)P/LPS+Gly (0.96 mg/kg) group compared with B(a)p/LPS group. Glyburide 147-150 prohibitin 2 Mus musculus 4-9 34037304-9 2021 The B(a)p/LPS increased the expression of NLRP3, IL-1beta, and Cleaved-IL-1beta protein significantly than Vehicle, whereas decreased in B(a)P/LPS+Gly (0.96 mg/kg) group compared with B(a)p/LPS group. Glyburide 147-150 prohibitin 2 Mus musculus 137-142 34037304-10 2021 Results suggested glyburide might inhibit NLRP3 inflammasome to attenuate inflammation-related lung tumorigenesis caused by intratracheal instillation of B(a)p/LPS in non-diabetes mice. Glyburide 18-27 NLR family, pyrin domain containing 3 Mus musculus 42-47 34037304-10 2021 Results suggested glyburide might inhibit NLRP3 inflammasome to attenuate inflammation-related lung tumorigenesis caused by intratracheal instillation of B(a)p/LPS in non-diabetes mice. Glyburide 18-27 prohibitin 2 Mus musculus 154-159 33987715-0 2021 Case report: coeliac disease as a cause of secondary failure of glibenclamide therapy in a patient with permanent neonatal diabetes due to KCNJ11/R201C mutation. Glyburide 64-77 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 139-145 33961902-8 2021 Blockade of ATP-sensitive potassium (K-ATP) channels with glibenclamide (Glib) prevented markedly the effect of NaHS on both the induction phase and survival of TH- positive neurons. Glyburide 58-71 tyrosine hydroxylase Rattus norvegicus 161-163 33961902-8 2021 Blockade of ATP-sensitive potassium (K-ATP) channels with glibenclamide (Glib) prevented markedly the effect of NaHS on both the induction phase and survival of TH- positive neurons. Glyburide 73-77 tyrosine hydroxylase Rattus norvegicus 161-163 33080394-2 2021 In the human and rodent retina, we show that the glibenclamide activated channel SUR1 is expressed in the retina and enriched in the macula; we also show that it co-localizes with the potassium channel Kir6.2, and with the cation channel transporter TRPM4. Glyburide 49-62 ATP binding cassette subfamily C member 8 Homo sapiens 81-85 33030052-6 2021 LY 294002 and glibenclamide reversed lipid emulsion-mediated inhibition of cleaved caspase-3 and -8 expression induced by amlodipine. Glyburide 14-27 caspase 3 Rattus norvegicus 83-99 33688783-5 2021 HighlightsActive m-calpain is present in the media generated from striatal synaptosomes.Glyburide prevents m-calpain release from striatal synaptosomes. Glyburide 88-97 calpain 2 Rattus norvegicus 17-26 33688783-5 2021 HighlightsActive m-calpain is present in the media generated from striatal synaptosomes.Glyburide prevents m-calpain release from striatal synaptosomes. Glyburide 88-97 calpain 2 Rattus norvegicus 107-116 33674849-5 2021 Furthermore, when the antagonists glibenclamide and valspodar were used to inhibit the function of ABCA1 and SR-BI or ABCA1 alone, respectively, cholesterol efflux was only marginally reduced (8-15)%. Glyburide 34-47 ATP binding cassette subfamily A member 1 Homo sapiens 99-104 33674849-5 2021 Furthermore, when the antagonists glibenclamide and valspodar were used to inhibit the function of ABCA1 and SR-BI or ABCA1 alone, respectively, cholesterol efflux was only marginally reduced (8-15)%. Glyburide 34-47 scavenger receptor class B member 1 Homo sapiens 109-114 33674849-5 2021 Furthermore, when the antagonists glibenclamide and valspodar were used to inhibit the function of ABCA1 and SR-BI or ABCA1 alone, respectively, cholesterol efflux was only marginally reduced (8-15)%. Glyburide 34-47 ATP binding cassette subfamily A member 1 Homo sapiens 118-123 33080394-2 2021 In the human and rodent retina, we show that the glibenclamide activated channel SUR1 is expressed in the retina and enriched in the macula; we also show that it co-localizes with the potassium channel Kir6.2, and with the cation channel transporter TRPM4. Glyburide 49-62 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 202-208 33080394-2 2021 In the human and rodent retina, we show that the glibenclamide activated channel SUR1 is expressed in the retina and enriched in the macula; we also show that it co-localizes with the potassium channel Kir6.2, and with the cation channel transporter TRPM4. Glyburide 49-62 transient receptor potential cation channel subfamily M member 4 Homo sapiens 250-255 33080394-4 2021 The down-regulation of SUR1 using a siRNA suppressed the neuroprotective effects of glibenclamide on excitotoxic stress-induced cell death. Glyburide 84-97 ATP binding cassette subfamily C member 8 Homo sapiens 23-27 32963077-13 2020 Glib abolished the inhibitory effects of AST IV on p-JNK and p-Cx43 both in vivo and in vitro. Glyburide 0-4 sulfotransferase family 1A member 1 Rattus norvegicus 41-47 33609028-6 2021 Glibenclamide was used as an ABCA1 antagonist. Glyburide 0-13 ATP binding cassette subfamily A member 1 Homo sapiens 29-34 33338529-0 2021 Glyburide inhibits non-enzymatic glycation of HSA: An approach for the management of AGEs associated diabetic complications. Glyburide 0-9 albumin Homo sapiens 46-49 33338529-2 2021 In this study, the antiglycation activity of glyburide was investigated using HSA as model protein both against glucose and methylglyoxal mediated glycation. Glyburide 45-54 albumin Homo sapiens 78-81 33338529-6 2021 Interaction studies revealed that glyburide showed moderate to strong binding affinity towards HSA with binding constant in the order of 106 M-1. Glyburide 34-43 albumin Homo sapiens 95-98 33338529-7 2021 The interaction of glyburide with HSA was entropically favourable and spontaneous in nature. Glyburide 19-28 albumin Homo sapiens 34-37 33338529-8 2021 Molecular dynamics simulation deciphered that glyburide-HSA complex was quite stable where RMSD, RMSF, Rg, SASA, and secondary structure of HSA remained approximately same over the entire simulation period. Glyburide 46-55 albumin Homo sapiens 56-59 33338529-8 2021 Molecular dynamics simulation deciphered that glyburide-HSA complex was quite stable where RMSD, RMSF, Rg, SASA, and secondary structure of HSA remained approximately same over the entire simulation period. Glyburide 46-55 albumin Homo sapiens 140-143 33338529-9 2021 The average binding energy of the MD simulation for glyburide-HSA complex was found to be -15.386 kJ mol-1. Glyburide 52-61 albumin Homo sapiens 62-65 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 ATP binding cassette subfamily C member 8 Homo sapiens 211-215 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 transient receptor potential cation channel subfamily M member 4 Homo sapiens 216-221 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 tumor necrosis factor Homo sapiens 222-231 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 ATP binding cassette subfamily C member 8 Homo sapiens 235-239 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 transient receptor potential cation channel subfamily M member 4 Homo sapiens 240-245 33463481-7 2022 For example, glibenclamide exerts an anti-inflammatory effect in respiratory, digestive, urological, and central nervous system (CNS) diseases, as well as in ischemia-reperfusion injury associated with abnormal SUR1-Trpm4/TNF-alpha or SUR1-Trpm4/ Nos2/ROS signaling. Glyburide 13-26 nitric oxide synthase 2 Homo sapiens 247-251 33788643-11 2021 The salutary effects of glibenclamide on pain behaviors correlated with reduced expression of IL-6, CCL2 and CXCL1 by dorsal horn astrocytes. Glyburide 24-37 interleukin 6 Mus musculus 94-98 33788643-11 2021 The salutary effects of glibenclamide on pain behaviors correlated with reduced expression of IL-6, CCL2 and CXCL1 by dorsal horn astrocytes. Glyburide 24-37 chemokine (C-C motif) ligand 2 Mus musculus 100-104 33788643-11 2021 The salutary effects of glibenclamide on pain behaviors correlated with reduced expression of IL-6, CCL2 and CXCL1 by dorsal horn astrocytes. Glyburide 24-37 chemokine (C-X-C motif) ligand 1 Mus musculus 109-114 33456300-11 2020 Hyperosmotic AQP8 gene expression was also reduced by autocrine/paracrine interleukin-1 signaling, the sulfonylureas glibenclamide and glipizide, which are known inhibitors of KATP channel activation, and a pannexin-blocking peptide. Glyburide 117-130 aquaporin 8 Homo sapiens 13-17 33375520-5 2020 Two additional novel inhibitors of DNMT1 are the approved drugs glyburide and panobinostat. Glyburide 64-73 DNA methyltransferase 1 Homo sapiens 35-40 33341937-0 2021 Hypoglycemia and glycemic control with glyburide in women with gestational diabetes and genetic variants of cytochrome P450 2C9 and/or OATP1B3. Glyburide 39-48 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 108-127 33341937-0 2021 Hypoglycemia and glycemic control with glyburide in women with gestational diabetes and genetic variants of cytochrome P450 2C9 and/or OATP1B3. Glyburide 39-48 solute carrier organic anion transporter family member 1B3 Homo sapiens 135-142 33341937-1 2021 Glyburide is mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme and enters the liver via the transporter OATP1B3. Glyburide 0-9 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 39-58 33341937-1 2021 Glyburide is mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme and enters the liver via the transporter OATP1B3. Glyburide 0-9 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 60-66 33341937-1 2021 Glyburide is mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme and enters the liver via the transporter OATP1B3. Glyburide 0-9 solute carrier organic anion transporter family member 1B3 Homo sapiens 116-123 33341937-2 2021 The variants OATP1B3*4 (699 G>A; rs7311358) and CYP2C9*2 and *3 are known to have a significant influence on the hepatic uptake and metabolism of glyburide, with lower clearance than in the wild type. Glyburide 146-155 solute carrier organic anion transporter family member 1B3 Homo sapiens 13-20 33341937-2 2021 The variants OATP1B3*4 (699 G>A; rs7311358) and CYP2C9*2 and *3 are known to have a significant influence on the hepatic uptake and metabolism of glyburide, with lower clearance than in the wild type. Glyburide 146-155 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 48-54 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 133-142 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 40-46 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 133-142 solute carrier organic anion transporter family member 1B3 Homo sapiens 53-60 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 133-142 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 261-267 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 133-142 solute carrier organic anion transporter family member 1B3 Homo sapiens 272-279 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 191-200 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 40-46 33341937-7 2021 In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3. Glyburide 191-200 solute carrier organic anion transporter family member 1B3 Homo sapiens 53-60 33293383-10 2020 The Sur1 inhibitor glibenclamide significantly reduced Vpr-induced apoptosis. Glyburide 19-32 ATP binding cassette subfamily C member 8 Homo sapiens 4-8 33293383-14 2020 We further show that an FDA-approved Sur1 inhibitory drug called glibenclamide significantly ameliorates apoptotic astrocytic cell death caused by HIV-1 Vpr, which could potentially open the possibility of repurposing glibenclamide for treating HAND. Glyburide 65-78 ATP binding cassette subfamily C member 8 Homo sapiens 37-41 33293383-14 2020 We further show that an FDA-approved Sur1 inhibitory drug called glibenclamide significantly ameliorates apoptotic astrocytic cell death caused by HIV-1 Vpr, which could potentially open the possibility of repurposing glibenclamide for treating HAND. Glyburide 218-231 ATP binding cassette subfamily C member 8 Homo sapiens 37-41 33292127-15 2021 GABA or Glib (10 mg/kg) significantly improved b.w., plasma insulin and GLUT-4 levels, and ameliorated FBG and blood lipid profile in diabetic rats. Glyburide 8-12 solute carrier family 2 member 4 Rattus norvegicus 72-78 33292127-16 2021 GABA and Glib (5 mg/kg) combination therapy achieved far better control over hyperglycaemia and related pathogenic conditions (b.w., water-intake, insulin, GLUT-4, lipids). Glyburide 9-13 solute carrier family 2 member 4 Rattus norvegicus 156-162 32737781-7 2020 DPE and/or GLI, an anti-diabetic drug, improved the pancreatic histoarchitecture and improved beta cell function and structure, which increased insulin levels and improved the insulin, Bcl-2, and caspase-3 immunoreactivity in diabetic rats. Glyburide 11-14 BCL2, apoptosis regulator Rattus norvegicus 185-190 32737781-7 2020 DPE and/or GLI, an anti-diabetic drug, improved the pancreatic histoarchitecture and improved beta cell function and structure, which increased insulin levels and improved the insulin, Bcl-2, and caspase-3 immunoreactivity in diabetic rats. Glyburide 11-14 caspase 3 Rattus norvegicus 196-205 32963077-12 2020 Additionally, the analgesic effect of AST IV was reversed by the adenosine triphosphate-sensitive potassium (KATP) channel blocker, glibenclamide (Glib). Glyburide 132-145 sulfotransferase family 1A member 1 Rattus norvegicus 38-44 32963077-12 2020 Additionally, the analgesic effect of AST IV was reversed by the adenosine triphosphate-sensitive potassium (KATP) channel blocker, glibenclamide (Glib). Glyburide 147-151 sulfotransferase family 1A member 1 Rattus norvegicus 38-44 33229413-0 2021 Alpha-synuclein aggregates increase the conductance of substantia nigra dopamine neurons, an effect partly reversed by the KATP channel inhibitor glibenclamide. Glyburide 146-159 synuclein alpha Homo sapiens 0-15 33229413-8 2021 The effects of alpha-syn aggregates could be significantly reduced by pre-incubation with the ATP-sensitive potassium channel (KATP) inhibitor glibenclamide. Glyburide 143-156 synuclein alpha Homo sapiens 15-24 33615172-3 2021 All these drugs were found to exhibit moderate to strong inhibitory efficiency on the neurotransmitter degrading enzyme acetylcholinesterase (AChE) with GLY (IC50 = 0.74 +- 0.02 muM) being the most potent, followed by CPM (IC50 = 5.72 +- 0.24 muM) and TBM (IC50 = 28.9 +- 1.60 muM). Glyburide 153-156 acetylcholinesterase (Cartwright blood group) Homo sapiens 142-146 33615172-5 2021 The larger size of GLY spans almost the full gorge of AChE ranging from catalytic active site (CAS) to the peripheral active site (PAS) with relatively strong binding affinity (6.0 x 105 M-1) and acts as a competitive inhibitor for AChE. Glyburide 19-22 acetylcholinesterase (Cartwright blood group) Homo sapiens 54-58 33615172-5 2021 The larger size of GLY spans almost the full gorge of AChE ranging from catalytic active site (CAS) to the peripheral active site (PAS) with relatively strong binding affinity (6.0 x 105 M-1) and acts as a competitive inhibitor for AChE. Glyburide 19-22 acetylcholinesterase (Cartwright blood group) Homo sapiens 232-236 31971103-8 2021 The development of NLRP3 inhibitors was described from the earliest glyburide in 2001 to the latest progress in 2019. Glyburide 68-77 NLR family pyrin domain containing 3 Homo sapiens 19-24 32963077-13 2020 Glib abolished the inhibitory effects of AST IV on p-JNK and p-Cx43 both in vivo and in vitro. Glyburide 0-4 mitogen-activated protein kinase 8 Rattus norvegicus 53-56 32963077-13 2020 Glib abolished the inhibitory effects of AST IV on p-JNK and p-Cx43 both in vivo and in vitro. Glyburide 0-4 gap junction protein, alpha 1 Rattus norvegicus 63-67 32962633-9 2020 Interestingly, the translocation of GLUT1 induced by hypoxia was inhibited by the ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, while the mitochondrial KATP channel inhibitor 5-HD did not influence GLUT1 translocation during hypoxia. Glyburide 131-144 solute carrier family 2 member 1 Homo sapiens 36-41 32721448-0 2020 Glibenclamide modulates microglial function and attenuates Abeta deposition in 5XFAD mice. Glyburide 0-13 amyloid beta (A4) precursor protein Mus musculus 59-64 32860822-4 2020 Interestingly, glybenclamide, a widely used inhibitor of NLRP3 inflammasome, significantly reduced NLRP3 inflammasome activation, which was associated with decreased GSDMD cleavage and axon degeneration as well as improved motor performance of HD-intoxicated rats. Glyburide 15-28 NLR family, pyrin domain containing 3 Rattus norvegicus 57-62 32860822-4 2020 Interestingly, glybenclamide, a widely used inhibitor of NLRP3 inflammasome, significantly reduced NLRP3 inflammasome activation, which was associated with decreased GSDMD cleavage and axon degeneration as well as improved motor performance of HD-intoxicated rats. Glyburide 15-28 NLR family, pyrin domain containing 3 Rattus norvegicus 99-104 32860822-5 2020 Subsequently, we found that inhibition of NLRP3 inflammasome by glybenclamide attenuated macrophage infiltration, activation and M1 polarization in sciatic nerves of HD-intoxicated rats. Glyburide 64-77 NLR family, pyrin domain containing 3 Rattus norvegicus 42-47 32815401-6 2020 Repurposing of drugs such as glyburide that inhibit the aberrant upregulation of ion channels such as SUR1-TRPM4, and novel agents, such as ZT-a1, which re-establish physiological regulation of ion channels such as NKCC1/KCC, could be useful adjuvants to prevent and even reverse fluid accumulation in the brain parenchyma. Glyburide 29-38 ATP binding cassette subfamily C member 8 Homo sapiens 102-106 32048199-2 2020 The effect of the "NACHT, LRR and PYD domain containing protein 3" (NLRP3)-inflammasome/caspase-1/galectin-3 pathway and the potential benefits of NLRP3-inflammasome inhibitor glibenclamide (GLB) on atrial remodeling in the DM state are still unknown. Glyburide 176-189 NACHT, LRR and PYD domains-containing protein 3 Oryctolagus cuniculus 68-73 32048199-2 2020 The effect of the "NACHT, LRR and PYD domain containing protein 3" (NLRP3)-inflammasome/caspase-1/galectin-3 pathway and the potential benefits of NLRP3-inflammasome inhibitor glibenclamide (GLB) on atrial remodeling in the DM state are still unknown. Glyburide 191-194 NACHT, LRR and PYD domains-containing protein 3 Oryctolagus cuniculus 68-73 32048199-4 2020 Atrial caspase-1 activity as well as serum IL-1beta and IL-18 levels were elevated in diabetic animals but suppressed by GLB. Glyburide 121-124 caspase-1 Oryctolagus cuniculus 7-16 32048199-5 2020 Moreover, GLB decreased the DM-induced protein expression enhancement of NLRP3, Gal-3, TGF-beta1, and CaV1.2 according to western blot analysis. Glyburide 10-13 NACHT, LRR and PYD domains-containing protein 3 Oryctolagus cuniculus 73-78 32048199-5 2020 Moreover, GLB decreased the DM-induced protein expression enhancement of NLRP3, Gal-3, TGF-beta1, and CaV1.2 according to western blot analysis. Glyburide 10-13 galectin-3 Oryctolagus cuniculus 80-85 32048199-7 2020 NLRP3-inflammasome inhibitor GLB prevents AF inducibility and moderates atrial structural remodeling in DM. Glyburide 29-32 NACHT, LRR and PYD domains-containing protein 3 Oryctolagus cuniculus 0-5 32522579-0 2020 Glibenclamide attenuates 2,5-hexanedione-induced neurotoxicity in the spinal cord of rats through mitigation of NLRP3 inflammasome activation, neuroinflammation and oxidative stress. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 112-117 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 43-48 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 82-87 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 gasdermin D Rattus norvegicus 149-160 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 gasdermin D Rattus norvegicus 162-167 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 neurofilament light chain Rattus norvegicus 179-202 32522579-5 2020 Glibenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, reduced HD-induced NLRP3 inflammasome activation, which was associated with mitigated gasdermin D (GSDMD) cleavage, neurofilament protein L (NF-L) reduction and demyelination as well as axon degeneration in the spinal cord of rats. Glyburide 0-13 neurofilament light chain Rattus norvegicus 204-208 32522579-6 2020 Subsequently, we found that inhibition of NLRP3 inflammasome by glibenclamide suppressed microglial activation and M1 polarization and simultaneously recovered M2 polarization in HD-intoxicated rats. Glyburide 64-77 NLR family, pyrin domain containing 3 Rattus norvegicus 42-47 32522579-9 2020 Inhibition of NLRP3 inflammasome by glibenclamide might a potential avenue to combat n-hexane-induced neuropathy. Glyburide 36-49 NLR family, pyrin domain containing 3 Rattus norvegicus 14-19 32668327-7 2020 Furthermore, through its anti-inflammatory potential, glibenclamide reduced tumor necrosis factor-alpha level. Glyburide 54-67 tumor necrosis factor Mus musculus 76-103 32592753-0 2020 Glibenclamide transfer across the perfused human placenta is determined by albumin binding not transporter activity. Glyburide 0-13 albumin Homo sapiens 75-82 32592753-4 2020 In the presence of maternal and fetal albumin, BSP increased placental glibenclamide uptake from the fetal circulation by displacing glibenclamide from BSA, increasing the free fraction of glibenclamide driving diffusive transport. Glyburide 71-84 albumin Homo sapiens 38-45 32592753-4 2020 In the presence of maternal and fetal albumin, BSP increased placental glibenclamide uptake from the fetal circulation by displacing glibenclamide from BSA, increasing the free fraction of glibenclamide driving diffusive transport. Glyburide 133-146 albumin Homo sapiens 38-45 32592753-4 2020 In the presence of maternal and fetal albumin, BSP increased placental glibenclamide uptake from the fetal circulation by displacing glibenclamide from BSA, increasing the free fraction of glibenclamide driving diffusive transport. Glyburide 133-146 albumin Homo sapiens 38-45 32592753-6 2020 Computational modelling confirmed that albumin binding and not transporter activity, is the dominant factor in the transfer of glibenclamide across the human placenta. Glyburide 127-140 albumin Homo sapiens 39-46 32592753-7 2020 The effect of BSP binding to albumin on promoting the diffusive transfer of glibenclamide highlights the importance of drug-protein binding interactions and their interpretation using computational modelling. Glyburide 76-89 albumin Homo sapiens 29-36 32167222-0 2020 Glyburide attenuates ozone-induced pulmonary inflammation and injury by blocking the NLRP3 inflammasome. Glyburide 0-9 NLR family, pyrin domain containing 3 Mus musculus 85-90 31721320-12 2020 The isozymes CYP3A and CYP2C were found to be involved in the metabolism of glyburide. Glyburide 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 32829287-0 2020 Glyburide Regulates UCP1 Expression in Adipocytes Independent of KATP Channel Blockade. Glyburide 0-9 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 20-24 32829287-2 2020 Here we reported that, glyburide, one of the FDA-approved drugs currently used to treat type 2 diabetes, can significantly enhance UCP1 expression in both brown and white adipocytes. Glyburide 23-32 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 131-135 32829287-3 2020 Glyburide-fed mice exhibited a clear resistance to high-fat diet-induced obesity, reduced blood triglyceride level, and increased UCP1 expression in brown adipose tissue. Glyburide 0-9 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 130-134 32829287-4 2020 Moreover, in situ injection of glyburide to inguinal white adipose tissue remarkably enhanced UCP1 expression and increased thermogenesis. Glyburide 31-40 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 94-98 32829287-5 2020 Further mechanistic studies indicated that the glyburide effect in UCP1 expression in adipocytes was KATP channel independent but may involve the regulation of the Ca2+-Calcineurin-NFAT signal pathway. Glyburide 47-56 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 67-71 32829287-6 2020 Overall, our findings revealed the significant effects of glyburide in regulating UCP1 expression and thermogenesis in adipocytes, which can be potentially repurposed to treat obesity. Glyburide 58-67 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 82-86 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 NLR family, pyrin domain containing 3 Mus musculus 51-56 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 interleukin 18 Mus musculus 58-63 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 interleukin 1 alpha Mus musculus 69-77 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 NLR family, pyrin domain containing 3 Mus musculus 123-128 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 caspase 1 Mus musculus 164-173 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 S100 calcium binding protein A10 (calpactin) Mus musculus 174-177 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 interleukin 1 alpha Mus musculus 186-194 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 interleukin 1 alpha Mus musculus 186-194 32167222-9 2020 In addition, glyburide inhibited the expression of NLRP3, IL-18, and IL-1beta protein in lung tissues, and also suppressed NLRP3 inflammasome activation, including caspase-1 p10, active IL-1beta protein in lung tissues, IL-1beta, and IL-18 in BALF. Glyburide 13-22 interleukin 18 Mus musculus 234-239 32167222-10 2020 These results demonstrate that glyburide effectively attenuates ozone-induced pulmonary inflammation and injury via blocking the NLRP3 inflammasome. Glyburide 31-40 NLR family, pyrin domain containing 3 Mus musculus 129-134 32353421-8 2020 NEK7 depletion and treatment with glibenclamide or oridonin exerted anti-inflammatory effects that alleviated VILI by blocking the interaction between NEK7 and NLRP3, inhibiting NLRP3 inflammasome activation. Glyburide 34-47 NIMA (never in mitosis gene a)-related expressed kinase 7 Mus musculus 151-155 32372450-4 2020 Smooth muscle-specific expression of Kir6.1 gain-of-function mutant (GoF) subunits results in profound lymphatic contractile dysfunction and LSM hyperpolarization that is partially rescued by the KATP inhibitor, glibenclamide. Glyburide 212-225 potassium inwardly-rectifying channel, subfamily J, member 8 Mus musculus 37-43 32274916-10 2020 EVIDENCE SYNTHESIS: The discovery of the pathogenesis of most forms of congenital diabetes has made it possible to adapt the therapy to the diagnosis and in the forms of alteration of the potassium channels of the pancreatic Beta cels the switch from insulin to Glibenclamide per os has greatly improved the quality of life. Glyburide 262-275 insulin Homo sapiens 251-258 32353421-8 2020 NEK7 depletion and treatment with glibenclamide or oridonin exerted anti-inflammatory effects that alleviated VILI by blocking the interaction between NEK7 and NLRP3, inhibiting NLRP3 inflammasome activation. Glyburide 34-47 NLR family, pyrin domain containing 3 Mus musculus 160-165 32353421-8 2020 NEK7 depletion and treatment with glibenclamide or oridonin exerted anti-inflammatory effects that alleviated VILI by blocking the interaction between NEK7 and NLRP3, inhibiting NLRP3 inflammasome activation. Glyburide 34-47 NLR family, pyrin domain containing 3 Mus musculus 178-183 32353421-9 2020 NEK7 is a vital mediator of NLRP3 inflammasome activation, and glibenclamide or oridonin may be candidates for the development of new therapeutics against VILI driven by the interaction between NEK7 and NLRP3. Glyburide 63-76 NIMA (never in mitosis gene a)-related expressed kinase 7 Mus musculus 194-198 32353421-9 2020 NEK7 is a vital mediator of NLRP3 inflammasome activation, and glibenclamide or oridonin may be candidates for the development of new therapeutics against VILI driven by the interaction between NEK7 and NLRP3. Glyburide 63-76 NLR family, pyrin domain containing 3 Mus musculus 203-208 32202959-3 2020 Recently, glyburide, a hypoglycemic sulfonylurea, has been reported to reduce IL-1beta activation by suppressing activation of the NLRP3 inflammasome. Glyburide 10-19 NLR family pyrin domain containing 3 Homo sapiens 131-136 32606720-10 2020 The findings also showed that the plasma level of sulfonylureas (i.e., glibenclamide and gliclazide) was the highest in the patients with the CYP2C9*3 allele. Glyburide 71-84 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 142-148 32202959-3 2020 Recently, glyburide, a hypoglycemic sulfonylurea, has been reported to reduce IL-1beta activation by suppressing activation of the NLRP3 inflammasome. Glyburide 10-19 interleukin 1 alpha Homo sapiens 78-86 32202959-4 2020 Therefore, we evaluated the possibility of targeting the NLRP3 inflammasome pathway by glyburide to suppress periodontal pathogen-induced inflammation. Glyburide 87-96 NLR family pyrin domain containing 3 Homo sapiens 57-62 32202959-8 2020 Glyburide treatment suppressed IL-1beta expression in culture supernatants and enhanced intracellular IL-1beta expression, suggesting that glyburide may have inhibited IL-1beta secretion. Glyburide 0-9 interleukin 1 alpha Homo sapiens 31-39 32202959-8 2020 Glyburide treatment suppressed IL-1beta expression in culture supernatants and enhanced intracellular IL-1beta expression, suggesting that glyburide may have inhibited IL-1beta secretion. Glyburide 0-9 interleukin 1 alpha Homo sapiens 102-110 32202959-8 2020 Glyburide treatment suppressed IL-1beta expression in culture supernatants and enhanced intracellular IL-1beta expression, suggesting that glyburide may have inhibited IL-1beta secretion. Glyburide 0-9 interleukin 1 alpha Homo sapiens 102-110 32452426-0 2020 Glibenclamide alters interleukin-8 and interleukin-1beta of primary human monocytes from diabetes patients against Mycobacterium tuberculosis infection. Glyburide 0-13 C-X-C motif chemokine ligand 8 Homo sapiens 21-34 32452426-0 2020 Glibenclamide alters interleukin-8 and interleukin-1beta of primary human monocytes from diabetes patients against Mycobacterium tuberculosis infection. Glyburide 0-13 interleukin 1 beta Homo sapiens 39-56 32452426-2 2020 Our previous study showed glibenclamide, an anti-diabetic drug used to control blood glucose concentration, reduced interleukin (IL)-8 secretion from primary human monocytes challenged with M. tuberculosis (Mtb). Glyburide 26-39 C-X-C motif chemokine ligand 8 Homo sapiens 116-134 32452426-4 2020 We hypothesize that glibenclamide may also interfere with monocyte mediated immune responses against Mtb and alter the balance between IL-1beta and IFNalpha-mediated immunity. Glyburide 20-33 interleukin 1 alpha Homo sapiens 135-143 32452426-6 2020 We demonstrate that monocytes from diabetes patients who were being treated with glibenclamide showed reduced IL-1beta and IL-8 secretion when exposed to Mtb. Glyburide 81-94 interleukin 1 alpha Homo sapiens 110-118 32452426-6 2020 We demonstrate that monocytes from diabetes patients who were being treated with glibenclamide showed reduced IL-1beta and IL-8 secretion when exposed to Mtb. Glyburide 81-94 C-X-C motif chemokine ligand 8 Homo sapiens 123-127 32452426-9 2020 Taken together, our data show that glibenclamide might exacerbate susceptibility of diabetes patients to Mtb infection by reducing IL-1beta and IL-8 production by monocytes. Glyburide 35-48 interleukin 1 alpha Homo sapiens 131-139 32452426-9 2020 Taken together, our data show that glibenclamide might exacerbate susceptibility of diabetes patients to Mtb infection by reducing IL-1beta and IL-8 production by monocytes. Glyburide 35-48 C-X-C motif chemokine ligand 8 Homo sapiens 144-148 32930209-5 2020 By applying the flower-like Ag@MIPs as an efficient and ultra-sensitive SERS platform, glibenclamide was quantitatively detected in trace concentrations as low as 1 ng mL-1. Glyburide 87-100 L1 cell adhesion molecule Mus musculus 168-172 32229236-0 2020 Glibenclamide inhibits BK polyomavirus infection in kidney cells through CFTR blockade. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 73-77 32229236-5 2020 Disrupting CFTR function through treatment with the clinically available drug glibenclamide, the CFTR inhibitor CFTR172, or CFTR-silencing, all reduced BKPyV infection. Glyburide 78-91 CF transmembrane conductance regulator Homo sapiens 11-15 32153049-3 2020 NLRP3 inflammasomes have been linked to IL-1beta expression, but it is currently unclear whether glyburide, the inhibiter of NLRP3 inflammasome, suppresses occlusal trauma in rats. Glyburide 97-106 NLR family, pyrin domain containing 3 Rattus norvegicus 125-130 32153049-6 2020 In the trauma + glyburide group, the NLRP3 inhibitor glyburide was administered orally every 24 hours from 1 day before induction of occlusal trauma. Glyburide 53-62 NLR family, pyrin domain containing 3 Rattus norvegicus 37-42 32483763-8 2020 The OATP2B1 inhibitors, including atorvastatin, bromosulfophthalein, glibenclamide, sulfasalazine, talinolol, and estrone 3-sulfate, inhibited the DBF and the 5-CF transport. Glyburide 69-82 solute carrier organic anion transporter family member 2B1 Homo sapiens 4-11 31834465-0 2020 NLRP3 inhibitor glibenclamide attenuates high-fat diet and streptozotocin-induced non-alcoholic fatty liver disease in rat: studies on oxidative stress, inflammation, DNA damage and insulin signalling pathway. Glyburide 16-29 NLR family, pyrin domain containing 3 Rattus norvegicus 0-5 32442232-16 2020 Glyburide-exposed neonates were heavier at birth (58.20 g, 95% confidence interval [CI] 10.10-106.31, p = 0.02) with increased risk of macrosomia (odds ratio [OR] 1.38, 95% CI 1.01-1.89, p = 0.04) versus neonates of insulin-treated mothers. Glyburide 0-9 insulin Homo sapiens 216-223 32442232-19 2020 Glyburide-exposed neonates had a nonsignificant increase in total fat mass (103.2 g, 95% CI -3.91 to 210.31, p = 0.06) and increased abdominal (0.90 cm, 95% CI 0.03-1.77, p = 0.04) and chest circumferences (0.80 cm, 95% CI 0.07-1.53, p = 0.03) versus insulin-exposed neonates. Glyburide 0-9 insulin Homo sapiens 251-258 32375810-13 2020 Furthermore, inhibition of NLRP3 inflammasome by glybenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, was found to be able to suppress microglial proinflammatory activation and nuclear factor-kappaB activation induced by paraquat and maneb. Glyburide 49-62 NLR family, pyrin domain containing 3 Mus musculus 27-32 32375810-13 2020 Furthermore, inhibition of NLRP3 inflammasome by glybenclamide, a sulfonylurea inhibitor of NLRP3 inflammasome, was found to be able to suppress microglial proinflammatory activation and nuclear factor-kappaB activation induced by paraquat and maneb. Glyburide 49-62 NLR family, pyrin domain containing 3 Mus musculus 92-97 32375810-14 2020 Moreover, reduced reactive oxygen species production, NADPH oxidase, and inducible nitric oxide synthase expressions as well as 4-hydroxynonenal and malondialdehyde levels were detected in combined glybenclamide and paraquat and maneb-treated mice compared with paraquat and maneb alone group. Glyburide 198-211 nitric oxide synthase 2, inducible Mus musculus 73-104 32375810-15 2020 Finally, we found that glybenclamide treatment ameliorated LC/NE neurodegeneration and alpha-synuclein aggregation in paraquat and maneb-treated mice. Glyburide 23-36 synuclein, alpha Mus musculus 87-102 31714001-4 2020 Since glyburide (a specific inhibitor of K+ efflux channels) inhibited the transcription of NLRP3, IL-1beta, and IL-18, the role of K+ efflux in the activation of inflammasomes in APOL1 risk milieu was implicated. Glyburide 6-15 NLR family pyrin domain containing 3 Homo sapiens 92-97 31714001-4 2020 Since glyburide (a specific inhibitor of K+ efflux channels) inhibited the transcription of NLRP3, IL-1beta, and IL-18, the role of K+ efflux in the activation of inflammasomes in APOL1 risk milieu was implicated. Glyburide 6-15 interleukin 1 beta Homo sapiens 99-107 31714001-4 2020 Since glyburide (a specific inhibitor of K+ efflux channels) inhibited the transcription of NLRP3, IL-1beta, and IL-18, the role of K+ efflux in the activation of inflammasomes in APOL1 risk milieu was implicated. Glyburide 6-15 interleukin 18 Homo sapiens 113-118 31714001-4 2020 Since glyburide (a specific inhibitor of K+ efflux channels) inhibited the transcription of NLRP3, IL-1beta, and IL-18, the role of K+ efflux in the activation of inflammasomes in APOL1 risk milieu was implicated. Glyburide 6-15 apolipoprotein L1 Homo sapiens 180-185 32500072-9 2020 Glibenclamide, a classic KATP channel blocker that inhibits the efflux of HSP70 from cytoplasm to extracellular environment, or HSP70 overexpression in neurons, could markedly suppress morphine-induced ER stress and hyperalgesia. Glyburide 0-13 heat shock protein family A (Hsp70) member 4 Homo sapiens 74-79 32229156-5 2020 To assess whether L-isoleucine, calcitriol, phenyl butyrate, metformin, glyburide or insulin induced RNase 7, keratinocytes were stimulated, and RNase 7 expression was evaluated. Glyburide 72-81 ribonuclease A family member 7 Homo sapiens 101-108 32229156-7 2020 Since most of the DM2 patients are treated with drugs to reduce glycemia, we investigated whether glyburide, metformin or insulin were able to induce any change regarding RNase 7 production. Glyburide 98-107 ribonuclease A family member 7 Homo sapiens 171-178 31834465-3 2020 Glibenclamide (GLB) is a potent NLRP3 inflammasome inhibitor and possesses anti-inflammatory and anti-oxidant properties. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 32-37 31834465-3 2020 Glibenclamide (GLB) is a potent NLRP3 inflammasome inhibitor and possesses anti-inflammatory and anti-oxidant properties. Glyburide 15-18 NLR family, pyrin domain containing 3 Rattus norvegicus 32-37 31834465-10 2020 Immunohistochemical and immunoblotting findings showed that GLB improved the hepatic expressions of inflammatory markers (NLRP3, ASC, caspase-1, IL-1beta, NF-kappaB), anti-oxidant markers (SOD, catalase) and insulin signalling markers (p-AKT, p-GSK-3beta, p-IRS). Glyburide 60-63 NLR family, pyrin domain containing 3 Rattus norvegicus 122-127 31834465-10 2020 Immunohistochemical and immunoblotting findings showed that GLB improved the hepatic expressions of inflammatory markers (NLRP3, ASC, caspase-1, IL-1beta, NF-kappaB), anti-oxidant markers (SOD, catalase) and insulin signalling markers (p-AKT, p-GSK-3beta, p-IRS). Glyburide 60-63 PYD and CARD domain containing Rattus norvegicus 129-132 31834465-10 2020 Immunohistochemical and immunoblotting findings showed that GLB improved the hepatic expressions of inflammatory markers (NLRP3, ASC, caspase-1, IL-1beta, NF-kappaB), anti-oxidant markers (SOD, catalase) and insulin signalling markers (p-AKT, p-GSK-3beta, p-IRS). Glyburide 60-63 caspase 1 Rattus norvegicus 134-143 31834465-10 2020 Immunohistochemical and immunoblotting findings showed that GLB improved the hepatic expressions of inflammatory markers (NLRP3, ASC, caspase-1, IL-1beta, NF-kappaB), anti-oxidant markers (SOD, catalase) and insulin signalling markers (p-AKT, p-GSK-3beta, p-IRS). Glyburide 60-63 interleukin 1 beta Rattus norvegicus 145-153 31834465-10 2020 Immunohistochemical and immunoblotting findings showed that GLB improved the hepatic expressions of inflammatory markers (NLRP3, ASC, caspase-1, IL-1beta, NF-kappaB), anti-oxidant markers (SOD, catalase) and insulin signalling markers (p-AKT, p-GSK-3beta, p-IRS). Glyburide 60-63 catalase Rattus norvegicus 194-202 32224233-5 2020 In diabetic patients, oral antidiabetic drugs (glyburide, metformin or pioglitazone) reduced circulating levels fractalkine and E-selectin (both P < .05), without affecting vascular responses (all P > .05). Glyburide 47-56 C-X3-C motif chemokine ligand 1 Homo sapiens 112-123 32086630-4 2020 METHODS: We performed accumulation assays with Hoechst 33342 (a model dual substrate of ABCB1 and ABCG2) and bi-directional transport studies with the ABCG2 substrate [3H]glyburide in transduced MDCKII cells, accumulation studies in choriocarcinoma-derived BeWo cells, and in situ dual perfusions of rat term placenta with glyburide. Glyburide 171-180 ATP binding cassette subfamily G member 2 Canis lupus familiaris 151-156 31957808-5 2020 The Kir6.2-D323K mutation gave rise to a constitutively active, glibenclamide and ATP-insensitive KATP complex, further confirming the importance of information transfer between the Kir6 and SUR2 subunits. Glyburide 64-77 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 4-10 31957808-5 2020 The Kir6.2-D323K mutation gave rise to a constitutively active, glibenclamide and ATP-insensitive KATP complex, further confirming the importance of information transfer between the Kir6 and SUR2 subunits. Glyburide 64-77 ATP binding cassette subfamily C member 9 Homo sapiens 191-195 33728270-7 2021 Results and conclusion: APE, like glibenclamide and metformin, showed significant hypoglycaemic effect. Glyburide 34-47 apurinic/apyrimidinic endonuclease 1 Mus musculus 24-27 31733313-10 2020 In contrast, GBC treatment improved memory impairment, increased insulin, and reduced glucose and hippocampal inflammation in rats with T2D and sporadic AD. Glyburide 13-16 insulin Homo sapiens 65-72 31851526-0 2020 TRPM4 channel inhibitors 9-phenanthrol and glibenclamide differentially decrease guinea pig detrusor smooth muscle whole-cell cation currents and phasic contractions. Glyburide 43-56 LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily M member 4 Cavia porcellus 0-5 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 159-165 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 171-175 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 176-181 31811853-0 2020 Glibenclamide ameliorates transplant-induced arteriosclerosis and inhibits macrophage migration and MCP-1 expression. Glyburide 0-13 chemokine (C-C motif) ligand 2 Mus musculus 100-105 31811853-9 2020 Furthermore, glibenclamide inhibited macrophage expression and secretion of inflammatory factors in vitro through suppressing activation of the nuclear factor-kappaB (NF-kappaB) pathway and MCP-1 production. Glyburide 13-26 chemokine (C-C motif) ligand 2 Mus musculus 190-195 31811853-10 2020 CONCLUSION: Glibenclamide protected against aorta transplantation-induced arteriosclerosis by reducing inflammatory factors in vivo and inhibited macrophage migration and MCP-1 production in vitro. Glyburide 12-25 chemokine (C-C motif) ligand 2 Mus musculus 171-176 31936452-4 2020 Targeted SUR1-TRPM4 channel inhibition with glibenclamide has been shown to reduce edema and progression of hemorrhage, particularly in preclinical models of contusional TBI. Glyburide 44-57 ATP binding cassette subfamily C member 8 Homo sapiens 9-13 31936452-4 2020 Targeted SUR1-TRPM4 channel inhibition with glibenclamide has been shown to reduce edema and progression of hemorrhage, particularly in preclinical models of contusional TBI. Glyburide 44-57 transient receptor potential cation channel subfamily M member 4 Homo sapiens 14-19 31936452-7 2020 In this comprehensive narrative review, we summarize the molecular basis of SUR1-TRPM4 related pathology and discuss TBI-specific expression patterns, biomarker potential, genetic variation, preclinical experiments, and clinical studies evaluating the utility of treatment with glibenclamide in this disease. Glyburide 278-291 ATP binding cassette subfamily C member 8 Homo sapiens 76-80 31655149-11 2020 Induction of diabetes increased FGF21 levels and both of the treatments could reduce its contents, however, glibenclamide was more effective than HESS. Glyburide 108-121 fibroblast growth factor 21 Rattus norvegicus 32-37 31761320-0 2020 Diethylnitrosamine and thioacetamide-induced hepatic damage and early carcinogenesis in rats: Role of Nrf2 activator dimethyl fumarate and NLRP3 inhibitor glibenclamide. Glyburide 155-168 NLR family, pyrin domain containing 3 Rattus norvegicus 139-144 31761320-3 2020 Glibenclamide (GLB), a sulphonylurea drug used to treat type II diabetes, possesses anti-inflammatory properties and inhibits NLRP3 inflammasomes. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 126-131 31761320-3 2020 Glibenclamide (GLB), a sulphonylurea drug used to treat type II diabetes, possesses anti-inflammatory properties and inhibits NLRP3 inflammasomes. Glyburide 15-18 NLR family, pyrin domain containing 3 Rattus norvegicus 126-131 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 NFE2 like bZIP transcription factor 2 Rattus norvegicus 105-109 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 heme oxygenase 1 Rattus norvegicus 111-115 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 superoxide dismutase 1 Rattus norvegicus 117-122 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 catalase Rattus norvegicus 124-132 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 NLR family, pyrin domain containing 3 Rattus norvegicus 160-165 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 PYD and CARD domain containing Rattus norvegicus 167-170 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 caspase 1 Rattus norvegicus 172-181 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 transforming growth factor, beta 1 Rattus norvegicus 196-205 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 glutathione S-transferase pi 1 Rattus norvegicus 256-261 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 hepatocyte growth factor Rattus norvegicus 263-266 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 MET proto-oncogene, receptor tyrosine kinase Rattus norvegicus 268-273 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 transforming growth factor alpha Rattus norvegicus 275-283 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 epidermal growth factor Rattus norvegicus 285-288 31761320-6 2020 DMF and GLB intervention significantly ameliorated the DEN + TAA-induced alterations in the antioxidant (Nrf2, HO-1, SOD-1, catalase), inflammatory (NF-kappaB, NLRP3, ASC, caspase-1), fibrogenic (TGF-beta1, collagen) and regenerative proliferative stress (GST-p, HGF, c-MET, TGFalpha, EGF, AFP) markers. Glyburide 8-11 alpha-fetoprotein Rattus norvegicus 290-293 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 71-74 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 112-116 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 117-123 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 125-137 31899311-2 2020 Glibenclamide is a potent inhibitor of numerous sulfonylurea receptor (SUR)-regulated channels, including KATP (SUR1-KIR6.2, SUR2A-KIR6.2, SUR2B-KIR6.2, SUR2B-KIR6.1) and SUR1-TRPM4. Glyburide 0-13 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 139-151 31989292-6 2020 The pooled estimate showed that glyburide significantly decreased the need for cesarean section (OR = 0.87, 95% CI [0.82, 0.92], p < 0.0001), fasting blood glucose (MD - 5.63 mg/dL, 95% CI [- 10.97, - 0.28], p = 0.04), and Apgar score at 5 min (MD - 0.30, 95% CI [- 0.36, - 0.23], p < 0.001) than insulin. Glyburide 32-41 insulin Homo sapiens 303-310 31989292-7 2020 However, glyburide significantly increased the risk of neonatal hypoglycemia (OR = 1.42, 95% CI [1.03, 1.95], p = 0.03) and neonatal intensive care unit admission duration (NICU) (MD 4.26 days, 95% CI [2.65, 5.86], p < 0.01) compared to insulin. Glyburide 9-18 insulin Homo sapiens 240-247 32793438-2 2020 The current study was undertaken to evaluate the effects of hydroalcoholic extract of S. securidaca seeds (HESS) alone, and in combination with a standard drug, glibenclamide (GB) on paraoxonase1 (PON1) activity, lipid profile and peroxidation, and cardiovascular risk indices in streptozotocin (STZ) induced diabetic rats. Glyburide 161-174 paraoxonase 1 Rattus norvegicus 183-195 32793438-2 2020 The current study was undertaken to evaluate the effects of hydroalcoholic extract of S. securidaca seeds (HESS) alone, and in combination with a standard drug, glibenclamide (GB) on paraoxonase1 (PON1) activity, lipid profile and peroxidation, and cardiovascular risk indices in streptozotocin (STZ) induced diabetic rats. Glyburide 161-174 paraoxonase 1 Rattus norvegicus 197-201 32793438-2 2020 The current study was undertaken to evaluate the effects of hydroalcoholic extract of S. securidaca seeds (HESS) alone, and in combination with a standard drug, glibenclamide (GB) on paraoxonase1 (PON1) activity, lipid profile and peroxidation, and cardiovascular risk indices in streptozotocin (STZ) induced diabetic rats. Glyburide 176-178 paraoxonase 1 Rattus norvegicus 183-195 32793438-8 2020 However, the higher doses (200 and 400 mg/kg) alone and in combination with GB could significantly improve lipid profile, restore PON1 activity, and decrease cardiovascular risk indices, MDA, as well. Glyburide 76-78 paraoxonase 1 Rattus norvegicus 130-134 31542963-11 2020 The effects of H2S were significantly antagonized by administration of glibenclamide as KATP channel blocker, Nomega-nitro-l-arginine, as eNOS inhibitor, or ruthenium red, as transient receptor potential vanilloid 1 (TRPV1) antagonist. Glyburide 71-84 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 175-215 33442181-2 2020 We report the first DEND syndrome in Malaysia with heterozygous missense mutation Q52R at KCNJ11 (Kir6.2) gene with delayed presentation beyond 6 months of age and failure to transition to glibenclamide. Glyburide 189-202 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 90-96 33442181-2 2020 We report the first DEND syndrome in Malaysia with heterozygous missense mutation Q52R at KCNJ11 (Kir6.2) gene with delayed presentation beyond 6 months of age and failure to transition to glibenclamide. Glyburide 189-202 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 98-104 31704276-1 2020 Glibenclamide protects against ischemic injury in both preclinical and clinical studies, presumably by blocking the de novo assembled sulfonylurea receptor 1-transient receptor potential M4 (Sur1-Trpm4) channel induced by ischemia. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 191-195 31704276-1 2020 Glibenclamide protects against ischemic injury in both preclinical and clinical studies, presumably by blocking the de novo assembled sulfonylurea receptor 1-transient receptor potential M4 (Sur1-Trpm4) channel induced by ischemia. Glyburide 0-13 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 196-201 31931306-1 2020 INTRODUCTION: Glyburide is an approved anti-diabetes drug binding to the sulfonylurea receptors-1 (SUR-1) and substrate of solute carrier (SLC) transporters, which can be isotopically radiolabelled with carbon-11 for PET imaging. Glyburide 14-23 ATP binding cassette subfamily C member 8 Homo sapiens 73-97 31931306-1 2020 INTRODUCTION: Glyburide is an approved anti-diabetes drug binding to the sulfonylurea receptors-1 (SUR-1) and substrate of solute carrier (SLC) transporters, which can be isotopically radiolabelled with carbon-11 for PET imaging. Glyburide 14-23 ATP binding cassette subfamily C member 8 Homo sapiens 99-104 32224233-5 2020 In diabetic patients, oral antidiabetic drugs (glyburide, metformin or pioglitazone) reduced circulating levels fractalkine and E-selectin (both P < .05), without affecting vascular responses (all P > .05). Glyburide 47-56 selectin E Homo sapiens 128-138 31742116-5 2019 Prolactin serum levels were higher in glyburide-treated patients compared with metformin-treated patients (P < 0.01). Glyburide 38-47 prolactin Homo sapiens 0-9 31678606-3 2019 By contrast, the inhibition of inward rectifier K+ (Kir) channels by pretreatment with barium (Ba2+), large-conductance calcium (Ca2+)-activated K+ (BKCa) channels with paxilline, and adenosine triphosphate (ATP)-sensitive K+ (KATP) channels with glibenclamide did not change this effect. Glyburide 247-260 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 52-55 31341030-0 2019 Glibenclamide targets sulfonylurea receptor 1 to inhibit p70S6K activity and upregulate KLF4 expression to suppress non-small-cell lung carcinoma. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 22-45 31341030-0 2019 Glibenclamide targets sulfonylurea receptor 1 to inhibit p70S6K activity and upregulate KLF4 expression to suppress non-small-cell lung carcinoma. Glyburide 0-13 ribosomal protein S6 kinase B1 Homo sapiens 57-63 31341030-0 2019 Glibenclamide targets sulfonylurea receptor 1 to inhibit p70S6K activity and upregulate KLF4 expression to suppress non-small-cell lung carcinoma. Glyburide 0-13 Kruppel like factor 4 Homo sapiens 88-92 31341030-1 2019 Sulfonylurea receptor 1 (SUR1) is the regulatory subunit of ATP-sensitive potassium channels (KATP channels) and the receptor of antidiabetic drugs, such as glibenclamide, that induce insulin secretion in pancreatic beta cells. Glyburide 157-170 ATP binding cassette subfamily C member 8 Homo sapiens 0-23 31341030-1 2019 Sulfonylurea receptor 1 (SUR1) is the regulatory subunit of ATP-sensitive potassium channels (KATP channels) and the receptor of antidiabetic drugs, such as glibenclamide, that induce insulin secretion in pancreatic beta cells. Glyburide 157-170 ATP binding cassette subfamily C member 8 Homo sapiens 25-29 31341030-5 2019 Targeting SUR1 with glibenclamide suppressed cell growth, cell cycle progression, the epithelial-mesenchymal transition, and cell migration. Glyburide 20-33 ATP binding cassette subfamily C member 8 Homo sapiens 10-14 31341030-7 2019 Additionally, glibenclamide inhibited p70S6K, and overexpression of p70S6K partially reversed the growth-inhibiting effect of glibenclamide. Glyburide 14-27 ribosomal protein S6 kinase B1 Homo sapiens 38-44 31341030-7 2019 Additionally, glibenclamide inhibited p70S6K, and overexpression of p70S6K partially reversed the growth-inhibiting effect of glibenclamide. Glyburide 126-139 ribosomal protein S6 kinase B1 Homo sapiens 68-74 31341030-8 2019 Furthermore, glibenclamide upregulated the expression of the tumor suppressor Kruppel-like factor 4 (KLF4), and silencing KLF4 partially reversed the inhibitory effect of glibenlcamide on cell growth, the EMT, and migration. Glyburide 13-26 Kruppel like factor 4 Homo sapiens 78-99 31341030-8 2019 Furthermore, glibenclamide upregulated the expression of the tumor suppressor Kruppel-like factor 4 (KLF4), and silencing KLF4 partially reversed the inhibitory effect of glibenlcamide on cell growth, the EMT, and migration. Glyburide 13-26 Kruppel like factor 4 Homo sapiens 101-105 31341030-10 2019 Finally, in xenograft mouse models, SUR1 expression silencing or glibenclamide treatment inhibited the growth of A549 tumors, downregulated p70S6K activity, and upregulated KLF4 expression. Glyburide 65-78 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 140-146 31341030-10 2019 Finally, in xenograft mouse models, SUR1 expression silencing or glibenclamide treatment inhibited the growth of A549 tumors, downregulated p70S6K activity, and upregulated KLF4 expression. Glyburide 65-78 Kruppel-like factor 4 (gut) Mus musculus 173-177 31341030-12 2019 Targeting SUR1 with glibenclamide inhibited NSCLC through downregulation of p70S6K activity and subsequent upregulationof the expression of the tumor suppressor gene KLF4. Glyburide 20-33 ATP binding cassette subfamily C member 8 Homo sapiens 10-14 31341030-12 2019 Targeting SUR1 with glibenclamide inhibited NSCLC through downregulation of p70S6K activity and subsequent upregulationof the expression of the tumor suppressor gene KLF4. Glyburide 20-33 ribosomal protein S6 kinase B1 Homo sapiens 76-82 31341030-12 2019 Targeting SUR1 with glibenclamide inhibited NSCLC through downregulation of p70S6K activity and subsequent upregulationof the expression of the tumor suppressor gene KLF4. Glyburide 20-33 Kruppel like factor 4 Homo sapiens 166-170 31341030-13 2019 SUR1 can be developed as a new target for cancer therapy and glibenclamide has potential anticancer effects. Glyburide 61-74 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 31386893-8 2019 The augmentation of NaHS-induced ANP secretion during hypoxia was blocked by the pretreatment with KATP channel blocker (glibenclamide) and was enhanced by the pretreatment with KATP channel activator (pinacidil). Glyburide 121-134 natriuretic peptide A Rattus norvegicus 33-36 31292311-0 2019 The differential influence of glimepiride and glibenclamide on insulin resistance and adiponectin levels in patients with type 2 diabetes. Glyburide 46-59 insulin Homo sapiens 63-70 31292311-8 2019 The serum adiponectin and HOMA-IR were inversely correlated within the group of glibenclamide (r = -0.667, p = 0.009). Glyburide 80-93 adiponectin, C1Q and collagen domain containing Homo sapiens 10-21 31601596-3 2019 Preclinical studies evaluating the use of the Food and Drug Administration-approved sulfonylurea receptor 1-transient receptor potential melastatin 4 channel blocker glyburide in rodent models have shown reduced secondary microhaemorrhage formation and the absence of capillary fragmentation, the pathological hallmark of PHN. Glyburide 166-175 ATP binding cassette subfamily C member 8 Homo sapiens 84-107 31408377-7 2019 In patients with T2D enrolled in the intervention trial, antidiabetic treatment with either glyburide, metformin or pioglitazone resulted in significant reduction of circulating OPG (P=0.001), without changes in the other biomarkers and vasodilator responses (all P>0.05). Glyburide 92-101 TNF receptor superfamily member 11b Homo sapiens 178-181 31780397-7 2019 Glibenclamide inhibited glucagon secretion from islets and the alpha- and beta-mixed cell-aggregates, but not from the alpha-cell-only aggregates, at 2.0 mM glucose. Glyburide 0-13 glucagon Homo sapiens 24-32 31623469-3 2019 Glibenclamide, a sulfonylurea drug and potent inhibitor of SUR1-TRPM4, was reformulated for intravenous injection, known as BIIB093. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 59-63 31623469-3 2019 Glibenclamide, a sulfonylurea drug and potent inhibitor of SUR1-TRPM4, was reformulated for intravenous injection, known as BIIB093. Glyburide 0-13 transient receptor potential cation channel subfamily M member 4 Homo sapiens 64-69 31479156-10 2019 The macrosomia rate was higher in the glibenclamide-exposed group than the insulin-alone group (12.2% vs 0%, P=0.025). Glyburide 38-51 insulin Homo sapiens 75-82 31885478-12 2019 The current study suggests that OL and GLB combination could cause herb-drug interactions through modulation of insulin receptor (INR), glucose transporter 2 (Slc2a2) and peroxisome proliferator-activated receptor alpha (PPAR-alpha) genes expression in the liver of diabetic rats. Glyburide 39-42 insulin receptor Rattus norvegicus 112-128 31885478-12 2019 The current study suggests that OL and GLB combination could cause herb-drug interactions through modulation of insulin receptor (INR), glucose transporter 2 (Slc2a2) and peroxisome proliferator-activated receptor alpha (PPAR-alpha) genes expression in the liver of diabetic rats. Glyburide 39-42 insulin receptor Rattus norvegicus 130-133 31885478-12 2019 The current study suggests that OL and GLB combination could cause herb-drug interactions through modulation of insulin receptor (INR), glucose transporter 2 (Slc2a2) and peroxisome proliferator-activated receptor alpha (PPAR-alpha) genes expression in the liver of diabetic rats. Glyburide 39-42 solute carrier family 2 member 2 Rattus norvegicus 159-165 31885478-12 2019 The current study suggests that OL and GLB combination could cause herb-drug interactions through modulation of insulin receptor (INR), glucose transporter 2 (Slc2a2) and peroxisome proliferator-activated receptor alpha (PPAR-alpha) genes expression in the liver of diabetic rats. Glyburide 39-42 peroxisome proliferator activated receptor alpha Rattus norvegicus 171-219 31885478-12 2019 The current study suggests that OL and GLB combination could cause herb-drug interactions through modulation of insulin receptor (INR), glucose transporter 2 (Slc2a2) and peroxisome proliferator-activated receptor alpha (PPAR-alpha) genes expression in the liver of diabetic rats. Glyburide 39-42 peroxisome proliferator activated receptor alpha Rattus norvegicus 221-231 31477246-0 2019 NLRP3 inflammasome inhibitor glyburide expedites diabetic-induced impaired fracture healing. Glyburide 29-38 NLR family, pyrin domain containing 3 Mus musculus 0-5 31477246-2 2019 The present study aims to investigate the therapeutic effects of glyburide, an NLRP3 inflammasome inhibitor, in a diabetic-induced fracture model. Glyburide 65-74 NLR family, pyrin domain containing 3 Mus musculus 79-84 31477246-8 2019 Our results showed that treatment of glyburide significantly decreased the expressions of IFN-gamma, TNF-alpha, and IL-6 in the fracture calluses in diabetic-induced fracture model, while bone callus volume and bone volume fraction were increased. Glyburide 37-46 interferon gamma Mus musculus 90-99 31477246-8 2019 Our results showed that treatment of glyburide significantly decreased the expressions of IFN-gamma, TNF-alpha, and IL-6 in the fracture calluses in diabetic-induced fracture model, while bone callus volume and bone volume fraction were increased. Glyburide 37-46 tumor necrosis factor Mus musculus 101-110 31477246-8 2019 Our results showed that treatment of glyburide significantly decreased the expressions of IFN-gamma, TNF-alpha, and IL-6 in the fracture calluses in diabetic-induced fracture model, while bone callus volume and bone volume fraction were increased. Glyburide 37-46 interleukin 6 Mus musculus 116-120 31537189-10 2019 Treatment with intravenous glibenclamide was associated with reduced NWU (beta=-2.80; 95% CI, -5.07 to -0.53; P=0.016) and reduced MLS (beta=-1.50; 95% CI, -2.71 to -0.28; P=0.016). Glyburide 27-40 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 74-81 31537189-10 2019 Treatment with intravenous glibenclamide was associated with reduced NWU (beta=-2.80; 95% CI, -5.07 to -0.53; P=0.016) and reduced MLS (beta=-1.50; 95% CI, -2.71 to -0.28; P=0.016). Glyburide 27-40 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 136-143 30874987-8 2019 However, further addition of glibenclamide, a CFTR channel blocker, abolished lubiprostone-evoked HCO3- secretion. Glyburide 29-42 cystic fibrosis transmembrane conductance regulator Mus musculus 46-50 30805250-6 2019 A significant increase in the AST, ALT and ALP levels (P < 0.05) was observed in the diabetic control and in the experimental groups with glibenclamide which was also significantly (P < 0.05) lowered after treatment with extracts at special doses. Glyburide 141-154 PDZ and LIM domain 3 Rattus norvegicus 43-46 31620350-10 2019 PRL serum level was high in glyburide-treated patients as compared with metformin-treated patients (P = 0.002). Glyburide 28-37 prolactin Homo sapiens 0-3 31184597-8 2019 Pull-down and co-immunoprecipitation experiments showed that Barr1 can directly interact with Epac2 and that SUs such as glibenclamide promote Barr1/Epac2 complex formation, triggering enhanced Rap1 signaling and insulin secretion. Glyburide 121-134 Rap guanine nucleotide exchange factor (GEF) 4 Mus musculus 94-99 31184597-8 2019 Pull-down and co-immunoprecipitation experiments showed that Barr1 can directly interact with Epac2 and that SUs such as glibenclamide promote Barr1/Epac2 complex formation, triggering enhanced Rap1 signaling and insulin secretion. Glyburide 121-134 Rap guanine nucleotide exchange factor (GEF) 4 Mus musculus 149-154 31184597-8 2019 Pull-down and co-immunoprecipitation experiments showed that Barr1 can directly interact with Epac2 and that SUs such as glibenclamide promote Barr1/Epac2 complex formation, triggering enhanced Rap1 signaling and insulin secretion. Glyburide 121-134 RAS-related protein 1a Mus musculus 194-198 31042750-5 2019 Glibenclamide, a hypoglycemic agent that inhibits Sur1-Trpm4, has been shown to reduce BBB damage and edema following infusion of autologous blood into the brain (ICH) as well as after other brain injuries. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 50-54 31042750-5 2019 Glibenclamide, a hypoglycemic agent that inhibits Sur1-Trpm4, has been shown to reduce BBB damage and edema following infusion of autologous blood into the brain (ICH) as well as after other brain injuries. Glyburide 0-13 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 55-60 30706637-7 2019 The effect of operative factors such as pH, buffer, contact time and concentration of CdTe QDs were investigated and in the optimized condition, a linear increase was achieved for the emission intensity of QDs by increasing GB concentration in the range 49-345 ng mL-1 , with a detection limit of 17.84 ng mL-1 . Glyburide 224-226 L1 cell adhesion molecule Mus musculus 264-268 30706637-7 2019 The effect of operative factors such as pH, buffer, contact time and concentration of CdTe QDs were investigated and in the optimized condition, a linear increase was achieved for the emission intensity of QDs by increasing GB concentration in the range 49-345 ng mL-1 , with a detection limit of 17.84 ng mL-1 . Glyburide 224-226 L1 cell adhesion molecule Mus musculus 306-310 31516323-13 2019 Moreover, GLB plus MCFE-500 was the most efficient in restoring INR, Slc2a2 and PPAR-alpha mRNA expression to their normal levels. Glyburide 10-13 insulin receptor Rattus norvegicus 64-67 31516323-13 2019 Moreover, GLB plus MCFE-500 was the most efficient in restoring INR, Slc2a2 and PPAR-alpha mRNA expression to their normal levels. Glyburide 10-13 solute carrier family 2 member 2 Rattus norvegicus 69-75 31516323-13 2019 Moreover, GLB plus MCFE-500 was the most efficient in restoring INR, Slc2a2 and PPAR-alpha mRNA expression to their normal levels. Glyburide 10-13 peroxisome proliferator activated receptor alpha Rattus norvegicus 80-90 31511772-0 2019 Glibenclamide-Induced Autophagy Inhibits Its Insulin Secretion-Improving Function in beta Cells. Glyburide 0-13 insulin Homo sapiens 45-52 31511772-6 2019 Herein, we showed that glibenclamide promoted insulin release and further activated autophagy through the adenosine 5"-monophosphate (AMP) activated protein kinase (AMPK) pathway in MIN-6 cells. Glyburide 23-36 insulin Homo sapiens 46-53 31511772-8 2019 These results suggest that glibenclamide-induced autophagy plays an inhibitory role in promoting insulin secretion by activating the AMPK pathway instead of altering the mammalian target of rapamycin (mTOR). Glyburide 27-40 mechanistic target of rapamycin kinase Homo sapiens 170-199 31511772-8 2019 These results suggest that glibenclamide-induced autophagy plays an inhibitory role in promoting insulin secretion by activating the AMPK pathway instead of altering the mammalian target of rapamycin (mTOR). Glyburide 27-40 mechanistic target of rapamycin kinase Homo sapiens 201-205 31412679-7 2019 Vindoline did not significantly alter the levels of inflammatory cytokines; however glibenclamide lowered the levels of TNF-alpha in kidney and heart tissues. Glyburide 84-97 tumor necrosis factor Rattus norvegicus 120-129 31175705-0 2019 Glibenclamide treatment in a Cantu syndrome patient with a pathogenic ABCC9 gain-of-function variant: Initial experience. Glyburide 0-13 ATP binding cassette subfamily C member 9 Homo sapiens 70-75 31119887-4 2019 We have been suggested that IKATP inhibitors, glibenclamide and HMR1098, normalize CS channels. Glyburide 46-59 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 28-33 31197747-9 2019 Metformin and glyburide pretreatment normalized the LPS-induced IL-1beta secretion in the control and diabetic cultures. Glyburide 14-23 interleukin 1 beta Rattus norvegicus 64-72 31197747-10 2019 Furthermore, glyburide diminished both: LPS-induced IL-6 and TNF-alpha secretion in the control and diabetic cultures and increased NF-kappaB p65 subunit phosphorylation. Glyburide 13-22 interleukin 6 Rattus norvegicus 52-56 31197747-10 2019 Furthermore, glyburide diminished both: LPS-induced IL-6 and TNF-alpha secretion in the control and diabetic cultures and increased NF-kappaB p65 subunit phosphorylation. Glyburide 13-22 tumor necrosis factor Rattus norvegicus 61-70 31197747-11 2019 Glyburide also diminished the levels of the NLRP3 subunit and caspase-1, but only in the diabetic cultures. Glyburide 0-9 NLR family, pyrin domain containing 3 Rattus norvegicus 44-49 31197747-11 2019 Glyburide also diminished the levels of the NLRP3 subunit and caspase-1, but only in the diabetic cultures. Glyburide 0-9 caspase 1 Rattus norvegicus 62-71 31350736-0 2019 In Vitro Modulation of Glibenclamide Transport by P-glycoprotein Inhibitory Antidiabetic African Plant Extracts. Glyburide 23-36 ATP binding cassette subfamily B member 1 Homo sapiens 50-64 31290245-6 2019 It is demonstrated that the resulting CXCR4-overexpressing membrane-coated NPs, termed CMNPs, significantly augment the efficacy of glyburide, an anti-edema agent, for stroke treatment. Glyburide 132-141 C-X-C motif chemokine receptor 4 Homo sapiens 38-43 31288831-2 2019 The effect of glibenclamide blocking the Sur1-Trpm4 channel was examined in models of subarachnoid hemorrhage and stroke, with findings of significantly reduced tight-junction abnormalities, resulting in less edema formation and considerably reduced transsynaptic apoptosis of hippocampal neurons and significantly ameliorated impairments in spatial learning. Glyburide 14-27 ATP binding cassette subfamily C member 8 Homo sapiens 41-45 31288831-2 2019 The effect of glibenclamide blocking the Sur1-Trpm4 channel was examined in models of subarachnoid hemorrhage and stroke, with findings of significantly reduced tight-junction abnormalities, resulting in less edema formation and considerably reduced transsynaptic apoptosis of hippocampal neurons and significantly ameliorated impairments in spatial learning. Glyburide 14-27 transient receptor potential cation channel subfamily M member 4 Homo sapiens 46-51 30995106-13 2019 MGO exposure enhanced the activation of all three MAPK pathways in H-HAECs, whereas glibenclamide reversed the activation of p-stress-activated protein kinase/JNK induced by MGO. Glyburide 84-97 mitogen-activated protein kinase 8 Homo sapiens 159-162 31946797-0 2019 Neuroprotection of Glibenclamide against Brain Injury after Cardiac Arrest via Modulation of NLRP3 Inflammasome. Glyburide 19-32 NLR family, pyrin domain containing 3 Rattus norvegicus 93-98 31946797-9 2019 Furthermore, on the molecular basis, the NLRP3 inflammasome was strongly activated in the hippocampal CA1 area 3 days after CA in control rats, which was suppressed with GBC treatment. Glyburide 170-173 NLR family, pyrin domain containing 3 Rattus norvegicus 41-46 31946797-9 2019 Furthermore, on the molecular basis, the NLRP3 inflammasome was strongly activated in the hippocampal CA1 area 3 days after CA in control rats, which was suppressed with GBC treatment. Glyburide 170-173 carbonic anhydrase 1 Rattus norvegicus 102-105 31123394-0 2019 Glibenclamide alleviates inflammation in oleic acid model of acute lung injury through NLRP3 inflammasome signaling pathway. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 87-92 31123394-14 2019 Pretreatment with glibenclamide partly inhibited the increase in NLRP3, caspase-1 and IL-1beta expression induced by OA, simultaneously attenuated the lung injury. Glyburide 18-31 NLR family, pyrin domain containing 3 Rattus norvegicus 65-70 31123394-14 2019 Pretreatment with glibenclamide partly inhibited the increase in NLRP3, caspase-1 and IL-1beta expression induced by OA, simultaneously attenuated the lung injury. Glyburide 18-31 caspase 1 Rattus norvegicus 72-81 31123394-14 2019 Pretreatment with glibenclamide partly inhibited the increase in NLRP3, caspase-1 and IL-1beta expression induced by OA, simultaneously attenuated the lung injury. Glyburide 18-31 interleukin 1 alpha Rattus norvegicus 86-94 31123394-17 2019 Glibenclamide can alleviate this kind of ALI by inhibiting rather the NLRP3/caspase-1/IL-1beta signaling pathway than the levels of FFAs or TLR4 pathway. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 70-75 31123394-17 2019 Glibenclamide can alleviate this kind of ALI by inhibiting rather the NLRP3/caspase-1/IL-1beta signaling pathway than the levels of FFAs or TLR4 pathway. Glyburide 0-13 caspase 1 Rattus norvegicus 76-85 31123394-17 2019 Glibenclamide can alleviate this kind of ALI by inhibiting rather the NLRP3/caspase-1/IL-1beta signaling pathway than the levels of FFAs or TLR4 pathway. Glyburide 0-13 interleukin 1 alpha Rattus norvegicus 86-94 29457517-8 2019 CONCLUSIONS: The combination of resveratrol with glibenclamide may alleviate reperfusion-induced arrhythmias via an underlying mechanism not be only associated with the restoration of the protein expression of Kir6.2 subunits but also associated with the other subunits or ion channels underlying cardiac action potential. Glyburide 49-62 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 210-216 30710517-3 2019 In prior studies, it has been demonstrated that A3AR-mediated ischemic protection is blocked by glibenclamide and is absent in Kir6.2 gene ablated mice that lack the pore-forming subunit of the ATP-sensitive potassium (KATP) channel, suggesting one contributing mechanism may involve accelerated activation of KATP channels. Glyburide 96-109 adenosine A3 receptor Mus musculus 48-52 31086662-0 2019 Frequency of CYP2C9 (*2, *3 and IVS8-109A>T) allelic variants, and their clinical implications, among Mexican patients with diabetes mellitus type 2 undergoing treatment with glibenclamide and metformin. Glyburide 178-191 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 13-19 30859754-0 2019 Glibenclamide ameliorates the disrupted blood-brain barrier in experimental intracerebral hemorrhage by inhibiting the activation of NLRP3 inflammasome. Glyburide 0-13 NLR family, pyrin domain containing 3 Mus musculus 133-138 30859754-13 2019 Glibenclamide treatment and NLRP3 knockdown significantly reduced hemin-induced activation of the NLRP3 inflammasome, release of extracellular lactate dehydrogenase, apoptosis, and loss of ZO-1 in b.End3 cells. Glyburide 0-13 NLR family, pyrin domain containing 3 Mus musculus 98-103 30859754-13 2019 Glibenclamide treatment and NLRP3 knockdown significantly reduced hemin-induced activation of the NLRP3 inflammasome, release of extracellular lactate dehydrogenase, apoptosis, and loss of ZO-1 in b.End3 cells. Glyburide 0-13 tight junction protein 1 Mus musculus 189-193 30859754-14 2019 However, NLRP3 knockdown abolished the protective effect of glibenclamide. Glyburide 60-73 NLR family, pyrin domain containing 3 Mus musculus 9-14 30859754-15 2019 CONCLUSION: Glibenclamide maintained BBB integrity in experimental ICH by inhibiting the activation of the NLRP3 inflammasome in microvessel endothelial cells. Glyburide 12-25 NLR family, pyrin domain containing 3 Mus musculus 107-112 30160201-2 2019 In humans and rodents with contusion-TBI, sulfonylurea receptor 1 (SUR1) is upregulated in microvessels and astrocytes, and in rodent models, blockade of SUR1 with glibenclamide reduces HPC. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 42-65 30160201-2 2019 In humans and rodents with contusion-TBI, sulfonylurea receptor 1 (SUR1) is upregulated in microvessels and astrocytes, and in rodent models, blockade of SUR1 with glibenclamide reduces HPC. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 67-71 30160201-2 2019 In humans and rodents with contusion-TBI, sulfonylurea receptor 1 (SUR1) is upregulated in microvessels and astrocytes, and in rodent models, blockade of SUR1 with glibenclamide reduces HPC. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 154-158 30160201-10 2019 Our findings demonstrate upregulation of SUR1-TRPM4 and KATP after contusion-TBI, identify SUR1-TRPM4 as the primary molecular mechanism that accounts for HPC, and indicate that SUR1-TRPM4 is a crucial target of glibenclamide. Glyburide 212-225 ATP binding cassette subfamily C member 8 Rattus norvegicus 41-45 30587573-5 2019 We found that ATP binding is sufficient to switch SUR1 alone between inward- or outward-facing conformations with low or high dissociation constant, KD , values for the conformation-sensitive channel antagonist [3H]glibenclamide ([3H]GBM), indicating that ATP can act as a pure agonist. Glyburide 215-228 ATP binding cassette subfamily C member 8 Homo sapiens 50-54 30583226-10 2019 In contrast, the vasorelaxant effects of TSC were markedly inhibited by the NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 10 muM), guanylyl cyclase inhibitor 1H- [1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ, 10 muM), K+ channel blockers, glibenclamide (100 muM) and clotrimazole (5 mM). Glyburide 257-270 solute carrier family 12 member 3 Rattus norvegicus 41-44 30210053-5 2019 Furthermore, the increase in the CEC of apoE-containing HDL induced by the LXR agonist was significantly reduced by treatment with glyburide, an inhibitor of ATP-binding cassette transporter A1 (ABCA1). Glyburide 131-140 apolipoprotein E Homo sapiens 40-44 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Glyburide 75-88 solute carrier organic anion transporter family member 1B1 Homo sapiens 151-158 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Glyburide 75-88 solute carrier organic anion transporter family member 1B3 Homo sapiens 160-167 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Glyburide 75-88 solute carrier organic anion transporter family member 2B1 Homo sapiens 172-179 30756197-6 2019 Prevalence of DM2 in the VHA increased after 2001 but plateaued by 2008; blood sugar testing by glycosylated hemoglobin increased consistently while glucose testing decreased; and the trend of insulin and metformin use was consistent with the trend in DM2 prevalence, while glyburide and rosiglitazone use dropped sharply. Glyburide 274-283 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 252-255 30210053-5 2019 Furthermore, the increase in the CEC of apoE-containing HDL induced by the LXR agonist was significantly reduced by treatment with glyburide, an inhibitor of ATP-binding cassette transporter A1 (ABCA1). Glyburide 131-140 ATP binding cassette subfamily A member 1 Homo sapiens 158-193 30210053-5 2019 Furthermore, the increase in the CEC of apoE-containing HDL induced by the LXR agonist was significantly reduced by treatment with glyburide, an inhibitor of ATP-binding cassette transporter A1 (ABCA1). Glyburide 131-140 ATP binding cassette subfamily A member 1 Homo sapiens 195-200 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 127-140 glucagon Homo sapiens 85-108 30673724-0 2019 An analog of glibenclamide selectively enhances autophagic degradation of misfolded alpha1-antitrypsin Z. Glyburide 13-26 serpin family A member 1 Homo sapiens 84-102 30353742-0 2019 Bladder decompensation and reduction in nerve density in a rat model of chronic bladder outlet obstruction are attenuated with the NLRP3 inhibitor glyburide. Glyburide 147-156 NLR family, pyrin domain containing 3 Rattus norvegicus 131-136 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 127-140 glucagon Homo sapiens 110-115 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 127-140 glucagon Homo sapiens 148-153 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 142-145 glucagon Homo sapiens 85-108 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 142-145 glucagon Homo sapiens 110-115 30404557-2 2019 In this report, we developed and tested a synthetic multivalent ligand consisting of glucagon-like peptide-1 (GLP-1) linked to glibenclamide (Glb) (GLP-1/Glb) for signaling efficacy in beta-cells. Glyburide 142-145 glucagon Homo sapiens 148-153 29679622-3 2018 We have more information regarding treatment of women with gestational diabetes mellitus where glyburide can induce a picture of fetal hyperinsulinism (higher birthweight and more neonatal hypoglycemia) whereas metformin requires supplemental insulin in a larger proportion of women but achieves satisfactory perinatal outcomes with the exception of preterm birth. Glyburide 95-104 insulin Homo sapiens 140-147 30584236-0 2018 OATP1B3 (699G>A) and CYP2C9*2, *3 significantly influenced the transport and metabolism of glibenclamide and glipizide. Glyburide 94-107 solute carrier organic anion transporter family member 1B3 Homo sapiens 0-7 30584236-0 2018 OATP1B3 (699G>A) and CYP2C9*2, *3 significantly influenced the transport and metabolism of glibenclamide and glipizide. Glyburide 94-107 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 24-30 30584236-2 2018 This study purposed to investigate the effect of OATP1B3 and CYP2C9 genetic polymorphisms on the transport and metabolism of glibenclamide and glipizide in human. Glyburide 125-138 solute carrier organic anion transporter family member 1B3 Homo sapiens 49-56 30584236-2 2018 This study purposed to investigate the effect of OATP1B3 and CYP2C9 genetic polymorphisms on the transport and metabolism of glibenclamide and glipizide in human. Glyburide 125-138 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 61-67 30584236-3 2018 An LC-MS method was used to determine the uptake of glibenclamide and glipizide in OATP1B3, OATP1B3 (344T > G) and OATP1B3 (699G > A)-HEK293T cells and their metabolism in CYP2C9*1, *2 and *3 recombinase system. Glyburide 52-65 solute carrier organic anion transporter family member 1B3 Homo sapiens 83-90 30584236-3 2018 An LC-MS method was used to determine the uptake of glibenclamide and glipizide in OATP1B3, OATP1B3 (344T > G) and OATP1B3 (699G > A)-HEK293T cells and their metabolism in CYP2C9*1, *2 and *3 recombinase system. Glyburide 52-65 solute carrier organic anion transporter family member 1B3 Homo sapiens 92-99 30584236-3 2018 An LC-MS method was used to determine the uptake of glibenclamide and glipizide in OATP1B3, OATP1B3 (344T > G) and OATP1B3 (699G > A)-HEK293T cells and their metabolism in CYP2C9*1, *2 and *3 recombinase system. Glyburide 52-65 solute carrier organic anion transporter family member 1B3 Homo sapiens 92-99 30584236-3 2018 An LC-MS method was used to determine the uptake of glibenclamide and glipizide in OATP1B3, OATP1B3 (344T > G) and OATP1B3 (699G > A)-HEK293T cells and their metabolism in CYP2C9*1, *2 and *3 recombinase system. Glyburide 52-65 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 178-184 30584236-5 2018 The internal clearance of glibenclamide and glipizide in OATP1B3 (699G > A) was less than that in wild-type. Glyburide 26-39 solute carrier organic anion transporter family member 1B3 Homo sapiens 57-64 30584236-6 2018 Glibenclamide can be metabolized in CYP2C9*1, *2 and *3 recombinase system with the Vmax values of 1.58 +- 0.71, 0.69 +- 0.25, and 0.41 +- 0.13 nmol/min/mg protein, while glipizide was metabolized with Vmax of 8.82 +- 2.78, 5.99 +- 1.95, and 2.87 +- 1.03 nmol/min/mg protein, respectively. Glyburide 0-13 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 36-42 30584236-7 2018 The internal clearance of glibenclamide and glipizide in CYP2C9*2 and *3 was markedly reduced compared to that in CYP2C9*1. Glyburide 26-39 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 57-63 30584236-7 2018 The internal clearance of glibenclamide and glipizide in CYP2C9*2 and *3 was markedly reduced compared to that in CYP2C9*1. Glyburide 26-39 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 114-120 30584236-8 2018 These results collectively demonstrate that OATP1B3 (699G > A) and CYP2C9*2 and *3 have a significant influence on the transport and metabolism of glibenclamide and glipizide. Glyburide 150-163 solute carrier organic anion transporter family member 1B3 Homo sapiens 44-51 30584236-8 2018 These results collectively demonstrate that OATP1B3 (699G > A) and CYP2C9*2 and *3 have a significant influence on the transport and metabolism of glibenclamide and glipizide. Glyburide 150-163 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 70-76 30446594-8 2018 In the subset of patients with malignant edema, those treated with IV glyburide had less midline shift (p < 0.01) and reduced MMP-9 (matrix metalloproteinase 9) levels (p < 0.01). Glyburide 70-79 matrix metallopeptidase 9 Homo sapiens 129-134 30446594-8 2018 In the subset of patients with malignant edema, those treated with IV glyburide had less midline shift (p < 0.01) and reduced MMP-9 (matrix metalloproteinase 9) levels (p < 0.01). Glyburide 70-79 matrix metallopeptidase 9 Homo sapiens 136-162 30265150-11 2018 The KATP inhibitor glibenclamide and the BK inhibitor paxilline blocked CSE/H2S-dependent dilation of pial arterioles to ET-1. Glyburide 19-32 endothelin 1 Homo sapiens 121-125 29802808-0 2018 CYP2C9*3 gene variant contributes independently to glycaemic control in patients with type 2 diabetes treated with glibenclamide. Glyburide 115-128 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 29802808-2 2018 In this cross-sectional study, the aim was to explore the association of genetic variants in CYP2C9, ABCC8, KCNJ11 and TCF7L2 with good glycaemic control in Mexican type 2 diabetes (T2D) treated with glibenclamide. Glyburide 200-213 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 93-99 29802808-2 2018 In this cross-sectional study, the aim was to explore the association of genetic variants in CYP2C9, ABCC8, KCNJ11 and TCF7L2 with good glycaemic control in Mexican type 2 diabetes (T2D) treated with glibenclamide. Glyburide 200-213 transcription factor 7 like 2 Homo sapiens 119-125 29802808-11 2018 WHAT IS NEW AND CONCLUSION: The findings suggest that CYP2C9*3 genetic variant independently contributes to good glycaemic control of patients with type 2 diabetes treated with glibenclamide. Glyburide 177-190 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 54-60 30172767-12 2019 CONCLUSIONS: A majority of hypoglycemic events occurred in elderly patients with type 2 DM, with a high prevalence of associated comorbidities and treated with insulin and sulfonylureas, particularly glibenclamide. Glyburide 200-213 insulin Homo sapiens 160-167 30131395-9 2018 Likewise, the KATP inhibitor glibenclamide resulted in a greater decrease in afferent arteriolar diameter in SS rats with STZ-induced diabetes than in STZ-treated SS p66ShcKO and p66Shc-S36A rats. Glyburide 29-42 SHC adaptor protein 1 Rattus norvegicus 166-172 30066023-0 2018 Glibenclamide protects against thioacetamide-induced hepatic damage in Wistar rat: investigation on NLRP3, MMP-2, and stellate cell activation. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 100-105 30066023-0 2018 Glibenclamide protects against thioacetamide-induced hepatic damage in Wistar rat: investigation on NLRP3, MMP-2, and stellate cell activation. Glyburide 0-13 matrix metallopeptidase 2 Rattus norvegicus 107-112 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 transforming growth factor, beta 1 Rattus norvegicus 61-70 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 NLR family, pyrin domain containing 3 Rattus norvegicus 83-88 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 PYD and CARD domain containing Rattus norvegicus 90-93 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 caspase 1 Rattus norvegicus 95-104 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 interleukin 1 beta Rattus norvegicus 110-118 30066023-12 2018 GLB treatment significantly downregulated the expressions of TGF-beta1, alpha-SMA, NLRP3, ASC, caspase-1, and IL-1beta, and upregulated MMP-2 and catalase against TAA-induced liver damage. Glyburide 0-3 matrix metallopeptidase 2 Rattus norvegicus 136-154 30147301-1 2018 Glyburide (also known as glibenclamide) is a second-generation sulfonylurea drug that inhibits sulfonylurea receptor 1 (Sur1) at nanomolar concentrations. Glyburide 0-9 ATP binding cassette subfamily C member 8 Homo sapiens 95-118 30094785-9 2018 The gene analysis revealed a de novo mutation (c.602G > A (p.R201H)) of the KCNJ11 gene, and oral glibenclamide successfully replaced insulin treatment in the patient. Glyburide 101-114 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 79-85 30094785-9 2018 The gene analysis revealed a de novo mutation (c.602G > A (p.R201H)) of the KCNJ11 gene, and oral glibenclamide successfully replaced insulin treatment in the patient. Glyburide 101-114 insulin Homo sapiens 137-144 30637228-4 2018 Upregulation of SUR1 receptor has been observed after stroke and traumatic brain injury, therefore, SUR such as glibenclamide inhibits brain edema and astrocyte swelling following brain insults. Glyburide 112-125 ATP binding cassette subfamily C member 8 Homo sapiens 16-20 30637228-4 2018 Upregulation of SUR1 receptor has been observed after stroke and traumatic brain injury, therefore, SUR such as glibenclamide inhibits brain edema and astrocyte swelling following brain insults. Glyburide 112-125 ATP binding cassette subfamily C member 8 Homo sapiens 16-19 30637228-5 2018 SUR drugs mainly glibenclamide is effective at a low dose in the management of cerebral stroke and could be a contestant with corticosteroid in controlling brain edema. Glyburide 17-30 ATP binding cassette subfamily C member 8 Homo sapiens 0-3 30527115-12 2018 Treatment with Glybenclamide at 200 muM was used to prevent NLRP3 inflammasome activation. Glyburide 15-28 NLR family pyrin domain containing 3 Homo sapiens 60-65 30283449-7 2018 We found that glibenclamide significantly reduced M1 (HLA-DR+ and CD86+) surface markers and TNF-alpha production on primary human monocytes against mycobacterial infection. Glyburide 14-27 tumor necrosis factor Homo sapiens 93-102 30283449-8 2018 In contrast, M2 (CD163+ and CD206+) surface markers and IL-10 production were enhanced by pretreatment with glibenclamide. Glyburide 108-121 interleukin 10 Homo sapiens 56-61 30180807-10 2018 RESULTS: Treatment with glibenclamide aggravated the apoptosis of HK-2 cells in high-glucose, as indicated by a significant decrease in the expression of Bcl-2 and increase in Bax. Glyburide 24-37 BCL2 apoptosis regulator Homo sapiens 154-159 30180807-10 2018 RESULTS: Treatment with glibenclamide aggravated the apoptosis of HK-2 cells in high-glucose, as indicated by a significant decrease in the expression of Bcl-2 and increase in Bax. Glyburide 24-37 BCL2 associated X, apoptosis regulator Homo sapiens 176-179 29933037-5 2018 We found that GLI could scavenge free radicals, reduce activated-caspase-3 expression, increase the Bcl-2/Bax ratio, inhibit apoptosis, and improve functional neurological outcomes in a rat model of ICH. Glyburide 14-17 caspase 3 Rattus norvegicus 65-74 29933037-5 2018 We found that GLI could scavenge free radicals, reduce activated-caspase-3 expression, increase the Bcl-2/Bax ratio, inhibit apoptosis, and improve functional neurological outcomes in a rat model of ICH. Glyburide 14-17 BCL2, apoptosis regulator Rattus norvegicus 100-105 29933037-5 2018 We found that GLI could scavenge free radicals, reduce activated-caspase-3 expression, increase the Bcl-2/Bax ratio, inhibit apoptosis, and improve functional neurological outcomes in a rat model of ICH. Glyburide 14-17 BCL2 associated X, apoptosis regulator Rattus norvegicus 106-109 30079884-5 2018 Inhibition of SUR1 with glyburide decreases edema and neuroinflammation by countering cytotoxic edema and apoptosis in rodent models of subarachnoid hemorrhage, stroke, trauma, and cerebral metastases. Glyburide 24-33 ATP binding cassette subfamily C member 8 Homo sapiens 14-18 29648981-2 2018 Glibenclamide may reduce cerebral edema by inhibiting sulfonylurea receptor-1 (Sur1); its effect on diffuse cerebral edema exacerbated by hypotension/resuscitation is unknown. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 54-77 29648981-2 2018 Glibenclamide may reduce cerebral edema by inhibiting sulfonylurea receptor-1 (Sur1); its effect on diffuse cerebral edema exacerbated by hypotension/resuscitation is unknown. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 79-83 29976759-7 2018 Moreover, inhibiting cellular potassium efflux with glyburide or increasing extracellular potassium also significantly reduced SAA-mediated IL-1beta secretion. Glyburide 52-61 serum amyloid A cluster Mus musculus 127-130 29976759-7 2018 Moreover, inhibiting cellular potassium efflux with glyburide or increasing extracellular potassium also significantly reduced SAA-mediated IL-1beta secretion. Glyburide 52-61 interleukin 1 beta Mus musculus 140-148 30147301-1 2018 Glyburide (also known as glibenclamide) is a second-generation sulfonylurea drug that inhibits sulfonylurea receptor 1 (Sur1) at nanomolar concentrations. Glyburide 0-9 ATP binding cassette subfamily C member 8 Homo sapiens 120-124 30147301-1 2018 Glyburide (also known as glibenclamide) is a second-generation sulfonylurea drug that inhibits sulfonylurea receptor 1 (Sur1) at nanomolar concentrations. Glyburide 25-38 ATP binding cassette subfamily C member 8 Homo sapiens 95-118 30147301-1 2018 Glyburide (also known as glibenclamide) is a second-generation sulfonylurea drug that inhibits sulfonylurea receptor 1 (Sur1) at nanomolar concentrations. Glyburide 25-38 ATP binding cassette subfamily C member 8 Homo sapiens 120-124 30147301-2 2018 Long used to target KATP (Sur1-Kir6.2) channels for the treatment of diabetes mellitus type 2, glyburide was recently repurposed to target Sur1-transient receptor potential melastatin 4 (Trpm4) channels in acute central nervous system injury. Glyburide 95-104 ATP binding cassette subfamily C member 8 Homo sapiens 26-30 30147301-2 2018 Long used to target KATP (Sur1-Kir6.2) channels for the treatment of diabetes mellitus type 2, glyburide was recently repurposed to target Sur1-transient receptor potential melastatin 4 (Trpm4) channels in acute central nervous system injury. Glyburide 95-104 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 31-37 30147301-2 2018 Long used to target KATP (Sur1-Kir6.2) channels for the treatment of diabetes mellitus type 2, glyburide was recently repurposed to target Sur1-transient receptor potential melastatin 4 (Trpm4) channels in acute central nervous system injury. Glyburide 95-104 transient receptor potential cation channel subfamily M member 4 Homo sapiens 139-185 30147301-2 2018 Long used to target KATP (Sur1-Kir6.2) channels for the treatment of diabetes mellitus type 2, glyburide was recently repurposed to target Sur1-transient receptor potential melastatin 4 (Trpm4) channels in acute central nervous system injury. Glyburide 95-104 transient receptor potential cation channel subfamily M member 4 Homo sapiens 187-192 30147301-7 2018 Additionally, recent work linked SUR1-TRPM4 to secretion of matrix metalloproteinase-9 (MMP-9) induced by recombinant tissue plasminogen activator in activated brain endothelial cells, with blockade of SUR1-TRPM4 by glyburide reducing MMP-9 and hemorrhagic transformation in preclinical models with recombinant tissue plasminogen activator. Glyburide 216-225 ATP binding cassette subfamily C member 8 Homo sapiens 33-37 30147301-7 2018 Additionally, recent work linked SUR1-TRPM4 to secretion of matrix metalloproteinase-9 (MMP-9) induced by recombinant tissue plasminogen activator in activated brain endothelial cells, with blockade of SUR1-TRPM4 by glyburide reducing MMP-9 and hemorrhagic transformation in preclinical models with recombinant tissue plasminogen activator. Glyburide 216-225 matrix metallopeptidase 9 Homo sapiens 60-86 30147301-7 2018 Additionally, recent work linked SUR1-TRPM4 to secretion of matrix metalloproteinase-9 (MMP-9) induced by recombinant tissue plasminogen activator in activated brain endothelial cells, with blockade of SUR1-TRPM4 by glyburide reducing MMP-9 and hemorrhagic transformation in preclinical models with recombinant tissue plasminogen activator. Glyburide 216-225 matrix metallopeptidase 9 Homo sapiens 88-93 30147301-8 2018 The recently completed GAMES (Glyburide Advantage in Malignant Edema and Stroke) clinical trials on patients with large hemispheric infarctions treated with intravenous glyburide (RP-1127) revealed promising findings with regard to brain swelling (midline shift), MMP-9, functional outcomes and mortality. Glyburide 30-39 matrix metallopeptidase 9 Homo sapiens 264-269 30147301-8 2018 The recently completed GAMES (Glyburide Advantage in Malignant Edema and Stroke) clinical trials on patients with large hemispheric infarctions treated with intravenous glyburide (RP-1127) revealed promising findings with regard to brain swelling (midline shift), MMP-9, functional outcomes and mortality. Glyburide 169-178 matrix metallopeptidase 9 Homo sapiens 264-269 29543503-5 2018 Increasing concentrations (10-10-10-6 M) of pinacidil, a KATP channel agonist, resulted in progressive hyperpolarization of SMCs of intact PAs (Delta Vm ~30 mV), which was blocked by glibenclamide (10-6 M), as was hyperpolarization of ECs and SMCs to CGRP. Glyburide 183-196 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 251-255 29498478-4 2018 The inhibitory effects of glibenclamide and glimepiride on sulfobromophthalein (BSP) uptake have been previously studied, and glibenclamide has been reported as the substrate of OATP1B3, but it remains unclear whether other SUs such as gliclazide, glipizide and gliquidone are substrates of OATP1B1 and OATP1B3. Glyburide 126-139 solute carrier organic anion transporter family member 1B3 Homo sapiens 178-185 29498478-4 2018 The inhibitory effects of glibenclamide and glimepiride on sulfobromophthalein (BSP) uptake have been previously studied, and glibenclamide has been reported as the substrate of OATP1B3, but it remains unclear whether other SUs such as gliclazide, glipizide and gliquidone are substrates of OATP1B1 and OATP1B3. Glyburide 126-139 solute carrier organic anion transporter family member 1B1 Homo sapiens 291-298 29498478-4 2018 The inhibitory effects of glibenclamide and glimepiride on sulfobromophthalein (BSP) uptake have been previously studied, and glibenclamide has been reported as the substrate of OATP1B3, but it remains unclear whether other SUs such as gliclazide, glipizide and gliquidone are substrates of OATP1B1 and OATP1B3. Glyburide 126-139 solute carrier organic anion transporter family member 1B3 Homo sapiens 303-310 29884910-6 2018 We found that OGD significantly increased the levels of caspase-1 cleaved p10, IL-1beta and ASC expression, caspase-1 activity and the frequency of pyroptotic AM, and promoted the cytoplasm transportation and secretion of HMGB1, which were significantly mitigated by ASC silencing or pre-treatment with glyburide (a Nlrp3 inhibitor) in AM. Glyburide 303-312 caspase 1 Rattus norvegicus 56-65 29884910-8 2018 Treatment with glyburide significantly mitigated the CPB-increased ASC, caspase-1 p10 and IL-1beta expression, and the percentages of AM pyroptosis in the lungs, as well as the levels of HMGB1 in serum and BALF in rats. Glyburide 15-24 PYD and CARD domain containing Rattus norvegicus 67-70 29884910-8 2018 Treatment with glyburide significantly mitigated the CPB-increased ASC, caspase-1 p10 and IL-1beta expression, and the percentages of AM pyroptosis in the lungs, as well as the levels of HMGB1 in serum and BALF in rats. Glyburide 15-24 caspase 1 Rattus norvegicus 72-81 29884910-8 2018 Treatment with glyburide significantly mitigated the CPB-increased ASC, caspase-1 p10 and IL-1beta expression, and the percentages of AM pyroptosis in the lungs, as well as the levels of HMGB1 in serum and BALF in rats. Glyburide 15-24 interleukin 1 beta Rattus norvegicus 90-98 29884910-8 2018 Treatment with glyburide significantly mitigated the CPB-increased ASC, caspase-1 p10 and IL-1beta expression, and the percentages of AM pyroptosis in the lungs, as well as the levels of HMGB1 in serum and BALF in rats. Glyburide 15-24 high mobility group box 1 Rattus norvegicus 187-192 29627526-8 2018 AKR1C3 was downregulated in the kidney and podocytes, whereas glibenclamide increased the expression of AKR1C3. Glyburide 62-75 aldo-keto reductase family 1, member C3 Rattus norvegicus 104-110 29150777-3 2018 In this study, we examined whether glibenclamide (GBC), a Sur1-TRPM4 channel inhibitor, attenuates cerebral edema following CA/CPR and further examined the efficacy of GBC combined with therapeutic hypothermia. Glyburide 35-48 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 58-62 29150777-3 2018 In this study, we examined whether glibenclamide (GBC), a Sur1-TRPM4 channel inhibitor, attenuates cerebral edema following CA/CPR and further examined the efficacy of GBC combined with therapeutic hypothermia. Glyburide 35-48 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 63-68 29150777-3 2018 In this study, we examined whether glibenclamide (GBC), a Sur1-TRPM4 channel inhibitor, attenuates cerebral edema following CA/CPR and further examined the efficacy of GBC combined with therapeutic hypothermia. Glyburide 50-53 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 58-62 30349568-5 2018 Urotensin-II efficacy was significantly increased in chtx, TEA and BaCl2 treated groups, while significantly decreased in glibenclamide and clotrimazole treated groups as compared with the control group. Glyburide 122-135 urotensin 2 Rattus norvegicus 0-12 29630758-9 2018 The docking study with current anti-diabetic therapeutics shows that the drugs Glibenclamide and Glyclopyramide have a partial affinity towards SOCS1. Glyburide 79-92 suppressor of cytokine signaling 1 Homo sapiens 144-149 29941940-11 2018 Moreover, LPS + ATP increased IL-1beta protein expression and production, which were prevented by glyburide. Glyburide 98-107 interleukin 1 beta Homo sapiens 30-38 29610263-10 2018 The effects of diabetes were reversible, as glibenclamide therapy restored euglycemia, cardiac metabolism and function, and PDK4/UCP3 levels. Glyburide 44-57 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 124-128 29610263-10 2018 The effects of diabetes were reversible, as glibenclamide therapy restored euglycemia, cardiac metabolism and function, and PDK4/UCP3 levels. Glyburide 44-57 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 129-133 29617457-3 2018 In humans and rodents with cerebral ischemia/reperfusion (I/R), the SUR1 antagonist, glibenclamide, reduces hemorrhagic transformation and plasma MMP-9, but the mechanism is unknown. Glyburide 85-98 ATP binding cassette subfamily C member 8 Homo sapiens 68-72 29159877-15 2018 Cell death induced by dental calculus was significantly inhibited by cytochalasin D, z-YVAD-fmk and glyburide, indicating NLRP3 inflammasome involvement. Glyburide 100-109 NLR family pyrin domain containing 3 Homo sapiens 122-127 29802529-6 2018 Inhibition of NLRP3 by glyburide strongly suppressed the expression of NLRP3 inflammasome proteins and IL-1beta, and markedly reduced brain tissue damage. Glyburide 23-32 NLR family, pyrin domain containing 3 Rattus norvegicus 14-19 29802529-6 2018 Inhibition of NLRP3 by glyburide strongly suppressed the expression of NLRP3 inflammasome proteins and IL-1beta, and markedly reduced brain tissue damage. Glyburide 23-32 NLR family, pyrin domain containing 3 Rattus norvegicus 71-76 29802529-6 2018 Inhibition of NLRP3 by glyburide strongly suppressed the expression of NLRP3 inflammasome proteins and IL-1beta, and markedly reduced brain tissue damage. Glyburide 23-32 interleukin 1 beta Rattus norvegicus 103-111 29789393-11 2018 Participants treated with intravenous glyburide had lower plasma levels of MMP-9 (189 versus 376 ng/mL; P<0.001) and decreased midline shift (4.7 versus 9 mm; P<0.001) compared with participants who received placebo. Glyburide 38-47 matrix metallopeptidase 9 Homo sapiens 75-80 29849783-13 2018 The effect of the KATP channel blocker glibenclamide on the proliferation of five different cervical cancer cell lines was studied, revealing that as Kir6.2 mRNA expression increased, the inhibitory effect of glibenclamide also increased. Glyburide 39-52 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 150-156 29849783-13 2018 The effect of the KATP channel blocker glibenclamide on the proliferation of five different cervical cancer cell lines was studied, revealing that as Kir6.2 mRNA expression increased, the inhibitory effect of glibenclamide also increased. Glyburide 209-222 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 150-156 29617457-3 2018 In humans and rodents with cerebral ischemia/reperfusion (I/R), the SUR1 antagonist, glibenclamide, reduces hemorrhagic transformation and plasma MMP-9, but the mechanism is unknown. Glyburide 85-98 matrix metallopeptidase 9 Homo sapiens 146-151 28551720-6 2018 RESULTS: Paricalcitol and glibenclamide treatment significantly (P < 0.05) decreased plasma glucose, insulin resistance, and pancreatic malondialdehyde and tumor necrosis factor-alpha levels. Glyburide 26-39 tumor necrosis factor Rattus norvegicus 159-186 29305569-0 2018 Emergence of insulin resistance following empirical glibenclamide therapy: a case report of neonatal diabetes with a recessive INS gene mutation. Glyburide 52-65 insulin Homo sapiens 13-20 29393427-8 2018 Moreover, persistent PMD was caused by different membrane-depolarizing agents; the use of the anti-type II diabetes drug, glibenclamide, alone caused mitochondrial fragmentation and enhanced TRAIL-induced Ca2+ modulation, mitochondrial network abnormalities and caspase-independent cell killing. Glyburide 122-135 TNF superfamily member 10 Homo sapiens 191-196 28984997-4 2018 METHODS: There were five groups of rats: (i) Control (no surgery); (ii) Sham-operated; (iii) BOO rats given vehicle; (iv) BOO rats given the NLRP3 inhibitor glyburide; and (v) BOO rats given the IL-1 receptor antagonist anakinra. Glyburide 157-166 NLR family, pyrin domain containing 3 Rattus norvegicus 141-146 29432801-8 2018 The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release. Glyburide 33-46 NLR family pyrin domain containing 3 Homo sapiens 82-87 29432801-8 2018 The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release. Glyburide 33-46 caspase 1 Homo sapiens 192-201 29432801-8 2018 The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release. Glyburide 33-46 NLR family pyrin domain containing 3 Homo sapiens 217-222 29432801-8 2018 The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release. Glyburide 33-46 interleukin 1 beta Homo sapiens 267-275 29432801-8 2018 The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release. Glyburide 33-46 interleukin 18 Homo sapiens 280-285 29563527-3 2018 We previously demonstrated that S1P is exported from erythrocytes by a glyburide-sensitive S1P transporter. Glyburide 71-80 sphingosine-1-phosphate receptor 1 Mus musculus 32-35 29563527-3 2018 We previously demonstrated that S1P is exported from erythrocytes by a glyburide-sensitive S1P transporter. Glyburide 71-80 sphingosine-1-phosphate receptor 1 Mus musculus 91-94 28984997-12 2018 The decrease in nerve density was blocked by glyburide or anakinra, clearly implicating the NLRP3 pathway in denervation. Glyburide 45-54 NLR family, pyrin domain containing 3 Rattus norvegicus 92-97 28971696-13 2017 The cardioprotective effects of NaHS were counteracted by Gli which inhibited the Akt/eNOS/NO pathway. Glyburide 58-61 AKT serine/threonine kinase 1 Rattus norvegicus 82-85 29197370-9 2017 Furthermore, in presence of apamin, 4-aminopyridine, glibenclamide or 1 mM TEA+, the relaxant potency of FGAL was attenuated, indicating the participation of SKCa, KV, KATP and highlighting BKCa. Glyburide 53-66 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 190-194 29291445-6 2018 The most potent compounds of both series, i.e. A15, A33 and B16, tested on aortic rings in the presence of glibenclamide or 80 mM KCl, suggested that they acted as voltage-gated Ca2+ channel blockers, like verapamil, instead of being ATP-potassium channel activators, as is cromakalim, the parent molecule. Glyburide 107-120 tetraspanin 7 Rattus norvegicus 47-50 29339732-0 2018 Glyburide and retinoic acid synergize to promote wound healing by anti-inflammation and RIP140 degradation. Glyburide 0-9 nuclear receptor interacting protein 1 Mus musculus 88-94 29339732-5 2018 Our data also delineate the mechanism underlying glyburide"s anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. Glyburide 49-58 nuclear receptor interacting protein 1 Mus musculus 158-190 29339732-5 2018 Our data also delineate the mechanism underlying glyburide"s anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. Glyburide 49-58 nuclear receptor interacting protein 1 Mus musculus 192-198 29339732-5 2018 Our data also delineate the mechanism underlying glyburide"s anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. Glyburide 49-58 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 215-258 29339732-5 2018 Our data also delineate the mechanism underlying glyburide"s anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. Glyburide 49-58 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 260-266 29339732-5 2018 Our data also delineate the mechanism underlying glyburide"s anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. Glyburide 49-58 nuclear receptor interacting protein 1 Mus musculus 309-315 29339732-6 2018 By stimulating RIP140 degradation, glyburide enhances M2 polarization and anti-inflammation. Glyburide 35-44 nuclear receptor interacting protein 1 Mus musculus 15-21 29339732-8 2018 Mechanistically, this study uncovers a new mechanism of action of glyburide and a new pathway modulating RIP140 protein degradation that is mediated by CamKII signaling. Glyburide 66-75 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 152-158 29178967-5 2017 Glibenclamide, a classic KATP channel blocker, can improve neuroinflammation by inhibiting the activation of NLRP3 inflammasome. Glyburide 0-13 NLR family, pyrin domain containing 3 Mus musculus 109-114 29178967-6 2017 Our present study investigated the effect and possible mechanism of glibenclamide in improving morphine tolerance via its specific inhibition on the release of HSP70 and activation of NLRP3 inflammasome induced by morphine. Glyburide 68-81 heat shock protein 1B Mus musculus 160-165 29178967-6 2017 Our present study investigated the effect and possible mechanism of glibenclamide in improving morphine tolerance via its specific inhibition on the release of HSP70 and activation of NLRP3 inflammasome induced by morphine. Glyburide 68-81 NLR family, pyrin domain containing 3 Mus musculus 184-189 29178967-16 2017 Glibenclamide as a classic KATP channel blocker markedly inhibited the release of HSP70 induced by morphine and suppressed HSP70-TLR4-NLRP3 inflammasome-mediated neuroinflammation, which consequently attenuated morphine tolerance. Glyburide 0-13 heat shock protein 1B Mus musculus 82-87 29178967-16 2017 Glibenclamide as a classic KATP channel blocker markedly inhibited the release of HSP70 induced by morphine and suppressed HSP70-TLR4-NLRP3 inflammasome-mediated neuroinflammation, which consequently attenuated morphine tolerance. Glyburide 0-13 heat shock protein 1B Mus musculus 123-128 29178967-16 2017 Glibenclamide as a classic KATP channel blocker markedly inhibited the release of HSP70 induced by morphine and suppressed HSP70-TLR4-NLRP3 inflammasome-mediated neuroinflammation, which consequently attenuated morphine tolerance. Glyburide 0-13 toll-like receptor 4 Mus musculus 129-133 29178967-16 2017 Glibenclamide as a classic KATP channel blocker markedly inhibited the release of HSP70 induced by morphine and suppressed HSP70-TLR4-NLRP3 inflammasome-mediated neuroinflammation, which consequently attenuated morphine tolerance. Glyburide 0-13 NLR family, pyrin domain containing 3 Mus musculus 134-139 28522373-7 2017 Even though data are limited, it appears that despite inhibition of CYP2C9 due to long-term glibenclamide administration to T2DM patients, overall no differences are observed in the total clearance of carvedilol when compared to healthy subjects (43.1 vs. 45.9L/h for (S)-(-)-carvedilol and 29.0 vs. 33.1L/h for (R)-(+)-carvedilol). Glyburide 92-105 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 68-74 29024691-10 2017 Glibenclamide and 4-aminopyridine inhibited the ANP-induced relaxations more in diabetic than in control rabbits. Glyburide 0-13 natriuretic peptides A Oryctolagus cuniculus 48-51 29056256-0 2017 Glibenclamide inhibits NLRP3 inflammasome-mediated IL-1beta secretion in human trophoblasts. Glyburide 0-13 NLR family pyrin domain containing 3 Homo sapiens 23-28 28961497-4 2017 In the present study, PC12 neuronal cells were exposed to oxygen-glucose deprivation (OGD), exogenous irisin (12.5, 25, 50nmol/L) or NLRP3 inhibitor glyburide (50, 100, 200mumol/L) were used as an intervention reagent, NLRP3 was over-expressed or suppressed by transfection with a NLRP3 expressing vector or NLRP3-specifc siRNA, respectively. Glyburide 149-158 NLR family, pyrin domain containing 3 Rattus norvegicus 133-138 29084550-10 2017 Furthermore, antidiabetic drug glyburide, an inhibitor of the NLRP3 inflammasome, was discovered to be effective in preventing the experimental comorbidity. Glyburide 31-40 NLR family, pyrin domain containing 3 Mus musculus 62-67 29035201-3 2017 Here, we present a cryo-EM structure of a hamster SUR1/rat Kir6.2 channel bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolution, which reveals unprecedented details of the ATP and glibenclamide binding sites. Glyburide 117-130 ATP binding cassette subfamily C member 8 Homo sapiens 50-54 29035201-3 2017 Here, we present a cryo-EM structure of a hamster SUR1/rat Kir6.2 channel bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolution, which reveals unprecedented details of the ATP and glibenclamide binding sites. Glyburide 117-130 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 59-65 29035201-3 2017 Here, we present a cryo-EM structure of a hamster SUR1/rat Kir6.2 channel bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolution, which reveals unprecedented details of the ATP and glibenclamide binding sites. Glyburide 212-225 ATP binding cassette subfamily C member 8 Homo sapiens 50-54 29035201-3 2017 Here, we present a cryo-EM structure of a hamster SUR1/rat Kir6.2 channel bound to a high-affinity sulfonylurea drug glibenclamide and ATP at 3.63 A resolution, which reveals unprecedented details of the ATP and glibenclamide binding sites. Glyburide 212-225 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 59-65 29035201-4 2017 Importantly, the structure shows for the first time that glibenclamide is lodged in the transmembrane bundle of the SUR1-ABC core connected to the first nucleotide binding domain near the inner leaflet of the lipid bilayer. Glyburide 57-70 ATP binding cassette subfamily C member 8 Homo sapiens 116-120 29035201-4 2017 Importantly, the structure shows for the first time that glibenclamide is lodged in the transmembrane bundle of the SUR1-ABC core connected to the first nucleotide binding domain near the inner leaflet of the lipid bilayer. Glyburide 57-70 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 121-124 28842488-7 2017 However, as a consequence of the increased open state stability, both Kir6.1(V65M) and Kir6.2(V64M) mutations essentially abolish high-affinity sensitivity to the KATP blocker glibenclamide in both intact cells and excised patches. Glyburide 176-189 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 70-76 28842488-7 2017 However, as a consequence of the increased open state stability, both Kir6.1(V65M) and Kir6.2(V64M) mutations essentially abolish high-affinity sensitivity to the KATP blocker glibenclamide in both intact cells and excised patches. Glyburide 176-189 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 87-93 28556992-7 2017 If the fetus inherits a KATP neonatal diabetes mutation from their mother they have greatly reduced insulin secretion in utero that reduces fetal growth by ~900 g. Treating the mother with glibenclamide in the third trimester treats the affected fetus in utero, normalising fetal growth, but is not desirable, especially in the high doses used in this condition, if the fetus is unaffected. Glyburide 189-202 insulin Homo sapiens 100-107 29056256-0 2017 Glibenclamide inhibits NLRP3 inflammasome-mediated IL-1beta secretion in human trophoblasts. Glyburide 0-13 interleukin 1 beta Homo sapiens 51-59 29056256-8 2017 These findings suggest that trophoblasts can secrete IL-1beta through the NLRP3/caspase-1 pathway, which is suppressed by glibenclamide, and that the TLR4-mediated NLRP3 inflammasome pathway is more likely to be stimulated in undifferentiated than differentiated trophoblasts. Glyburide 122-135 interleukin 1 beta Homo sapiens 53-61 29056256-8 2017 These findings suggest that trophoblasts can secrete IL-1beta through the NLRP3/caspase-1 pathway, which is suppressed by glibenclamide, and that the TLR4-mediated NLRP3 inflammasome pathway is more likely to be stimulated in undifferentiated than differentiated trophoblasts. Glyburide 122-135 NLR family pyrin domain containing 3 Homo sapiens 74-79 29056256-8 2017 These findings suggest that trophoblasts can secrete IL-1beta through the NLRP3/caspase-1 pathway, which is suppressed by glibenclamide, and that the TLR4-mediated NLRP3 inflammasome pathway is more likely to be stimulated in undifferentiated than differentiated trophoblasts. Glyburide 122-135 caspase 1 Homo sapiens 80-89 28801533-8 2017 In conclusion, Gli treatment significantly induced cell apoptosis by promoting ROS-dependent JNK pathway activation in HCC cells. Glyburide 15-18 mitogen-activated protein kinase 8 Homo sapiens 93-96 28865458-12 2017 In primary astrocyte cultures, activation by TNF plus IFNgamma induced de novo expression of SUR1-TRPM4 channels and upregulated Tnf, Baff, Ccl2, and Nos2 mRNA, with glibenclamide blockade of SUR1-TRPM4 reducing these mRNA increases. Glyburide 166-179 tumor necrosis factor Mus musculus 45-48 28801533-0 2017 Glibenclamide induces apoptosis by activating reactive oxygen species dependent JNK pathway in hepatocellular carcinoma cells. Glyburide 0-13 mitogen-activated protein kinase 8 Homo sapiens 80-83 28801533-4 2017 We found that Gli treatment significantly inhibited cell viability, induced a significant cell-cycle arrest in G2/M-phase and induced apoptosis in both HepG-2 and Huh7 cells. Glyburide 14-17 MIR7-3 host gene Homo sapiens 163-167 28801533-5 2017 We further verified that apoptosis induction by Gli was accompanied by increase in ROS levels and activation of the JNK pathway. Glyburide 48-51 mitogen-activated protein kinase 8 Homo sapiens 116-119 28801533-6 2017 Scavenging of the intracellular ROS with its blocker N-acetyl-L-cysteine (NAC) could mitigate the Gli-induced apoptosis and JNK activation in the two HCC cell lines. Glyburide 98-101 X-linked Kx blood group Homo sapiens 74-77 28801533-6 2017 Scavenging of the intracellular ROS with its blocker N-acetyl-L-cysteine (NAC) could mitigate the Gli-induced apoptosis and JNK activation in the two HCC cell lines. Glyburide 98-101 mitogen-activated protein kinase 8 Homo sapiens 124-127 28801533-7 2017 Furthermore, inhibition of JNK pathway by its inhibitor SP100625 effectively reduced Gli-induced apoptosis in HCC cells. Glyburide 85-88 mitogen-activated protein kinase 8 Homo sapiens 27-30 28938877-12 2017 The combination of metformin and glibenclamide should be reserved for women with GDM with true needle phobia or inability to use insulin therapy. Glyburide 33-46 insulin Homo sapiens 129-136 28877214-12 2017 The actions of SUR1 and Trpm4 modulators were informative: like ghrelin, diazoxide, a SUR1 agonist, elevated [Ca2+]c and glibenclamide, a SUR1 antagonist, partially suppressed ghrelin action, while 9-phenanthrol and flufenamic acid, selective Trpm4 antagonists, blocked ghrelin actions on isolated neurons. Glyburide 121-134 transient receptor potential cation channel subfamily M member 4 Homo sapiens 24-29 28877214-12 2017 The actions of SUR1 and Trpm4 modulators were informative: like ghrelin, diazoxide, a SUR1 agonist, elevated [Ca2+]c and glibenclamide, a SUR1 antagonist, partially suppressed ghrelin action, while 9-phenanthrol and flufenamic acid, selective Trpm4 antagonists, blocked ghrelin actions on isolated neurons. Glyburide 121-134 transient receptor potential cation channel subfamily M member 4 Homo sapiens 243-248 28865458-12 2017 In primary astrocyte cultures, activation by TNF plus IFNgamma induced de novo expression of SUR1-TRPM4 channels and upregulated Tnf, Baff, Ccl2, and Nos2 mRNA, with glibenclamide blockade of SUR1-TRPM4 reducing these mRNA increases. Glyburide 166-179 interferon gamma Mus musculus 54-62 28865458-12 2017 In primary astrocyte cultures, activation by TNF plus IFNgamma induced de novo expression of SUR1-TRPM4 channels and upregulated Tnf, Baff, Ccl2, and Nos2 mRNA, with glibenclamide blockade of SUR1-TRPM4 reducing these mRNA increases. Glyburide 166-179 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 93-97 28083968-1 2017 In this report, we present the first known case of intermediate developmental delay, epilepsy and permanent neonatal diabetes (DEND) syndrome caused by a Q52R mutation in the KCNJ11 gene who was successfully switched (at age 1.3 years) to sulphonylurea monotherapy, namely glibenclamide. Glyburide 273-286 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 175-181 28930827-14 2017 Ranking results showed that glyburide might be the optimum treatment regarding average glucose control, and metformin is the fastest in glucose control for GDM patients; glyburide have the highest incidence of macrosomia, preeclampsia, hyperbilirubinemia, neonatal hypoglycemia, shortest gestational age at delivery, and lowest mean birth weight; metformin (plus insulin when required) have the lowest incidence of macrosomia, PIH, LGA, RDS, low gestational age at delivery, and low birth weight. Glyburide 170-179 insulin Homo sapiens 363-370 28930827-8 2017 The results of the NAM showed that regarding the incidence of macrosomia and LGA, metformin had lower incidence than glyburide (OR, 0.5411 and 0.4177). Glyburide 117-126 SH3 and cysteine rich domain 3 Homo sapiens 19-22 28930827-14 2017 Ranking results showed that glyburide might be the optimum treatment regarding average glucose control, and metformin is the fastest in glucose control for GDM patients; glyburide have the highest incidence of macrosomia, preeclampsia, hyperbilirubinemia, neonatal hypoglycemia, shortest gestational age at delivery, and lowest mean birth weight; metformin (plus insulin when required) have the lowest incidence of macrosomia, PIH, LGA, RDS, low gestational age at delivery, and low birth weight. Glyburide 170-179 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 427-430 28930827-14 2017 Ranking results showed that glyburide might be the optimum treatment regarding average glucose control, and metformin is the fastest in glucose control for GDM patients; glyburide have the highest incidence of macrosomia, preeclampsia, hyperbilirubinemia, neonatal hypoglycemia, shortest gestational age at delivery, and lowest mean birth weight; metformin (plus insulin when required) have the lowest incidence of macrosomia, PIH, LGA, RDS, low gestational age at delivery, and low birth weight. Glyburide 170-179 glutaminase 2 Homo sapiens 432-435 28930827-14 2017 Ranking results showed that glyburide might be the optimum treatment regarding average glucose control, and metformin is the fastest in glucose control for GDM patients; glyburide have the highest incidence of macrosomia, preeclampsia, hyperbilirubinemia, neonatal hypoglycemia, shortest gestational age at delivery, and lowest mean birth weight; metformin (plus insulin when required) have the lowest incidence of macrosomia, PIH, LGA, RDS, low gestational age at delivery, and low birth weight. Glyburide 170-179 peripherin 2 Homo sapiens 437-440 28864019-6 2017 Additionally, we determined GLUT1 expression by confocal microscopy in cultured primary human trophoblasts (PHT) after exposure to glyburide. Glyburide 131-140 solute carrier family 2 member 1 Homo sapiens 28-33 28864019-10 2017 Glyburide increased membrane expression of GLUT1 in a dose-dependent manner in cultured PHT. Glyburide 0-9 solute carrier family 2 member 1 Homo sapiens 43-48 28864019-11 2017 This data is the first to show that glyburide increases GLUT1 expression in syncytiotrophoblast MVM and BM in GDM pregnancies, and may promote transplacental glucose delivery contributing to fetal overgrowth. Glyburide 36-45 solute carrier family 2 member 1 Homo sapiens 56-61 28662892-3 2017 Pharmacological inhibition of sulfonylurea receptor 1 (SUR1) with glibenclamide was shown previously to reduce glial activation and improve cognition in contusive models of CNS trauma, but has not been examined in bTBI. Glyburide 66-79 ATP binding cassette subfamily C member 8 Rattus norvegicus 30-53 28662892-3 2017 Pharmacological inhibition of sulfonylurea receptor 1 (SUR1) with glibenclamide was shown previously to reduce glial activation and improve cognition in contusive models of CNS trauma, but has not been examined in bTBI. Glyburide 66-79 ATP binding cassette subfamily C member 8 Rattus norvegicus 55-59 28342366-5 2017 It also showed an increase of 2-fold in the [Ca2+]i level allowing an increment on insulin release, being as active as the positive control (glibenclamide), causing also an increase of 2-fold in mRNA expression of GPR40. Glyburide 141-154 free fatty acid receptor 1 Mus musculus 214-219 28486736-1 2017 We compared the individual effects of mitiglinide and glibenclamide administered in combination with the dipeptidyl peptidase-IV (DPP-IV) inhibitor sitagliptin on plasma DPP-IV activity and blood glucose levels in rats with streptozotocin-nicotinamide-induced type 2 diabetes (STZ-NA rats). Glyburide 54-67 dipeptidylpeptidase 4 Rattus norvegicus 170-176 28444661-2 2017 Recent research has demonstrated that SLCO1B3 functions as a determinant of the insulinotropic effect of glibenclamide at the tissue level. Glyburide 105-118 solute carrier organic anion transporter family member 1B3 Homo sapiens 38-45 28380448-0 2017 Glibenclamide, a diabetic drug, prevents acute radiation induced liver injury of mice via up-regulating intracellular ROS and subsequently activating Akt-NF-kappaB pathway. Glyburide 0-13 thymoma viral proto-oncogene 1 Mus musculus 150-153 28380448-0 2017 Glibenclamide, a diabetic drug, prevents acute radiation induced liver injury of mice via up-regulating intracellular ROS and subsequently activating Akt-NF-kappaB pathway. Glyburide 0-13 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 154-163 28380448-7 2017 RESULTS: Glibenclamide mitigated acute radiation-induced liver injury of mice, indicating as regression of hepatocellular edema, reduction of hepatic sinusoid, decline in serum ALP level and reduction of hepatocellular apoptosis. Glyburide 9-22 alopecia, recessive Mus musculus 177-180 28380448-15 2017 CONCLUSIONS: Glibenclamide, prevents acute radiation-induced liver injury of mice via up-regulating intracellular reactive oxygen species and subsequently activating Akt-NF-kappaB pathway. Glyburide 13-26 thymoma viral proto-oncogene 1 Mus musculus 166-169 28380448-15 2017 CONCLUSIONS: Glibenclamide, prevents acute radiation-induced liver injury of mice via up-regulating intracellular reactive oxygen species and subsequently activating Akt-NF-kappaB pathway. Glyburide 13-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 170-179 28592027-0 2017 [Glyburide prevents pulmonary artery smooth muscle cell proliferation and migration via inhibiting NLRP3 activation]. Glyburide 1-10 NLR family pyrin domain containing 3 Homo sapiens 99-104 28592027-1 2017 Objective: To investigate whether glyburide prevents platelet-derived growth factor (PDGF) induced pulmonary artery smooth muscle cells(PASMCs) proliferation and migration via inhibiting nucleotide binding domain leucine-rich repeat-containing receptors protein 3(NLRP3) inflammasome activation. Glyburide 34-43 NLR family pyrin domain containing 3 Homo sapiens 264-269 28592027-10 2017 Conclusion: Glyburide could ameliorate PDGF-induced PASMCs proliferation and migration by inhibiting NLRP3 inflammasome activation. Glyburide 12-21 NLR family pyrin domain containing 3 Homo sapiens 101-106 28412320-1 2017 Glibenclamide (GBC), a sulfonylurea receptor 1 blocker, emerges recently as a promising neuron protectant in various neurological disorders. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 23-46 28412320-1 2017 Glibenclamide (GBC), a sulfonylurea receptor 1 blocker, emerges recently as a promising neuron protectant in various neurological disorders. Glyburide 15-18 ATP binding cassette subfamily C member 8 Rattus norvegicus 23-46 27993998-11 2017 Glyburide markedly suppressed NLRP3 inflammasome expression/activation in IL-10-/- mice, leading to not only alleviation of ongoing colitis but also prevention/delay of disease onset. Glyburide 0-9 NLR family, pyrin domain containing 3 Mus musculus 30-35 27993998-11 2017 Glyburide markedly suppressed NLRP3 inflammasome expression/activation in IL-10-/- mice, leading to not only alleviation of ongoing colitis but also prevention/delay of disease onset. Glyburide 0-9 interleukin 10 Mus musculus 74-79 28342877-4 2017 Furthermore, we demonstrated the effect of an antidiabetic drug, glibenclamide, on synchronized insulin secretion from 2D- and 3D-cultured iGL cells. Glyburide 65-78 immunoglobulin lambda chain complex Rattus norvegicus 139-142 28077460-11 2017 In the glyburide group, nine (17%) patients were eventually treated with insulin compared with two (4%) in the metformin group (P = 0.03). Glyburide 7-16 insulin Homo sapiens 73-80 28496181-5 2017 Inhibition of KCC2 activity in clonal MIN6 beta-cells increases basal and glucose-stimulated insulin secretion and Ca2+ uptake in the presence of glibenclamide, an inhibitor of the ATP-dependent potassium (KATP)-channels, thus suggesting a possible mechanism underlying KCC2-dependent insulin release. Glyburide 146-159 solute carrier family 12, member 5 Mus musculus 14-18 28496181-5 2017 Inhibition of KCC2 activity in clonal MIN6 beta-cells increases basal and glucose-stimulated insulin secretion and Ca2+ uptake in the presence of glibenclamide, an inhibitor of the ATP-dependent potassium (KATP)-channels, thus suggesting a possible mechanism underlying KCC2-dependent insulin release. Glyburide 146-159 solute carrier family 12, member 5 Mus musculus 270-274 28320833-6 2017 Many molecules produced by adipocytes activate the NLRP3 inflammasome, and the NLRP3 inhibitor, glibenclamide, restored B lymphopoiesis and minimized induction of myeloid cells induced by adipocyte-conditioned medium in vitro. Glyburide 96-109 NLR family pyrin domain containing 3 Homo sapiens 79-84 28119170-16 2017 CONCLUSIONS: These results indicate that human PDL cells express KATP channels subunit including Sur2B and Kir6.1 and Kir6.2 which are sensitive to ATP but insensitive to glibenclamide. Glyburide 171-184 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 107-113 28153878-8 2017 Finally, blocking this cascade with the inflammasome inhibitor, glyburide (an antidiabetic medication), reduced angiotensin II-induced AAD formation. Glyburide 64-73 angiotensinogen Homo sapiens 112-126 27807801-10 2017 Glibenclamide protected BBB integrity and improved neurological outcomes after ICH by inhibiting the Sur1-Trpm4 channel, which reduces the expression of MMPs and thereby increases BBB tight-junction protein levels. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 101-105 27807801-10 2017 Glibenclamide protected BBB integrity and improved neurological outcomes after ICH by inhibiting the Sur1-Trpm4 channel, which reduces the expression of MMPs and thereby increases BBB tight-junction protein levels. Glyburide 0-13 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 106-111 28099049-7 2017 This increase in outflow induced by l-cysteine was significantly (P < 0.001) antagonized by AOAA (30 muM) and glibenclamide (100 muM). Glyburide 113-126 latexin Homo sapiens 132-135 28804207-5 2017 As genetic analysis identified a missense mutation within ABCC8, the insulin was replaced by glibenclamide at five months of age. Glyburide 93-106 ATP binding cassette subfamily C member 8 Homo sapiens 58-63 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 0-13 mitogen-activated protein kinase 8 Mus musculus 53-56 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 0-13 jun proto-oncogene Mus musculus 57-62 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 0-13 mitogen-activated protein kinase 8 Mus musculus 230-233 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 0-13 jun proto-oncogene Mus musculus 234-239 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 182-195 mitogen-activated protein kinase 8 Mus musculus 230-233 27297934-8 2017 Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01).Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). Glyburide 182-195 jun proto-oncogene Mus musculus 234-239 28092267-6 2017 The SUR1-ABC core is found in an unusual inward-facing conformation whereby the two nucleotide binding domains are misaligned along a two-fold symmetry axis, revealing a possible mechanism by which glibenclamide inhibits channel activity. Glyburide 198-211 ATP binding cassette subfamily C member 8 Homo sapiens 4-8 28092267-6 2017 The SUR1-ABC core is found in an unusual inward-facing conformation whereby the two nucleotide binding domains are misaligned along a two-fold symmetry axis, revealing a possible mechanism by which glibenclamide inhibits channel activity. Glyburide 198-211 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 9-12 28086082-5 2017 Glibenclamide-bound SUR1 uses TMD0-L0 fragment to stabilize Kir6.2 channel in a closed conformation. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 20-24 28086082-5 2017 Glibenclamide-bound SUR1 uses TMD0-L0 fragment to stabilize Kir6.2 channel in a closed conformation. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 60-66 28086082-6 2017 In another structural population, a putative co-purified phosphatidylinositol 4,5-bisphosphate (PIP2) molecule uncouples Kir6.2 from glibenclamide-bound SUR1. Glyburide 133-146 ATP binding cassette subfamily C member 8 Homo sapiens 153-157 27316908-0 2017 Mechanism of Action of Novel Glibenclamide Derivatives on Potassium and Calcium Channels for Insulin Secretion. Glyburide 29-42 insulin Homo sapiens 93-100 29201919-4 2017 Glibenclamide, a Kir 6.2 potassium channel blocker, and Bay K 8644, an opener of the voltage-sensitive Ca2+ channel, also potentiated glucose-induced insulin secretion. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 17-24 28740332-4 2017 Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 40-44 28740332-4 2017 Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glyburide 0-13 transient receptor potential cation channel subfamily M member 4 Homo sapiens 45-50 28740332-4 2017 Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glyburide 0-13 NLR family pyrin domain containing 3 Homo sapiens 109-114 28740332-4 2017 Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glyburide 0-13 tumor necrosis factor Homo sapiens 195-204 28740332-4 2017 Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-alpha, IL-1beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glyburide 0-13 interleukin 1 beta Homo sapiens 206-214 28006000-2 2016 In parallel, the anti-diabetic sulphonylurea glibenclamide was shown to promote the assembly and function of Cx36 channels. Glyburide 45-58 gap junction protein, delta 2 Mus musculus 109-113 27496642-5 2016 Treatment with either naringin or glibenclamide significantly reduced lipid peroxidation, Superoxide Dismutase (SOD) activities and also increased glutathione (GSH) and ATP levels in the cells that were treated with PIs. Glyburide 34-47 superoxide dismutase 1 Homo sapiens 90-110 27496642-5 2016 Treatment with either naringin or glibenclamide significantly reduced lipid peroxidation, Superoxide Dismutase (SOD) activities and also increased glutathione (GSH) and ATP levels in the cells that were treated with PIs. Glyburide 34-47 superoxide dismutase 1 Homo sapiens 112-115 27496642-6 2016 Furthermore, naringin or glibenclamide significantly reduced caspase-3 and caspase-9 activities in cells that were treated with PIs. Glyburide 25-38 caspase 3 Homo sapiens 61-70 27496642-6 2016 Furthermore, naringin or glibenclamide significantly reduced caspase-3 and caspase-9 activities in cells that were treated with PIs. Glyburide 25-38 caspase 9 Homo sapiens 75-84 27086859-5 2016 KCOs inhibited oxytocin (OXT)- and prostaglandin F2alpha (PGF2alpha)-induced phasic contractions in a glibenclamide-sensitive manner. Glyburide 102-115 oxytocin Mus musculus 15-23 27614764-5 2016 Moreover, human nasal epithelial cells (HNECs) were used to evaluate the effects of lipopolysaccharide (LPS) and glyburide on NLRP3 inflammasome signaling pathway. Glyburide 113-122 NLR family pyrin domain containing 3 Homo sapiens 126-131 27614764-9 2016 NLRP3 inflammasome signaling pathway was augmented by LPS but suppressed by glyburide. Glyburide 76-85 NLR family pyrin domain containing 3 Homo sapiens 0-5 27614764-11 2016 NLRP3 inflammasome signaling pathway was augmented by LPS, but suppressed by glyburide. Glyburide 77-86 NLR family pyrin domain containing 3 Homo sapiens 0-5 27686831-6 2016 The concentration-response curve to glabridin (0.1 to 30muM) was downshifted by the KATP channel blocker glibenclamide (10muM), the KV channel blocker 4-aminopyridine (300muM), and the KIR blocker BaCl2 (30muM). Glyburide 105-118 latexin Homo sapiens 56-59 27686831-6 2016 The concentration-response curve to glabridin (0.1 to 30muM) was downshifted by the KATP channel blocker glibenclamide (10muM), the KV channel blocker 4-aminopyridine (300muM), and the KIR blocker BaCl2 (30muM). Glyburide 105-118 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 185-188 27561267-1 2016 PURPOSE: Glibenclamide (Gb) is used in type II diabetes mellitus but also in the last 10 years, off label, in patients with neonatal syndromic hyperglycemia carrying a mutation of Kir6.2 or SUR1. Glyburide 9-22 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 180-186 27561267-1 2016 PURPOSE: Glibenclamide (Gb) is used in type II diabetes mellitus but also in the last 10 years, off label, in patients with neonatal syndromic hyperglycemia carrying a mutation of Kir6.2 or SUR1. Glyburide 9-22 ATP binding cassette subfamily C member 8 Homo sapiens 190-194 27561267-1 2016 PURPOSE: Glibenclamide (Gb) is used in type II diabetes mellitus but also in the last 10 years, off label, in patients with neonatal syndromic hyperglycemia carrying a mutation of Kir6.2 or SUR1. Glyburide 24-26 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 180-186 27561267-1 2016 PURPOSE: Glibenclamide (Gb) is used in type II diabetes mellitus but also in the last 10 years, off label, in patients with neonatal syndromic hyperglycemia carrying a mutation of Kir6.2 or SUR1. Glyburide 24-26 ATP binding cassette subfamily C member 8 Homo sapiens 190-194 27561267-8 2016 A variant genotype of CYP2C9 (i.e., *1/*2 and *1/*3) explained also a part of the remaining variability on Gb clearance. Glyburide 107-109 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 22-28 27573238-5 2016 In the present study, we identified 13 novel SUR1 mutations that cause channel trafficking defects, the majority of which are amenable to pharmacological rescue by glibenclamide and carbamazepine. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 45-49 27497881-5 2016 Treatment with glibenclamide, a Kir6.1 (ATP-sensitive) potassium channel blocker, inhibited vasodilation induced by 100 and 300 nmol isoquercitrin, but only partially reduced the effect of 1000 nmol isoquercitrin. Glyburide 15-28 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 32-38 27560494-4 2016 Glibenclamide, an SUR1 antagonist, appears to have neuroprotective effect against cerebral stroke in an open-label small clinical trial and great effectiveness in reducing damage after varied experimental CNS injury models. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 18-22 27560494-6 2016 Furthermore, the SUR1 antagonist glibenclamide administered immediately after rAION injury provided no protection to proximal ON microvasculature 1 day post-injury but may reduce optic nerve head edema in a manner unrelated to ON SUR1 expression. Glyburide 33-46 ATP binding cassette subfamily C member 8 Rattus norvegicus 17-21 27217490-5 2016 In contrast, glibenclamide, metabolized by hepatic CYP3A, canagliflozin, metabolized mainly by UDP-glucuronosyltransferases (UGT), and troglitazone, metabolized by sulfotransferase and UGT, exhibited significantly lower plasma clearance in ZDF than in SD rats after a single intravenous administration. Glyburide 13-26 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 51-56 27833799-10 2016 CaSR agonist spermine and KATP blocker glibenclamide offset IPC"s effects on CaSR expression and [Ca2+]i modulation. Glyburide 39-52 calcium-sensing receptor Rattus norvegicus 0-4 27833799-10 2016 CaSR agonist spermine and KATP blocker glibenclamide offset IPC"s effects on CaSR expression and [Ca2+]i modulation. Glyburide 39-52 calcium-sensing receptor Rattus norvegicus 77-81 27353597-8 2016 This effect was inhibited by a leptin antagonist (mutant L39A/D40A/F41A) and by ATP gated K(+) (KATP) channel closer glibenclamide, suggesting that leptin affects sweet taste responses of enteroendocrine cells via activation of leptin receptor and KATP channel expressed in these cells. Glyburide 117-130 leptin Mus musculus 148-154 27353597-8 2016 This effect was inhibited by a leptin antagonist (mutant L39A/D40A/F41A) and by ATP gated K(+) (KATP) channel closer glibenclamide, suggesting that leptin affects sweet taste responses of enteroendocrine cells via activation of leptin receptor and KATP channel expressed in these cells. Glyburide 117-130 leptin Mus musculus 148-154 27528423-5 2016 The inhibition of NLRP3 by means of glybenclamide significantly reduced IL-1beta release. Glyburide 36-49 NLR family, pyrin domain containing 3 Mus musculus 18-23 27528423-5 2016 The inhibition of NLRP3 by means of glybenclamide significantly reduced IL-1beta release. Glyburide 36-49 interleukin 1 beta Mus musculus 72-80 27753906-8 2016 Diazoxide (300 muM), cromakalim (10 muM) nicorandil (10 muM) which is known to activate KATP channel also completely blocked vasomotion in a glibenclamide sensitive manner. Glyburide 141-154 latexin Homo sapiens 15-18 27753906-8 2016 Diazoxide (300 muM), cromakalim (10 muM) nicorandil (10 muM) which is known to activate KATP channel also completely blocked vasomotion in a glibenclamide sensitive manner. Glyburide 141-154 latexin Homo sapiens 36-39 27753906-8 2016 Diazoxide (300 muM), cromakalim (10 muM) nicorandil (10 muM) which is known to activate KATP channel also completely blocked vasomotion in a glibenclamide sensitive manner. Glyburide 141-154 latexin Homo sapiens 36-39 26831749-9 2016 Moreover, as showed in the first two case-reports, when the treatment was switched from insulin to glibenclamide, according to identification of Kir 6.2 mutation and diagnosis of NPDM, the CSII therapy demonstrated to be helpful in allowing gradual insulin suspension and progressive introduction of sulfonylurea. Glyburide 99-112 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 145-152 26831749-9 2016 Moreover, as showed in the first two case-reports, when the treatment was switched from insulin to glibenclamide, according to identification of Kir 6.2 mutation and diagnosis of NPDM, the CSII therapy demonstrated to be helpful in allowing gradual insulin suspension and progressive introduction of sulfonylurea. Glyburide 99-112 insulin Homo sapiens 249-256 27217490-5 2016 In contrast, glibenclamide, metabolized by hepatic CYP3A, canagliflozin, metabolized mainly by UDP-glucuronosyltransferases (UGT), and troglitazone, metabolized by sulfotransferase and UGT, exhibited significantly lower plasma clearance in ZDF than in SD rats after a single intravenous administration. Glyburide 13-26 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 95-123 27217490-5 2016 In contrast, glibenclamide, metabolized by hepatic CYP3A, canagliflozin, metabolized mainly by UDP-glucuronosyltransferases (UGT), and troglitazone, metabolized by sulfotransferase and UGT, exhibited significantly lower plasma clearance in ZDF than in SD rats after a single intravenous administration. Glyburide 13-26 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 125-128 27217490-5 2016 In contrast, glibenclamide, metabolized by hepatic CYP3A, canagliflozin, metabolized mainly by UDP-glucuronosyltransferases (UGT), and troglitazone, metabolized by sulfotransferase and UGT, exhibited significantly lower plasma clearance in ZDF than in SD rats after a single intravenous administration. Glyburide 13-26 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 185-188 27086859-5 2016 KCOs inhibited oxytocin (OXT)- and prostaglandin F2alpha (PGF2alpha)-induced phasic contractions in a glibenclamide-sensitive manner. Glyburide 102-115 oxytocin Mus musculus 25-28 27431258-9 2016 RESULTS: GLP-1 prevented stunning even with glibenclamide pretreatment; the Delta % dP/dtmax 30-min post-BO1 normalized to baseline after GLP-1: 0.3 +- 6.8 % (p = 0.02) and GLP-1 + glibenclamide: -0.8 +- 9.0 % (p = 0.04) compared to control: -11.5 +- 10.0 %. Glyburide 44-57 glucagon like peptide 1 receptor Homo sapiens 9-14 27413041-1 2016 BACKGROUND: We previously have shown that glibenclamide (GBC), a sulfonylurea receptor 1-transient receptor potential M4 (SUR1-TRPM4) channel inhibitor, improves survival and neurological outcome after asphyxial cardiac arrest and cardiopulmonary resuscitation (ACA/CPR). Glyburide 42-55 ATP binding cassette subfamily C member 8 Rattus norvegicus 122-126 27413041-1 2016 BACKGROUND: We previously have shown that glibenclamide (GBC), a sulfonylurea receptor 1-transient receptor potential M4 (SUR1-TRPM4) channel inhibitor, improves survival and neurological outcome after asphyxial cardiac arrest and cardiopulmonary resuscitation (ACA/CPR). Glyburide 42-55 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 127-132 27413041-1 2016 BACKGROUND: We previously have shown that glibenclamide (GBC), a sulfonylurea receptor 1-transient receptor potential M4 (SUR1-TRPM4) channel inhibitor, improves survival and neurological outcome after asphyxial cardiac arrest and cardiopulmonary resuscitation (ACA/CPR). Glyburide 57-60 ATP binding cassette subfamily C member 8 Rattus norvegicus 122-126 27413041-1 2016 BACKGROUND: We previously have shown that glibenclamide (GBC), a sulfonylurea receptor 1-transient receptor potential M4 (SUR1-TRPM4) channel inhibitor, improves survival and neurological outcome after asphyxial cardiac arrest and cardiopulmonary resuscitation (ACA/CPR). Glyburide 57-60 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 127-132 27246103-5 2016 Pharmacological inhibition of Sur1 (glibenclamide), Trpm4 (9-phenanthrol), or gene silencing of Abcc8 or Trpm4 reduced Nos2 upregulation. Glyburide 36-49 nitric oxide synthase 2 Rattus norvegicus 119-123 27487277-0 2016 Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide. Glyburide 112-125 tumor necrosis factor Rattus norvegicus 55-60 27487277-7 2016 CONCLUSIONS: Hemorrhage and glibenclamide elevated TNF-alpha and IL-1 concentrations in serum and kidneys. Glyburide 28-41 tumor necrosis factor Rattus norvegicus 51-60 27487277-8 2016 High levels of TNF-alpha already present before the hemorrhage in the glibenclamide group may have attenuated the damages found in the kidneys after the ischemia event. Glyburide 70-83 tumor necrosis factor Rattus norvegicus 15-24 27329029-10 2016 Five of the patients with an ABCC8 or KCNJ11 mutation have successfully transferred from insulin to glibenclamide whist 1 child demonstrated a partial response to sulfonylurea treatment. Glyburide 100-113 ATP binding cassette subfamily C member 8 Homo sapiens 29-34 27329029-10 2016 Five of the patients with an ABCC8 or KCNJ11 mutation have successfully transferred from insulin to glibenclamide whist 1 child demonstrated a partial response to sulfonylurea treatment. Glyburide 100-113 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 38-44 27383173-3 2016 In contrast, glibenclamide significantly reduced the inhibitory effect of atrial natriuretic peptide. Glyburide 13-26 natriuretic peptide A Bos taurus 74-100 26901099-8 2016 Notably, L-Cys-evoked enhancement of nutrient transport was alleviated by glibenclamide (Gli;0.1 mmol/L; 10 min before the administration of L-Cys), a K(+) channel blocker. Glyburide 74-87 GLI family zinc finger 1 Rattus norvegicus 89-92 27066297-5 2016 Glyburide (a NLRP3 inhibitor) or vehicle was administered orally prior to and after injection. Glyburide 0-9 NLR family, pyrin domain containing 3 Rattus norvegicus 13-18 27163280-4 2016 Insulin has traditionally been the treatment of choice but since 2007, glyburide, a second generation sulfonylurea has become the most prescribed medication for GDM. Glyburide 71-80 insulin Homo sapiens 0-7 26707508-7 2016 Rats with bladder outlet obstruction were given vehicle (10% ethanol) or 10 mg/kg glyburide (a NLRP3 inhibitor) orally daily for 12 days. Glyburide 82-91 NLR family, pyrin domain containing 3 Rattus norvegicus 95-100 26739488-7 2016 Furthermore, UCP2 inhibition using small interfering RNA (siRNA) and the application of glibenclamide, an ATP-sensitive potassium (KATP(+)) channel blocker, reverse the GLP-1 secretion defect induced by chronic high-glucose treatment. Glyburide 88-101 glucagon Homo sapiens 169-174 26850786-9 2016 Overall, this research provides important mechanistic data regarding how the environment (dietary genistein) and a frequent genetic variant (ABCG2, C421A) may alter the maternal-fetal disposition of glyburide. Glyburide 199-208 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 141-146 27087100-3 2016 Metgod: In present work six different formulations of Atenolol (AF1-AF6) and Glyburide (GF1-GF6) were prepared by direct compression method using Avicel, Lactose DC, Crospovidone and Magnesium Stearate in different proportions and encapsulated in hard gelatin shells. Glyburide 77-86 GATA binding protein 1 Homo sapiens 88-95 26796130-3 2016 Glyburide failure was defined as reaching glyburide 20 mg day(-1) and receiving insulin. Glyburide 0-9 insulin Homo sapiens 80-87 26796130-4 2016 Glyburide success was defined as any glyburide dose without insulin and >70% of visits with glycemic control. Glyburide 0-9 insulin Homo sapiens 60-67 26850786-0 2016 Genetic and Dietary Regulation of Glyburide Efflux by the Human Placental Breast Cancer Resistance Protein Transporter. Glyburide 34-43 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 74-106 26850786-1 2016 Glyburide is frequently used to treat gestational diabetes owing to its low fetal accumulation resulting from placental efflux by the breast cancer resistance protein (BCRP)/ABCG2 transporter. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 134-166 26850786-1 2016 Glyburide is frequently used to treat gestational diabetes owing to its low fetal accumulation resulting from placental efflux by the breast cancer resistance protein (BCRP)/ABCG2 transporter. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 168-172 26850786-1 2016 Glyburide is frequently used to treat gestational diabetes owing to its low fetal accumulation resulting from placental efflux by the breast cancer resistance protein (BCRP)/ABCG2 transporter. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 174-179 26850786-2 2016 Here we sought to determine how exposure to the dietary phytoestrogen genistein and expression of a loss-of-function polymorphism in the ABCG2 gene (C421A) impacted the transport of glyburide by BCRP using stably transfected human embryonic kidney 293 (HEK) cells, human placental choriocarcinoma BeWo cells, and human placental explants. Glyburide 182-191 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 137-142 26850786-2 2016 Here we sought to determine how exposure to the dietary phytoestrogen genistein and expression of a loss-of-function polymorphism in the ABCG2 gene (C421A) impacted the transport of glyburide by BCRP using stably transfected human embryonic kidney 293 (HEK) cells, human placental choriocarcinoma BeWo cells, and human placental explants. Glyburide 182-191 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 195-199 27008632-4 2016 METHODS: We genotyped 5 variants of these genes in a total of 747 diabetic patients enrolled in a trial of glibenclamide (CYP2C9, KCNJ11, TCF7L2, KCNQ1 and CDKN2A/2B gene). Glyburide 107-120 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 122-128 27008632-10 2016 After adjusting for sex, age, BMI, total dose of glibenclamide and baseline HbA1c, Cox regression showed a borderline significant association between the number of risk alleles and glibenclamide treatment failure (HR=1.125, 95%CI 1.016-1.246, P=0.023). Glyburide 181-194 cytochrome c oxidase subunit 8A Homo sapiens 83-86 27008632-13 2016 CONCLUSION: Our study demonstrated that the combined genetic variants were borderline significantly associated with the efficacy of glibenclamide, and there are gene-gene interaction between KCNJ11 and CDKN2A/2B. Glyburide 132-145 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 191-197 27008632-13 2016 CONCLUSION: Our study demonstrated that the combined genetic variants were borderline significantly associated with the efficacy of glibenclamide, and there are gene-gene interaction between KCNJ11 and CDKN2A/2B. Glyburide 132-145 cyclin dependent kinase inhibitor 2A Homo sapiens 202-211 27066297-8 2016 RESULTS: Injection of LPS stimulated inflammasome activation (caspase-1 activity) and the release of IL-1beta into the urine which was prevented by glyburide. Glyburide 148-157 caspase 1 Rattus norvegicus 62-71 27066297-8 2016 RESULTS: Injection of LPS stimulated inflammasome activation (caspase-1 activity) and the release of IL-1beta into the urine which was prevented by glyburide. Glyburide 148-157 interleukin 1 beta Rattus norvegicus 101-109 26211973-4 2016 Chronic treatment of db/db mice with antidiabetic drugs such as metformin, glibenclamide and insulin glargine significantly decreased Abeta influx across the BBB determined by intra-arterial infusion of (125)I-Abeta(1-40), and expression of the receptor for advanced glycation end products (RAGE) participating in Abeta influx. Glyburide 75-88 amyloid beta (A4) precursor protein Mus musculus 134-139 26211973-4 2016 Chronic treatment of db/db mice with antidiabetic drugs such as metformin, glibenclamide and insulin glargine significantly decreased Abeta influx across the BBB determined by intra-arterial infusion of (125)I-Abeta(1-40), and expression of the receptor for advanced glycation end products (RAGE) participating in Abeta influx. Glyburide 75-88 advanced glycosylation end product-specific receptor Mus musculus 245-289 26211973-4 2016 Chronic treatment of db/db mice with antidiabetic drugs such as metformin, glibenclamide and insulin glargine significantly decreased Abeta influx across the BBB determined by intra-arterial infusion of (125)I-Abeta(1-40), and expression of the receptor for advanced glycation end products (RAGE) participating in Abeta influx. Glyburide 75-88 advanced glycosylation end product-specific receptor Mus musculus 291-295 26211973-4 2016 Chronic treatment of db/db mice with antidiabetic drugs such as metformin, glibenclamide and insulin glargine significantly decreased Abeta influx across the BBB determined by intra-arterial infusion of (125)I-Abeta(1-40), and expression of the receptor for advanced glycation end products (RAGE) participating in Abeta influx. Glyburide 75-88 amyloid beta (A4) precursor protein Mus musculus 210-215 27928958-9 2016 CONCLUSION: The use of either NPH insulin or a DPP-4 inhibitor as add-on treatments improves glucose control in patients with T2D failing on metformin plus glyburide therapy. Glyburide 156-165 dipeptidyl peptidase 4 Homo sapiens 47-52 26474038-2 2016 Here we present a novel approach to beta-cell imaging by targeting the sulphonylurea receptor subtype 1 (SUR1), using multivalent derivatives of the anti-diabetic drug glibenclamide. Glyburide 168-181 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 71-103 26474038-2 2016 Here we present a novel approach to beta-cell imaging by targeting the sulphonylurea receptor subtype 1 (SUR1), using multivalent derivatives of the anti-diabetic drug glibenclamide. Glyburide 168-181 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 105-109 26474038-3 2016 Since glibenclamide has a high affinity for SUR1 but does not contain a suitable functional group to be linked to an imaging probe, we have synthesized 11 glibenclamide derivatives and evaluated their affinity to SUR1 in MIN6 cells. Glyburide 6-19 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 44-48 26609764-6 2016 We found that few studies reported information on beta-cell function effects in GDM, despite some agents, such as glyburide, are well known insulin secretagogues. Glyburide 114-123 insulin Homo sapiens 140-147 26581714-1 2015 BACKGROUND: In experimental autoimmune encephalomyelitis (EAE), deletion of transient receptor potential melastatin 4 (Trpm4) and administration of glibenclamide were found to ameliorate disease progression, prompting speculation that glibenclamide acts by directly inhibiting Trpm4. Glyburide 148-161 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 119-124 26331221-9 2015 Interestingly, C-peptide levels raise during glibenclamide administration support some degree of improvement in insulin secretory capacity induced by the treatment. Glyburide 45-58 insulin Homo sapiens 112-119 26132275-5 2015 Dose-dependent decreases in blood glucose and increases in plasma insulin concentrations were seen with the combination of MK-467 and glibenclamide; the combinations were much more potent than glibenclamide or MK-467 alone. Glyburide 134-147 insulin Homo sapiens 66-73 26254913-11 2015 Also, 5HD and Gli inhibited the effect of RIPC on MDA level and CAT activity (P < 0.05). Glyburide 14-17 catalase Homo sapiens 64-67 26611836-5 2015 Treatment of hyperoxia-exposed mice with either IL1 receptor antagonist to block IL1beta or glyburide to block the Nlrp3 inflammasome results in decreased inflammation and increased alveolarization. Glyburide 92-101 interleukin 1 complex Mus musculus 48-51 26611836-5 2015 Treatment of hyperoxia-exposed mice with either IL1 receptor antagonist to block IL1beta or glyburide to block the Nlrp3 inflammasome results in decreased inflammation and increased alveolarization. Glyburide 92-101 NLR family, pyrin domain containing 3 Mus musculus 115-120 26581714-1 2015 BACKGROUND: In experimental autoimmune encephalomyelitis (EAE), deletion of transient receptor potential melastatin 4 (Trpm4) and administration of glibenclamide were found to ameliorate disease progression, prompting speculation that glibenclamide acts by directly inhibiting Trpm4. Glyburide 148-161 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 277-282 26581714-1 2015 BACKGROUND: In experimental autoimmune encephalomyelitis (EAE), deletion of transient receptor potential melastatin 4 (Trpm4) and administration of glibenclamide were found to ameliorate disease progression, prompting speculation that glibenclamide acts by directly inhibiting Trpm4. Glyburide 235-248 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 76-117 26581714-1 2015 BACKGROUND: In experimental autoimmune encephalomyelitis (EAE), deletion of transient receptor potential melastatin 4 (Trpm4) and administration of glibenclamide were found to ameliorate disease progression, prompting speculation that glibenclamide acts by directly inhibiting Trpm4. Glyburide 235-248 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 119-124 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 29-34 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 82-105 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 107-111 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 121-125 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 126-131 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 121-125 26581714-2 2015 We hypothesized that in EAE, Trpm4 upregulation is accompanied by upregulation of sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which are highly sensitive to glibenclamide, and that Sur1-Trpm4 channels are required for EAE progression. Glyburide 172-185 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 126-131 26581714-5 2015 WT/EAE mice were administered with the Sur1 inhibitor, glibenclamide, beginning on post-induction day 10. Glyburide 55-68 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 39-43 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 72-77 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 protein tyrosine phosphatase, receptor type, C Mus musculus 162-166 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 membrane-spanning 4-domains, subfamily A, member 1 Mus musculus 193-197 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 integrin subunit alpha M Homo sapiens 226-231 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 tumor necrosis factor Homo sapiens 289-298 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 interferon gamma Homo sapiens 300-309 26581714-9 2015 At 30 days, the lumbar spinal cords of glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice showed significantly fewer invading immune cells, including leukocytes (CD45), T cells (CD3), B cells (CD20) and macrophages/microglia (CD11b), and fewer cells expressing pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17). Glyburide 39-52 interleukin 17A Homo sapiens 311-316 26581714-10 2015 In both glibenclamide-treated WT/EAE and Abcc8-/-/EAE mice, the reduced inflammatory burden correlated with better preservation of myelin, better preservation of axons, and more numerous mature and precursor oligodendrocytes. Glyburide 8-21 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 41-46 26506473-7 2015 The blockade of type I interferon receptor and of AIM2 via the addition of LL-37 significantly reduced the release of IL-1alpha, which was still high after Nod-like receptor P3 inhibition via glibenclamide. Glyburide 192-205 absent in melanoma 2 Homo sapiens 50-54 26506473-7 2015 The blockade of type I interferon receptor and of AIM2 via the addition of LL-37 significantly reduced the release of IL-1alpha, which was still high after Nod-like receptor P3 inhibition via glibenclamide. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 75-80 26506473-7 2015 The blockade of type I interferon receptor and of AIM2 via the addition of LL-37 significantly reduced the release of IL-1alpha, which was still high after Nod-like receptor P3 inhibition via glibenclamide. Glyburide 192-205 interleukin 1 alpha Homo sapiens 118-127 26503124-10 2015 Glyburide, ranitidine, gemfibrozil, carvedilol, and allopurinol accounted for 47% of renally misprescribed drugs for individuals with a CrCl of 15 to 29 mL/min. Glyburide 0-9 CRCL Homo sapiens 136-140 26438710-4 2015 However, contemporary administration of insulin with an insulin secretagogue (glyburide), and of additional drugs, can make the diagnostic pathway problematic. Glyburide 78-87 insulin Homo sapiens 40-47 26438710-4 2015 However, contemporary administration of insulin with an insulin secretagogue (glyburide), and of additional drugs, can make the diagnostic pathway problematic. Glyburide 78-87 insulin Homo sapiens 56-63 26010685-11 2015 In addition, glibenclamide reduced the messenger RNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1 in the cortex after return of spontaneous circulation. Glyburide 13-26 tumor necrosis factor Rattus norvegicus 67-94 26172081-6 2015 KATP channel blockers, glibenclamide or tolbutamide, abolished any inhibitory effects of NaHS and enhanced NaHS-mediated [Ca(2+)]i increases, which were inhibited by extracellular Ca(2+) removal, HC030031 (a TRPA1 antagonist), and disulfide bond-reducing agents. Glyburide 23-36 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 208-213 26568660-0 2015 A case of a Japanese patient with neonatal diabetes mellitus caused by a novel mutation in the ABCC8 gene and successfully controlled with oral glibenclamide. Glyburide 144-157 ATP binding cassette subfamily C member 8 Homo sapiens 95-100 26209275-8 2015 Similarly, glibenclamide only exhibited a blocking effect on hCFTR but both blocked and potentiated mCFTR in excised membrane patches and in intact oocytes. Glyburide 11-24 CF transmembrane conductance regulator Homo sapiens 61-66 26010685-11 2015 In addition, glibenclamide reduced the messenger RNA expression of tumor necrosis factor-alpha and monocyte chemoattractant protein-1 in the cortex after return of spontaneous circulation. Glyburide 13-26 C-C motif chemokine ligand 2 Rattus norvegicus 99-133 26010685-12 2015 Furthermore, the sulfonylurea receptor 1 and transient receptor potential M4 heteromers, the putative therapeutic targets of glibenclamide, were up-regulated after cardiac arrest and cardiopulmonary resuscitation, indicating that they might be involved in neuroprotective effect of glibenclamide. Glyburide 125-138 ATP binding cassette subfamily C member 8 Rattus norvegicus 17-40 26010685-12 2015 Furthermore, the sulfonylurea receptor 1 and transient receptor potential M4 heteromers, the putative therapeutic targets of glibenclamide, were up-regulated after cardiac arrest and cardiopulmonary resuscitation, indicating that they might be involved in neuroprotective effect of glibenclamide. Glyburide 282-295 ATP binding cassette subfamily C member 8 Rattus norvegicus 17-40 26548081-4 2015 In the present study, we explored the binding interactions of antidiabetic drugs i.e., sulfonylurea drugs (glimepiride, glipizide, glyburide) and rapid acting insulin secretagogues viz., nateglinide, repaglinide and rosiglitazone; and Pgp inhibitors i.e., Generation I (verapamil and tamoxifen), III (tetradrine and tariquidar), and natural inhibitors (fumagillin and piperine) in mouse Pgp model. Glyburide 131-140 insulin Homo sapiens 159-166 25977483-5 2015 The KATP inhibitors glibenclamide and 5-hydroxydecanoate (5-HD) reduced basal and abolished CNP-induced CAM angiogenesis. Glyburide 20-33 natriuretic peptide type C Mus musculus 92-95 26028562-8 2015 The Kir 6.2 potassium channel blocker glibenclamide and Bay K 8644, an opener of the voltage-sensitive Ca(2+) channel significantly potentiated GSIS. Glyburide 38-51 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 4-11 26434126-5 2015 Furthermore, diabetic rats treated with thymoquinone demonstrated a marked decrease in hepatic protein expressions of CYP3A2 and CYP2C 11 enzymes that are responsible for the metabolism of glibenclamide. Glyburide 189-202 cytochrome P450, family 3, subfamily a, polypeptide 2 Rattus norvegicus 118-124 26434126-5 2015 Furthermore, diabetic rats treated with thymoquinone demonstrated a marked decrease in hepatic protein expressions of CYP3A2 and CYP2C 11 enzymes that are responsible for the metabolism of glibenclamide. Glyburide 189-202 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 129-137 26205024-10 2015 Glibenclamide (100 muM) treatment significantly blocked the anti-apoptotic effects of EPO (10 IU/ml) under both normoxic and hypoxic conditions. Glyburide 0-13 latexin Homo sapiens 19-22 26205024-10 2015 Glibenclamide (100 muM) treatment significantly blocked the anti-apoptotic effects of EPO (10 IU/ml) under both normoxic and hypoxic conditions. Glyburide 0-13 erythropoietin Homo sapiens 86-89 26205024-11 2015 EPO (10 IU/ml) and diazoxide (100 muM) treatments significantly increased (p <0.01) whereas glibenclamide decreased ( p<0.05) HIF-1 alpha mRNA expression. Glyburide 95-108 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-143 26205024-12 2015 Glibenclamide significantly ( p<0.01) decreased EPO induced HIF-1 alpha mRNA expression when compared with the EPO alone group. Glyburide 0-13 erythropoietin Homo sapiens 51-54 26205024-12 2015 Glibenclamide significantly ( p<0.01) decreased EPO induced HIF-1 alpha mRNA expression when compared with the EPO alone group. Glyburide 0-13 hypoxia inducible factor 1 subunit alpha Homo sapiens 63-74 26205024-12 2015 Glibenclamide significantly ( p<0.01) decreased EPO induced HIF-1 alpha mRNA expression when compared with the EPO alone group. Glyburide 0-13 erythropoietin Homo sapiens 114-117 25763566-7 2015 Like human CFTR, ovine CFTR formed a weakly inwardly rectifying Cl(-) channel regulated by PKA-dependent phosphorylation, inhibited by the open-channel blocker glibenclamide. Glyburide 160-173 CF transmembrane conductance regulator Homo sapiens 11-15 25763566-7 2015 Like human CFTR, ovine CFTR formed a weakly inwardly rectifying Cl(-) channel regulated by PKA-dependent phosphorylation, inhibited by the open-channel blocker glibenclamide. Glyburide 160-173 CF transmembrane conductance regulator Homo sapiens 23-27 25765720-13 2015 However, during moderate hyperinsulinemic hypoglycemia (2.9mmol/L) glyburide resulted in increased C-peptide and insulin, but blunted glucagon, sympathetic nervous system and EGP responses. Glyburide 67-76 insulin Homo sapiens 30-37 25739357-4 2015 We found that enhanced vasodilation to A2AAR agonist, CGS 21680, in HS-fed A2AAR(+/+) mice was blocked by PPARgamma antagonist (T0070907) and KATP channel blocker (Glibenclamide). Glyburide 164-177 adenosine A2a receptor Mus musculus 39-44 25739357-4 2015 We found that enhanced vasodilation to A2AAR agonist, CGS 21680, in HS-fed A2AAR(+/+) mice was blocked by PPARgamma antagonist (T0070907) and KATP channel blocker (Glibenclamide). Glyburide 164-177 adenosine A2a receptor Mus musculus 75-80 25637631-3 2015 Here we investigate how two chemically distinct compounds, glibenclamide and carbamazepine, correct biogenesis defects in ATP-sensitive potassium (KATP) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2. Glyburide 59-72 ATP binding cassette subfamily C member 8 Homo sapiens 174-197 25900651-7 2015 Intravaginal administration of wild-type (WT) mice with glyburide, a potent inhibitor of the NLRP3 inflammasome, reduced PMN infiltration and IL-1beta to levels comparable to those observed in Nlrp3(-/-) mice. Glyburide 56-65 NLR family, pyrin domain containing 3 Mus musculus 93-98 25900651-7 2015 Intravaginal administration of wild-type (WT) mice with glyburide, a potent inhibitor of the NLRP3 inflammasome, reduced PMN infiltration and IL-1beta to levels comparable to those observed in Nlrp3(-/-) mice. Glyburide 56-65 interleukin 1 beta Mus musculus 142-150 25900651-7 2015 Intravaginal administration of wild-type (WT) mice with glyburide, a potent inhibitor of the NLRP3 inflammasome, reduced PMN infiltration and IL-1beta to levels comparable to those observed in Nlrp3(-/-) mice. Glyburide 56-65 NLR family, pyrin domain containing 3 Mus musculus 193-198 25849717-9 2015 Treatment with anti-diabetic drugs metformin and glibenclamide also reduced IL-1alpha and IL-1beta secretion in infection and cytokine-primed adipose tissue. Glyburide 49-62 interleukin 1 alpha Homo sapiens 76-85 25849717-9 2015 Treatment with anti-diabetic drugs metformin and glibenclamide also reduced IL-1alpha and IL-1beta secretion in infection and cytokine-primed adipose tissue. Glyburide 49-62 interleukin 1 beta Homo sapiens 90-98 25315008-7 2015 Activation of Rap1 was enhanced by the combination of an Epac-selective cAMP analog with glibenclamide or glimepiride but not gliclazide. Glyburide 89-102 RAS-related protein 1a Mus musculus 14-18 25315008-7 2015 Activation of Rap1 was enhanced by the combination of an Epac-selective cAMP analog with glibenclamide or glimepiride but not gliclazide. Glyburide 89-102 Rap guanine nucleotide exchange factor (GEF) 3 Mus musculus 57-61 25113133-8 2015 Glibenclamide also downregulated OVA-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and phosphorylated signal transducer and activator of transcription 6 (p-STAT6) in the lung. Glyburide 0-13 vascular cell adhesion molecule 1 Mus musculus 60-93 25113133-8 2015 Glibenclamide also downregulated OVA-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and phosphorylated signal transducer and activator of transcription 6 (p-STAT6) in the lung. Glyburide 0-13 vascular cell adhesion molecule 1 Mus musculus 95-101 25113133-8 2015 Glibenclamide also downregulated OVA-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and phosphorylated signal transducer and activator of transcription 6 (p-STAT6) in the lung. Glyburide 0-13 signal transducer and activator of transcription 6 Mus musculus 122-172 25803314-3 2015 The mutagenic potential of glibenclamide in therapeutically plasma (0.6 muM) and higher concentrations (10 muM, 100 muM, 240 muM and 480 muM) was assessed by the in vitro mammalian cell micronucleus test in human lymphocytes. Glyburide 27-40 latexin Homo sapiens 72-75 25803314-3 2015 The mutagenic potential of glibenclamide in therapeutically plasma (0.6 muM) and higher concentrations (10 muM, 100 muM, 240 muM and 480 muM) was assessed by the in vitro mammalian cell micronucleus test in human lymphocytes. Glyburide 27-40 latexin Homo sapiens 107-110 25803314-3 2015 The mutagenic potential of glibenclamide in therapeutically plasma (0.6 muM) and higher concentrations (10 muM, 100 muM, 240 muM and 480 muM) was assessed by the in vitro mammalian cell micronucleus test in human lymphocytes. Glyburide 27-40 latexin Homo sapiens 107-110 25803314-3 2015 The mutagenic potential of glibenclamide in therapeutically plasma (0.6 muM) and higher concentrations (10 muM, 100 muM, 240 muM and 480 muM) was assessed by the in vitro mammalian cell micronucleus test in human lymphocytes. Glyburide 27-40 latexin Homo sapiens 107-110 25803314-3 2015 The mutagenic potential of glibenclamide in therapeutically plasma (0.6 muM) and higher concentrations (10 muM, 100 muM, 240 muM and 480 muM) was assessed by the in vitro mammalian cell micronucleus test in human lymphocytes. Glyburide 27-40 latexin Homo sapiens 107-110 25803314-4 2015 Since the loss of heterozygosity arising from allelic recombination is an important biologically significant consequence of oxidative damage, the glibenclamide recombinogenic activity at 1 muM, 10 muM and 100 muM concentrations was evaluated by the in vivo homozygotization assay. Glyburide 146-159 latexin Homo sapiens 189-192 25803314-4 2015 Since the loss of heterozygosity arising from allelic recombination is an important biologically significant consequence of oxidative damage, the glibenclamide recombinogenic activity at 1 muM, 10 muM and 100 muM concentrations was evaluated by the in vivo homozygotization assay. Glyburide 146-159 latexin Homo sapiens 197-200 25803314-4 2015 Since the loss of heterozygosity arising from allelic recombination is an important biologically significant consequence of oxidative damage, the glibenclamide recombinogenic activity at 1 muM, 10 muM and 100 muM concentrations was evaluated by the in vivo homozygotization assay. Glyburide 146-159 latexin Homo sapiens 197-200 25803314-6 2015 On the other hand, glibenclamide changed the cell-proliferation kinetics when used at 480 muM. Glyburide 19-32 latexin Homo sapiens 90-93 25639477-6 2015 Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082. Glyburide 180-189 interleukin 1 beta Homo sapiens 40-48 25639477-6 2015 Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082. Glyburide 180-189 GLI family zinc finger 2 Homo sapiens 62-67 25639477-6 2015 Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082. Glyburide 180-189 NLR family pyrin domain containing 3 Homo sapiens 163-168 25891870-3 2015 RESULTS: beta2-AR agonist induced myometrial relaxation was inhibited by glibenclamide and enhanced by pinacidil on day 6, when SUR1 expression levels were high. Glyburide 73-86 adrenoceptor beta 2 Rattus norvegicus 9-17 25637631-3 2015 Here we investigate how two chemically distinct compounds, glibenclamide and carbamazepine, correct biogenesis defects in ATP-sensitive potassium (KATP) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2. Glyburide 59-72 ATP binding cassette subfamily C member 8 Homo sapiens 199-203 25637631-3 2015 Here we investigate how two chemically distinct compounds, glibenclamide and carbamazepine, correct biogenesis defects in ATP-sensitive potassium (KATP) channels composed of sulfonylurea receptor 1 (SUR1) and Kir6.2. Glyburide 59-72 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 209-215 25749474-4 2015 Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1-transient receptor potential melastatin 4 (Sur1-Trpm4) channels and, in some cases, microglial KATP (Sur1-Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Glyburide 219-232 ATP binding cassette subfamily C member 8 Homo sapiens 133-137 25749474-4 2015 Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1-transient receptor potential melastatin 4 (Sur1-Trpm4) channels and, in some cases, microglial KATP (Sur1-Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Glyburide 219-232 transient receptor potential cation channel subfamily M member 4 Homo sapiens 138-143 25540100-3 2015 Luminal GN reversed serosa-negative PD, probably by enhancing Cl(-) secretion into the lumen, as the GN effect was blocked by apical Cl(-) channel blockers [diphenylamine-2-carboxylic acid (DPC), 5-nitro-2-(3-phenylpropylamino) benzoic acid, glibenclamide but not cystic fibrosis transmembrane regulator (CFTR)inh-172] or replacement of luminal fluid by MgCl2 Ringer. Glyburide 242-255 guanylate cyclase activator 2A Homo sapiens 8-10 25540100-3 2015 Luminal GN reversed serosa-negative PD, probably by enhancing Cl(-) secretion into the lumen, as the GN effect was blocked by apical Cl(-) channel blockers [diphenylamine-2-carboxylic acid (DPC), 5-nitro-2-(3-phenylpropylamino) benzoic acid, glibenclamide but not cystic fibrosis transmembrane regulator (CFTR)inh-172] or replacement of luminal fluid by MgCl2 Ringer. Glyburide 242-255 guanylate cyclase activator 2A Homo sapiens 101-103 25411819-11 2015 Addition of the KATP channel blocker glibenclamide eliminated the beneficial effects of nicorandil against hypertrophy and on connexin43. Glyburide 37-50 gap junction protein, alpha 1 Rattus norvegicus 126-136 25297572-0 2015 The effect of glibenclamide on insulin secretion at normal glucose concentrations. Glyburide 14-27 insulin Homo sapiens 31-38 25742954-11 2015 It is concluded that not all fibers are dependent on the myoprotection of KATP channels and that the decrease in unstimulated force by verapamil reported in a previous studies in glibenclamide-exposed fibers is due to a reduction in Ca(2+) load by reducing Ca(2+) influx through CaV1.1 channels between and during contractions. Glyburide 179-192 calcium channel, voltage-dependent, L type, alpha 1S subunit Mus musculus 279-285 26269444-1 2015 OBJECTIVE: To observe the effects, and study the mechanism of islet amyloid polypeptide (IAPP) on insulin secretion in INS-1 cells stimulated by glibenclamide. Glyburide 145-158 islet amyloid polypeptide Rattus norvegicus 89-93 26269444-5 2015 RESULTS: (1) Insulin secretion stimulated by 1 micomol/L glibenclamide was significantly decreased from (11.43 +/- 1.22) microg/L to (9.40 +/- 0.87) microg/L and to (7.11 +/- 1.85) microg/L after 1 micromol/L and 10 micromol/L IAPP incubation, respectively. Glyburide 57-70 islet amyloid polypeptide Rattus norvegicus 227-231 26269444-6 2015 (2) Glibenclamide-stimulated calcium influx was dose dependently inhibited by IAPP from 1 micromol/L to 10 micromol/L, with the AUC of fluorescence intensity-time reduced from 427.78 +/- 2.32 to 380.59 +/- 1.49, and to 246.53 +/- 8.41, respectively. Glyburide 4-17 islet amyloid polypeptide Rattus norvegicus 78-82 26269444-7 2015 (3) Compared with that in control cells (14.59 +/- 0.69) mV, the half activation voltage of KA, channel in response to glibenclamide was significantly increased to (28.75 +/- 0.77) mV and to (46.95 +/- 1.81) mV in cells pretreated with 1 micromol/L and 10 micromol/L IAPP, implicating an inhibitory effect of IAPP on activation of K(ATP) channel. Glyburide 119-132 islet amyloid polypeptide Rattus norvegicus 267-271 26269444-7 2015 (3) Compared with that in control cells (14.59 +/- 0.69) mV, the half activation voltage of KA, channel in response to glibenclamide was significantly increased to (28.75 +/- 0.77) mV and to (46.95 +/- 1.81) mV in cells pretreated with 1 micromol/L and 10 micromol/L IAPP, implicating an inhibitory effect of IAPP on activation of K(ATP) channel. Glyburide 119-132 islet amyloid polypeptide Rattus norvegicus 309-313 26269444-8 2015 CONCLUSION: Short-term exposure to high concentration of IAPP inhibited glibenclamide-induced closure of K(ATP) channels and decreased calcium influx, which may ultimately lead to the reduction of insulin secretion in INS-1 cells Glyburide 72-85 islet amyloid polypeptide Rattus norvegicus 57-61 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 NLR family, pyrin domain containing 3 Rattus norvegicus 0-5 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 NLR family, pyrin domain containing 3 Rattus norvegicus 91-96 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 PYD and CARD domain containing Rattus norvegicus 98-101 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 caspase 1 Rattus norvegicus 107-116 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 interleukin 1 beta Rattus norvegicus 141-149 25338942-8 2015 NLRP3 inflammasome blocker glybenclamide pretreatment attenuated lung edema, inhibited the NLRP3, ASC, and caspase-1 activation, and reduced IL-1beta and IL-18 levels in BALF. Glyburide 27-40 interleukin 18 Rattus norvegicus 154-159 25338942-9 2015 In the in vitro experiments, IL-1beta and IL-18 secreted from RAW264.7 mouse macrophages treated with paraquat were attenuated by glybenclamide. Glyburide 130-143 interleukin 1 beta Mus musculus 29-37 25338942-9 2015 In the in vitro experiments, IL-1beta and IL-18 secreted from RAW264.7 mouse macrophages treated with paraquat were attenuated by glybenclamide. Glyburide 130-143 interleukin 18 Mus musculus 42-47 25338942-5 2015 Moreover, rats were pretreated with 10, 30, and 50 mg/kg NLRP3 inflammasome blocker glybenclamide, respectively, 1 h before PQ exposure. Glyburide 84-97 NLR family, pyrin domain containing 3 Rattus norvegicus 57-62 25876805-17 2015 Glyburide increases the expression of AKR1C3 and have therapeutic effect for preeclampsia. Glyburide 0-9 aldo-keto reductase family 1, member C3 Rattus norvegicus 38-44 25297572-9 2015 CONCLUSIONS/INTERPRETATION: At low-normal glucose, glibenclamide exerted a disproportionate effect on insulin secretion. Glyburide 51-64 insulin Homo sapiens 102-109 26435646-10 2015 Glyburide inhibited urate-induced caspase-1 activation, IL-1beta secretion and proliferation. Glyburide 0-9 caspase 1 Homo sapiens 34-43 26435646-10 2015 Glyburide inhibited urate-induced caspase-1 activation, IL-1beta secretion and proliferation. Glyburide 0-9 interleukin 1 beta Homo sapiens 56-64 25665835-0 2015 Lack of glibenclamide response in a case of permanent neonatal diabetes caused by incomplete inactivation of glucokinase. Glyburide 8-21 glucokinase Homo sapiens 109-120 25665835-12 2015 However, glibenclamide treatment of the patient on a reduced dose of insulin did not reduce HbA1c levels, and C-peptide increased only very slightly. Glyburide 9-22 insulin Homo sapiens 69-76 25315294-1 2014 Oral hypoglycemic agents such as glyburide (second-generation sulfonylurea) and metformin (biguanide) are attractive alternatives to insulin due to lower cost, ease of administration, and better patient adherence. Glyburide 33-42 insulin Homo sapiens 133-140 25450675-0 2014 Identification of CYP3A7 for glyburide metabolism in human fetal livers. Glyburide 29-38 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 18-24 25450675-4 2014 In this study, we determined the kinetic parameters for glyburide depletion by CYP3A isoenzymes; characterized glyburide metabolism by human fetal liver tissues collected during the first or early second trimester of pregnancy; and identified the major enzyme responsible for glyburide metabolism in human fetal livers. Glyburide 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 25450675-5 2014 CYP3A4 had the highest metabolic capacity towards glyburide, followed by CYP3A7 and CYP3A5 (Clint,u=37.1, 13.0, and 8.7ml/min/nmol P450, respectively). Glyburide 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25450675-5 2014 CYP3A4 had the highest metabolic capacity towards glyburide, followed by CYP3A7 and CYP3A5 (Clint,u=37.1, 13.0, and 8.7ml/min/nmol P450, respectively). Glyburide 50-59 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 84-90 25450675-8 2014 CYP3A7 protein levels in HFLMs were highly correlated with glyburide Clint, 16alpha-OH DHEA formation, and 4"-OH midazolam formation. Glyburide 59-68 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 0-6 25450675-11 2014 These results indicate that human fetal livers metabolize glyburide predominantly to M5 and that CYP3A7 is the major enzyme responsible for glyburide metabolism in human fetal livers. Glyburide 140-149 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 97-103 25320353-8 2014 A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. Glyburide 184-197 ATP binding cassette subfamily C member 8 Rattus norvegicus 98-119 25320353-8 2014 A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. Glyburide 184-197 ATP binding cassette subfamily C member 8 Rattus norvegicus 121-124 25320353-8 2014 A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. Glyburide 184-197 ATP binding cassette subfamily C member 8 Rattus norvegicus 175-178 25320353-8 2014 A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. Glyburide 184-197 superoxide dismutase 2 Rattus norvegicus 206-211 25320353-8 2014 A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. Glyburide 184-197 sirtuin 3 Rattus norvegicus 216-221 24744252-6 2014 Consistent with the electrophysiology data, the PACAP-induced vasodilations of cannulated cerebellar artery preparations were attenuated by approximately 50 % in the presence of glibenclamide (a KATP channel blocker) or paxilline (a BK channel blocker). Glyburide 178-191 adenylate cyclase activating polypeptide 1 Rattus norvegicus 48-53 24917577-7 2014 Fluvastatin-induced activation of the NLRP3/caspase-1 pathway was required for the development of insulin resistance in adipose tissue explants, an effect also prevented by glyburide. Glyburide 173-182 NLR family, pyrin domain containing 3 Mus musculus 38-43 24917577-7 2014 Fluvastatin-induced activation of the NLRP3/caspase-1 pathway was required for the development of insulin resistance in adipose tissue explants, an effect also prevented by glyburide. Glyburide 173-182 caspase 1 Mus musculus 44-53 24744252-6 2014 Consistent with the electrophysiology data, the PACAP-induced vasodilations of cannulated cerebellar artery preparations were attenuated by approximately 50 % in the presence of glibenclamide (a KATP channel blocker) or paxilline (a BK channel blocker). Glyburide 178-191 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 233-243 24657787-7 2014 Conversely, another caspase 1 inhibitor, glyburide, significantly inhibited virus infection suggesting it had off-target effects on related enzymes or interfered with infection via non-enzymatic mechanisms. Glyburide 41-50 caspase 1 Homo sapiens 20-29 25422710-6 2014 Our study indicates that glibenclamide may decrease cerebral edema by blocking SUR1 receptors in ischemic stroke and non-ischemic etiologies. Glyburide 25-38 ATP binding cassette subfamily C member 8 Homo sapiens 79-83 24907587-7 2014 Caspase-1 KO mice, IL-1R1 KO mice, A2A AR KO mice and WT mice treated with the KATP channel blocker, glyburide, were resistant to adenosine-induced anxiety-like behaviors. Glyburide 101-110 caspase 1 Mus musculus 0-9 24907587-7 2014 Caspase-1 KO mice, IL-1R1 KO mice, A2A AR KO mice and WT mice treated with the KATP channel blocker, glyburide, were resistant to adenosine-induced anxiety-like behaviors. Glyburide 101-110 cytochrome P450, family 19, subfamily a, polypeptide 1 Mus musculus 39-44 24671831-2 2014 Preclinical data suggest that glyburide, an inhibitor of SUR1-TRPM4, is effective in preventing edema. Glyburide 30-39 ATP binding cassette subfamily C member 8 Homo sapiens 57-61 24671831-2 2014 Preclinical data suggest that glyburide, an inhibitor of SUR1-TRPM4, is effective in preventing edema. Glyburide 30-39 transient receptor potential cation channel subfamily M member 4 Homo sapiens 62-67 25077824-18 2014 Glibenclamide treatment suppressed the increase of IL-1beta level induced by high glucose and LPS. Glyburide 0-13 interleukin 1 beta Mus musculus 51-59 25077824-19 2014 Furthermore, Nalp3 and Caspase-1 levels were markedly increased by high glucose plus LPS, and both proteins were significantly inhibited by glibenclamide treatment. Glyburide 140-153 NLR family, pyrin domain containing 3 Mus musculus 13-18 25077824-19 2014 Furthermore, Nalp3 and Caspase-1 levels were markedly increased by high glucose plus LPS, and both proteins were significantly inhibited by glibenclamide treatment. Glyburide 140-153 caspase 1 Mus musculus 23-32 25077824-20 2014 CONCLUSIONS: We conclude that glibenclamide could attenuate myocardial injury induced by LPS challenge in STZ-mice, which was possibly related to inhibiting inflammation through Nalp3 inflammasomes. Glyburide 30-43 NLR family, pyrin domain containing 3 Mus musculus 178-183 24751713-7 2014 Inhibition of K(+) channels with tetraethylammonium and glibenclamide attenuated the emodin-induced changes in ANP secretion and atrial dynamics. Glyburide 56-69 natriuretic peptides A Oryctolagus cuniculus 111-114 24792709-3 2014 Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 33-38 24839071-1 2014 The purpose of this study is to characterize the involvement of hepato-biliary transport and cytochrome-P450 (CYP)-mediated metabolism in the disposition of glyburide and predict its pharmacokinetic variability due to drug interactions and genetic variations. Glyburide 157-166 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 93-108 24839071-1 2014 The purpose of this study is to characterize the involvement of hepato-biliary transport and cytochrome-P450 (CYP)-mediated metabolism in the disposition of glyburide and predict its pharmacokinetic variability due to drug interactions and genetic variations. Glyburide 157-166 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 110-113 24839071-2 2014 Comprehensive in vitro studies suggested that glyburide is a highly permeable drug with substrate affinity to multiple efflux pumps and to organic anion transporting polypeptide (OATP)1B1 and OATP2B1. Glyburide 46-55 solute carrier organic anion transporter family member 1B1 Homo sapiens 179-187 24839071-2 2014 Comprehensive in vitro studies suggested that glyburide is a highly permeable drug with substrate affinity to multiple efflux pumps and to organic anion transporting polypeptide (OATP)1B1 and OATP2B1. Glyburide 46-55 solute carrier organic anion transporter family member 2B1 Homo sapiens 192-199 24839071-4 2014 In vitro, glyburide is metabolized (intrinsic clearance, 52.9 muL/min/mg-microsomal protein) by CYP3A4, CYP2C9, and CYP2C8 with fraction metabolism of 0.53, 0.36, and 0.11, respectively. Glyburide 10-19 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 104-110 24839071-4 2014 In vitro, glyburide is metabolized (intrinsic clearance, 52.9 muL/min/mg-microsomal protein) by CYP3A4, CYP2C9, and CYP2C8 with fraction metabolism of 0.53, 0.36, and 0.11, respectively. Glyburide 10-19 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 116-122 25580176-13 2014 CONCLUSION: Glyburide and metformin appear to be safe and effective to manage blood glucose in patients with gestational diabetes who prefer to not utilize insulin or who cannot afford insulin therapy. Glyburide 12-21 insulin Homo sapiens 185-192 25152324-5 2014 We hypothesized that inhibition of the NLRP3 inflammasome with the sulfonylurea drug glyburide would reduce disease severity in obese mice with cerulein-induced SAP. Glyburide 85-94 NLR family, pyrin domain containing 3 Mus musculus 39-44 25152324-7 2014 Glyburide administration in ob/ob mice with cerulein-induced SAP also resulted in significantly reduced serum levels of interleukin 6, lipase, and amylase and led to lower production of lipopolysaccharide-stimulated interleukin 1beta release in cultured peritoneal cells, compared with vehicle-treated ob/ob mice with SAP. Glyburide 0-9 lipase, endothelial Mus musculus 135-141 25152324-7 2014 Glyburide administration in ob/ob mice with cerulein-induced SAP also resulted in significantly reduced serum levels of interleukin 6, lipase, and amylase and led to lower production of lipopolysaccharide-stimulated interleukin 1beta release in cultured peritoneal cells, compared with vehicle-treated ob/ob mice with SAP. Glyburide 0-9 interleukin 1 beta Mus musculus 216-233 25216263-6 2014 In addition, the genetic (small interfering ribonucleic acid [siRNA]) and pharmacological (glyburide) inhibition of the NLRP3 inflammasome in CFs can block this signaling pathway. Glyburide 91-100 NLR family, pyrin domain containing 3 Mus musculus 120-125 25200305-8 2014 8-pCPT-2"-O-Me-cAMP, an Epac-selective cAMP analogue, and glibenclamide, a sulfonylurea, synergistically activate Epac2A and Rap1, whereas adrenaline, which suppresses cAMP production in pancreatic beta-cells, blocks activation of Epac2A and Rap1 by glibenclamide. Glyburide 58-71 RAP1A, member of RAS oncogene family Homo sapiens 125-129 25200305-8 2014 8-pCPT-2"-O-Me-cAMP, an Epac-selective cAMP analogue, and glibenclamide, a sulfonylurea, synergistically activate Epac2A and Rap1, whereas adrenaline, which suppresses cAMP production in pancreatic beta-cells, blocks activation of Epac2A and Rap1 by glibenclamide. Glyburide 58-71 RAP1A, member of RAS oncogene family Homo sapiens 242-246 25200305-8 2014 8-pCPT-2"-O-Me-cAMP, an Epac-selective cAMP analogue, and glibenclamide, a sulfonylurea, synergistically activate Epac2A and Rap1, whereas adrenaline, which suppresses cAMP production in pancreatic beta-cells, blocks activation of Epac2A and Rap1 by glibenclamide. Glyburide 250-263 RAP1A, member of RAS oncogene family Homo sapiens 125-129 24713348-8 2014 pretreatment with tolbutamide, glyburide or glipizide attenuated the KA-induced neuronal cell death in CA3 region of the hippocampus and hyperglycemia. Glyburide 31-40 carbonic anhydrase 3 Mus musculus 103-106 24713348-17 2014 Our results suggest that supraspinally administered tolbutamide, glyburide and glipizide exert a protective effect against KA-induced neuronal cells death in CA3 region of the hippocampus. Glyburide 65-74 carbonic anhydrase 3 Mus musculus 158-161 24741335-1 2014 BACKGROUND: The purpose of this study was to investigate the effect of glibenclamide dose escalation on blood glucose and insulin in patients with poorly controlled type 2 diabetes. Glyburide 71-84 insulin Homo sapiens 122-129 24725740-8 2014 In addition, the expression of MYH10 gene encoding non-muscle myosin heavy chain-B decreased in diabetic rats treated with glibenclamide. Glyburide 123-136 myosin heavy chain 10 Rattus norvegicus 31-36 24725740-8 2014 In addition, the expression of MYH10 gene encoding non-muscle myosin heavy chain-B decreased in diabetic rats treated with glibenclamide. Glyburide 123-136 myosin heavy chain 10 Rattus norvegicus 51-82 24356749-11 2014 CONCLUSIONS/INTERPRETATION: Our study demonstrated that the CDKN2A/CDKN2B gene may be nominally associated with the efficacy of glibenclamide, and that CDKN2A/CDKN2B is associated with beta cell function. Glyburide 128-141 cyclin dependent kinase inhibitor 2B Homo sapiens 67-73 24477542-9 2014 Inactivating K ATP channels with 200 nM glibenclamide increased oxytocin and vasopressin release (OT: P < 0.003; VP: P < 0.05). Glyburide 40-53 arginine vasopressin Rattus norvegicus 77-88 24477542-9 2014 Inactivating K ATP channels with 200 nM glibenclamide increased oxytocin and vasopressin release (OT: P < 0.003; VP: P < 0.05). Glyburide 40-53 arginine vasopressin Rattus norvegicus 116-118 24356749-11 2014 CONCLUSIONS/INTERPRETATION: Our study demonstrated that the CDKN2A/CDKN2B gene may be nominally associated with the efficacy of glibenclamide, and that CDKN2A/CDKN2B is associated with beta cell function. Glyburide 128-141 cyclin dependent kinase inhibitor 2A Homo sapiens 60-66 24356749-11 2014 CONCLUSIONS/INTERPRETATION: Our study demonstrated that the CDKN2A/CDKN2B gene may be nominally associated with the efficacy of glibenclamide, and that CDKN2A/CDKN2B is associated with beta cell function. Glyburide 128-141 cyclin dependent kinase inhibitor 2B Homo sapiens 159-165 24072459-2 2014 Glyburide is reported to prevent brain swelling in preclinical rodent models of ischemic stroke through inhibition of a non-selective channel composed of sulfonylurea receptor 1 and transient receptor potential cation channel subfamily M member 4. Glyburide 0-9 ATP binding cassette subfamily C member 8 Homo sapiens 154-246 24184803-3 2014 Glyburide was adsorbed onto the porous silica, as confirmed by the SEM images and BET analysis. Glyburide 0-9 delta/notch like EGF repeat containing Homo sapiens 82-85 24552576-4 2014 In this focused review, we explore preclinical data linking Sur1 channel formation to development of edema and reference evidence suggesting that the antidiabetic sulfonylurea drug glyburide (a Sur1 inhibitor) is an inexpensive and well-tolerated agent that can be clinically tested to reduce or prevent malignancy and/or treatment-associated edema. Glyburide 181-190 ATP binding cassette subfamily C member 8 Homo sapiens 60-64 24552576-4 2014 In this focused review, we explore preclinical data linking Sur1 channel formation to development of edema and reference evidence suggesting that the antidiabetic sulfonylurea drug glyburide (a Sur1 inhibitor) is an inexpensive and well-tolerated agent that can be clinically tested to reduce or prevent malignancy and/or treatment-associated edema. Glyburide 181-190 ATP binding cassette subfamily C member 8 Homo sapiens 194-198 24336017-2 2014 Glyburide has NLRP3 inhibitory activity in vitro but requires very high doses in vivo, associated with hypoglycemia. Glyburide 0-9 NLR family, pyrin domain containing 3 Mus musculus 14-19 24336017-8 2014 CONCLUSIONS: The small molecule 16673-34-0, an intermediate substrate in the glyburide synthesis free of the cyclohexylurea moiety, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size after myocardial ischemia-reperfusion in the mouse, without affecting glucose metabolism. Glyburide 77-86 NLR family, pyrin domain containing 3 Mus musculus 162-167 24072459-7 2014 RESULTS: We report that IV glyburide was associated with T2 fluid-attenuated inversion recovery signal intensity ratio on brain MRI, diminished the lesional water diffusivity between days 1 and 2 (pseudo-normalization), and reduced blood MMP-9 level. Glyburide 27-36 matrix metallopeptidase 9 Homo sapiens 238-243 24361899-8 2014 The soluble guanylyl cyclase inhibitor ODQ and the specific blocker of ATP-sensitive K+ channels glibenclamide (40, 80 and 160 mug/paw) antagonized the Ang-(1-7) response. Glyburide 97-110 angiogenin Rattus norvegicus 152-160 23834474-5 2014 For verification, the pregnancy-related changes in the disposition of methadone (cleared by CYP2B6, 3A and 2C19) and glyburide (cleared by CYP3A, 2C9 and 2C19) were predicted. Glyburide 117-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-158 25016858-0 2014 [Glybenclamide regulate ERK1/2 signal pathway during hypoxia hypercapnia pulmonary vasoconstriction in rats]. Glyburide 1-14 mitogen activated protein kinase 3 Rattus norvegicus 24-30 24117047-4 2014 KEY RESULTS: When added to the intracellular solution, loop diuretics inhibited CFTR Cl(-) currents with potency approaching that of glibenclamide, a widely used CFTR blocker with some structural similarity to loop diuretics. Glyburide 133-146 CF transmembrane conductance regulator Homo sapiens 80-84 24285499-8 2014 Glyburide completely blocked CP-induced activation of caspase-1 and the production of IL-1beta at 4 h. At 24 h, glyburide reduced two markers of inflammation by 30-50% and reversed much of the inflammatory morphology. Glyburide 0-9 caspase 1 Homo sapiens 54-63 24285499-8 2014 Glyburide completely blocked CP-induced activation of caspase-1 and the production of IL-1beta at 4 h. At 24 h, glyburide reduced two markers of inflammation by 30-50% and reversed much of the inflammatory morphology. Glyburide 0-9 interleukin 1 beta Homo sapiens 86-94 24150606-0 2014 OATP1B3 is expressed in pancreatic beta-islet cells and enhances the insulinotropic effect of the sulfonylurea derivative glibenclamide. Glyburide 122-135 solute carrier organic anion transporter family member 1B3 Homo sapiens 0-7 24150606-4 2014 Transport studies using OATP1B3-overexpressing MDCKII cells revealed significant inhibition of the cellular uptake of the known substrate cholecystokinin-8 in the presence of the insulinotropic antidiabetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identified glibenclamide as a novel substrate of OATP1B3. Glyburide 230-243 solute carrier organic anion transporter family member 1B3 Homo sapiens 24-31 24150606-4 2014 Transport studies using OATP1B3-overexpressing MDCKII cells revealed significant inhibition of the cellular uptake of the known substrate cholecystokinin-8 in the presence of the insulinotropic antidiabetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identified glibenclamide as a novel substrate of OATP1B3. Glyburide 289-302 solute carrier organic anion transporter family member 1B3 Homo sapiens 24-31 24150606-6 2014 Here, we show that transient overexpression of human OATP1B3 in a murine beta-cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insulin secretion. Glyburide 122-135 solute carrier organic anion transporter family member 1B3 Homo sapiens 53-60 24150606-6 2014 Here, we show that transient overexpression of human OATP1B3 in a murine beta-cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insulin secretion. Glyburide 122-135 insulin Homo sapiens 146-153 24150606-6 2014 Here, we show that transient overexpression of human OATP1B3 in a murine beta-cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insulin secretion. Glyburide 216-229 solute carrier organic anion transporter family member 1B3 Homo sapiens 53-60 24150606-6 2014 Here, we show that transient overexpression of human OATP1B3 in a murine beta-cell line (MIN6)-which exhibits glucose and glibenclamide-sensitive insulin secretion-significantly enhances the insulinotropic effect of glibenclamide without affecting glucose-stimulated insulin secretion. Glyburide 216-229 insulin Homo sapiens 191-198 24150606-7 2014 Taken together, our data provide evidence that the drug transporter OATP1B3 functions as a determinant of the insulinotropic effect of glibenclamide on the tissue level. Glyburide 135-148 solute carrier organic anion transporter family member 1B3 Homo sapiens 68-75 24311472-8 2014 Using primary mixed glial and pure microglial cultures, glibenclamide specifically targeted reactive microglia to restore neurogenesis and increased the microglial production of the chemokine monocyte chemoattractant protein-1 (MCP-1). Glyburide 56-69 chemokine (C-C motif) ligand 2 Mus musculus 192-226 24311472-8 2014 Using primary mixed glial and pure microglial cultures, glibenclamide specifically targeted reactive microglia to restore neurogenesis and increased the microglial production of the chemokine monocyte chemoattractant protein-1 (MCP-1). Glyburide 56-69 chemokine (C-C motif) ligand 2 Mus musculus 228-233 24176035-7 2014 Pituitary adenylate cyclase-activating polypeptide (PACAP), a well-documented stimulant of VEGF secretion, caused a robust increase in VEGF secretion over 24 h. Glyburide, an ABCA1 and K(ATP) channel blocker, also caused an increase in VEGF secretion when applied alone, and amplified the response to PACAP. Glyburide 161-170 adenylate cyclase activating polypeptide 1 Mus musculus 0-50 24176035-7 2014 Pituitary adenylate cyclase-activating polypeptide (PACAP), a well-documented stimulant of VEGF secretion, caused a robust increase in VEGF secretion over 24 h. Glyburide, an ABCA1 and K(ATP) channel blocker, also caused an increase in VEGF secretion when applied alone, and amplified the response to PACAP. Glyburide 161-170 adenylate cyclase activating polypeptide 1 Mus musculus 52-57 24176035-7 2014 Pituitary adenylate cyclase-activating polypeptide (PACAP), a well-documented stimulant of VEGF secretion, caused a robust increase in VEGF secretion over 24 h. Glyburide, an ABCA1 and K(ATP) channel blocker, also caused an increase in VEGF secretion when applied alone, and amplified the response to PACAP. Glyburide 161-170 vascular endothelial growth factor A Mus musculus 91-95 24176035-7 2014 Pituitary adenylate cyclase-activating polypeptide (PACAP), a well-documented stimulant of VEGF secretion, caused a robust increase in VEGF secretion over 24 h. Glyburide, an ABCA1 and K(ATP) channel blocker, also caused an increase in VEGF secretion when applied alone, and amplified the response to PACAP. Glyburide 161-170 vascular endothelial growth factor A Mus musculus 135-139 24176035-7 2014 Pituitary adenylate cyclase-activating polypeptide (PACAP), a well-documented stimulant of VEGF secretion, caused a robust increase in VEGF secretion over 24 h. Glyburide, an ABCA1 and K(ATP) channel blocker, also caused an increase in VEGF secretion when applied alone, and amplified the response to PACAP. Glyburide 161-170 vascular endothelial growth factor A Mus musculus 135-139 24176035-9 2014 Exposure of TtT/GF cells to cycloheximide with PACAP or glyburide inhibited the increased secretion of VEGF, consistent with control of secretion at the transcription level. Glyburide 56-65 vascular endothelial growth factor A Mus musculus 103-107 24176035-11 2014 Diazoxide, a K(ATP) activator, inhibited PACAP- and PACAP + glyburide-stimulated VEGF secretion but not that of glyburide alone. Glyburide 60-69 adenylate cyclase activating polypeptide 1 Mus musculus 52-57 24176035-11 2014 Diazoxide, a K(ATP) activator, inhibited PACAP- and PACAP + glyburide-stimulated VEGF secretion but not that of glyburide alone. Glyburide 60-69 vascular endothelial growth factor A Mus musculus 81-85 24176035-11 2014 Diazoxide, a K(ATP) activator, inhibited PACAP- and PACAP + glyburide-stimulated VEGF secretion but not that of glyburide alone. Glyburide 112-121 adenylate cyclase activating polypeptide 1 Mus musculus 52-57 24443056-6 2014 Blocking SUR1 with glibenclamide significantly reduced the ammonia-induced cell swelling in cultured astrocytes. Glyburide 19-32 ATP binding cassette subfamily C member 8 Rattus norvegicus 9-13 24767162-6 2014 The coverage rates of acarbose (48.9%), metformin(40.7%) and human insulin (31.1%) were higher than those of glimepiride (9.4%), glipizide (3.0%), glibenclamide (0.6%) and animal insulin (0.2%). Glyburide 147-160 insulin Homo sapiens 67-74 24767162-9 2014 The coverage rates of acarbose (49.7%), metformin (36.3%) and insulin (30.4%) were still higher than those of glimepiride (6.3%), glipizide (2.2%) , glibenclamide (0.4%) and animal insulin(0.0%). Glyburide 149-162 insulin Homo sapiens 62-69 24259278-5 2014 A heterobivalent ligand was assembled from the active fragment of GLP-1 (7-36 GLP-1) and glibenclamide, a small organic ligand for SUR1. Glyburide 89-102 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 131-135 24122011-9 2014 The specific KATP channel opener pinacidil (10 mumol/L) could fully activate Kir6.1/SUR2B channels, which was inhibited by the specific KATP channel blocker glibenclamide (10 mumol/L). Glyburide 157-170 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 77-83 24122011-11 2014 The activation of Kir6.1/SUR2B channels by MGO was reversible upon washout, and could be inhibited completely by glibenclamide. Glyburide 113-126 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 18-24 24117047-4 2014 KEY RESULTS: When added to the intracellular solution, loop diuretics inhibited CFTR Cl(-) currents with potency approaching that of glibenclamide, a widely used CFTR blocker with some structural similarity to loop diuretics. Glyburide 133-146 CF transmembrane conductance regulator Homo sapiens 162-166 25176281-9 2014 Invivo study revealed that the glibenclamide incorporated niosomal gel formulation; GNG-1 is more efficient in lowering blood glucose levels in experimental animals. Glyburide 31-44 G protein subunit gamma transducin 1 Homo sapiens 84-89 24558086-0 2014 Long-term efficacy of glibenclamide and sitagliptin therapy in adult patients with KCNJ11 permanent diabetes. Glyburide 22-35 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 83-89 24147174-9 2013 Glyburide treatment did not affect glucose levels but was associated with reduced pulmonary cellular influx, reduced bacterial dissemination to both liver and spleen and reduced IL1beta production when compared to untreated controls. Glyburide 0-9 interleukin 1 beta Mus musculus 178-185 24380477-3 2014 Among these proteins involved in ion homeostasis, the ischemia-induced, nonselective cation conductance formed by the SUR1-TRPM4 protein complex appears to play a prominent role and is potently inhibited by glibenclamide, an FDA-approved drug commonly used in patients with Type 2 diabetes. Glyburide 207-220 ATP binding cassette subfamily C member 8 Homo sapiens 118-122 24380477-3 2014 Among these proteins involved in ion homeostasis, the ischemia-induced, nonselective cation conductance formed by the SUR1-TRPM4 protein complex appears to play a prominent role and is potently inhibited by glibenclamide, an FDA-approved drug commonly used in patients with Type 2 diabetes. Glyburide 207-220 transient receptor potential cation channel subfamily M member 4 Homo sapiens 123-128 24380477-4 2014 Several robust preclinical studies have demonstrated the efficacy of glibenclamide blockade of SUR1-TRPM4 activity in reducing edema and hemorrhagic conversion in rodent models of ischemic stroke, prompting the study of the potential protective effects of glibenclamide in humans in an ongoing prospective phase II clinical trial. Glyburide 69-82 ATP binding cassette subfamily C member 8 Homo sapiens 95-99 24380477-4 2014 Several robust preclinical studies have demonstrated the efficacy of glibenclamide blockade of SUR1-TRPM4 activity in reducing edema and hemorrhagic conversion in rodent models of ischemic stroke, prompting the study of the potential protective effects of glibenclamide in humans in an ongoing prospective phase II clinical trial. Glyburide 69-82 transient receptor potential cation channel subfamily M member 4 Homo sapiens 100-105 24642889-8 2014 Moreover, although glibenclamide or ODQ each partly inhibited the induction of COX-2 mRNA by nicorandil, their combined application significantly inhibited it. Glyburide 19-32 cytochrome c oxidase II, mitochondrial Rattus norvegicus 79-84 24114458-9 2013 In rats, inhibiting Sur1 using antisense or the selective Sur1 inhibitor glibenclamide reduced SAH-induced immunoglobulin G extravasation and tumor necrosis alpha overexpression. Glyburide 73-86 ATP binding cassette subfamily C member 8 Rattus norvegicus 20-24 24114458-9 2013 In rats, inhibiting Sur1 using antisense or the selective Sur1 inhibitor glibenclamide reduced SAH-induced immunoglobulin G extravasation and tumor necrosis alpha overexpression. Glyburide 73-86 ATP binding cassette subfamily C member 8 Rattus norvegicus 58-62 24285369-4 2013 Purified PMNs from diabetic patients who had been treated with glibenclamide (an ATP-sensitive potassium channel blocker for anti-diabetes therapy), showed reduction of interleukin (IL)-1beta and IL-8 secretion when exposed to B. pseudomallei. Glyburide 63-76 interleukin 1 beta Homo sapiens 169-191 24285369-4 2013 Purified PMNs from diabetic patients who had been treated with glibenclamide (an ATP-sensitive potassium channel blocker for anti-diabetes therapy), showed reduction of interleukin (IL)-1beta and IL-8 secretion when exposed to B. pseudomallei. Glyburide 63-76 C-X-C motif chemokine ligand 8 Homo sapiens 196-200 24285369-6 2013 These findings suggest that glibenclamide might be responsible for the increased susceptibility of diabetic patients, with poor glycemic control, to bacterial infections as a result of its effect on reducing IL-1beta production by PMNs. Glyburide 28-41 interleukin 1 beta Homo sapiens 208-216 24037327-8 2013 However, the SUR2A-55 KATP were 70-fold less sensitive to block by ATP, and twice as resistant to intracellular Ca (2+) inhibition compared with the SUR2A KATP, and were markedly insensitive to KATP drugs, pinacidil, diazoxide, and glybenclamide. Glyburide 232-245 ATP binding cassette subfamily C member 9 Homo sapiens 13-21 24291534-3 2014 NOD-like receptor protein-3 (NLRP-3) is pro-inflammatory in the kidney; glibenclamide inhibits production of NLRP-3. Glyburide 72-85 NLR family, pyrin domain containing 3 Rattus norvegicus 0-27 24291534-3 2014 NOD-like receptor protein-3 (NLRP-3) is pro-inflammatory in the kidney; glibenclamide inhibits production of NLRP-3. Glyburide 72-85 NLR family, pyrin domain containing 3 Rattus norvegicus 109-115 24291534-8 2014 Glibenclamide decreased infiltration of chronic inflammatory cells, fibrosis, tubular damage and expression of HO-1, TNF-alpha and NLRP-3 in the kidney. Glyburide 0-13 heme oxygenase 1 Rattus norvegicus 111-115 24291534-8 2014 Glibenclamide decreased infiltration of chronic inflammatory cells, fibrosis, tubular damage and expression of HO-1, TNF-alpha and NLRP-3 in the kidney. Glyburide 0-13 tumor necrosis factor Rattus norvegicus 117-126 24291534-8 2014 Glibenclamide decreased infiltration of chronic inflammatory cells, fibrosis, tubular damage and expression of HO-1, TNF-alpha and NLRP-3 in the kidney. Glyburide 0-13 NLR family, pyrin domain containing 3 Rattus norvegicus 131-137 23933222-6 2013 RESULTS: (1) Cannabidoil inhibition of breast cancer resistance protein-dependent mitoxantrone efflux was concentration dependent and of a noncell type specific nature (P < .0001); (2) In the cotyledon perfusion assay, the administration of cannabidoil to the maternal perfusion media increased the female/male ratio of glyburide concentrations (1.3 +- 0.1 vs 0.8 +- 0.1 at 120 minutes of perfusion, P < .001). Glyburide 323-332 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 39-71 23933222-7 2013 CONCLUSION: (1) Placental breast cancer resistance protein function is inhibited following even a short-term exposure to cannabidoil; (2) the ex vivo perfusion assay emphasize this effect by increased placental penetration of glyburide to the fetal compartment; and (3) these findings suggest that marijuana consumption enhances placental barrier permeability to xenobiotics and could endanger the developing fetus. Glyburide 226-235 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 26-58 24349947-12 2013 RESULTS: All the doses of UFD and glibenclamide decrease the level of serum glucose, glycated hemoglobin, glucose-6-phosphatase, fructose-1-6-biphosphate and increased the level of plasma insulin, hexokinase. Glyburide 34-47 glucose-6-phosphatase catalytic subunit 1 Rattus norvegicus 106-127 24188560-0 2013 Improvement of superoxide dismutase and catalase in streptozotocin-nicotinamide-induced type 2-diabetes in mice by berberine and glibenclamide. Glyburide 129-142 catalase Mus musculus 40-48 23921548-3 2013 (2) Interestingly, therapies to improve glucose homeostasis in diabetic patients usually involve the use of glibenclamide, an oral hypoglycemic drug that blocks ATP-sensitive K(+) channels (KATP), (3)(,) (4) forcing beta cells to release more insulin to overcome peripheral insulin resistance. Glyburide 108-121 insulin Homo sapiens 243-250 23921548-3 2013 (2) Interestingly, therapies to improve glucose homeostasis in diabetic patients usually involve the use of glibenclamide, an oral hypoglycemic drug that blocks ATP-sensitive K(+) channels (KATP), (3)(,) (4) forcing beta cells to release more insulin to overcome peripheral insulin resistance. Glyburide 108-121 insulin Homo sapiens 274-281 23835339-8 2013 Glibenclamide block was also reduced in beta-cells expressing Kir6.2-V59M channels. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 62-68 24147174-12 2013 Glyburide directly reduced the secretion of IL1beta by BMDMs in a dose-dependent fashion. Glyburide 0-9 interleukin 1 beta Mus musculus 44-51 24147174-14 2013 We further show, for the first time in any model of sepsis, that glyburide acts as an anti-inflammatory agent by reducing IL1beta secretion accompanied by diminished cellular influx and reduced bacterial dissemination to distant organs. Glyburide 65-74 interleukin 1 beta Mus musculus 122-129 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 49-62 insulin Homo sapiens 207-214 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 49-62 ATP binding cassette subfamily C member 8 Homo sapiens 244-267 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 49-62 ATP binding cassette subfamily C member 8 Homo sapiens 269-273 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 49-62 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 275-281 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 81-90 insulin Homo sapiens 207-214 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 81-90 ATP binding cassette subfamily C member 8 Homo sapiens 244-267 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 81-90 ATP binding cassette subfamily C member 8 Homo sapiens 269-273 24275850-1 2013 First introduced into clinical practice in 1969, glibenclamide (US adopted name, glyburide) is known best for its use in the treatment of diabetes mellitus type 2, where it is used to promote the release of insulin by blocking pancreatic KATP [sulfonylurea receptor 1 (Sur1)-Kir6.2] channels. Glyburide 81-90 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 275-281 24275850-3 2013 Acting via inhibition of the recently characterized Sur1-Trpm4 channel (formerly, the Sur1-regulated NCCa-ATP channel) and, in some cases, via brain KATP channels, glibenclamide has been shown to be beneficial in several clinically relevant rodent models of ischemic and hemorrhagic stroke, traumatic brain injury, spinal cord injury, neonatal encephalopathy of prematurity, and metastatic brain tumor. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 52-56 24275850-3 2013 Acting via inhibition of the recently characterized Sur1-Trpm4 channel (formerly, the Sur1-regulated NCCa-ATP channel) and, in some cases, via brain KATP channels, glibenclamide has been shown to be beneficial in several clinically relevant rodent models of ischemic and hemorrhagic stroke, traumatic brain injury, spinal cord injury, neonatal encephalopathy of prematurity, and metastatic brain tumor. Glyburide 164-177 ATP binding cassette subfamily C member 8 Homo sapiens 86-90 24275850-4 2013 Glibenclamide acts on microvessels to reduce edema formation and secondary hemorrhage, it inhibits necrotic cell death, it exerts potent anti-inflammatory effects and it promotes neurogenesis-all via inhibition of Sur1. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 214-218 24275850-6 2013 These recent findings, which implicate Sur1 in a number of acute pathological conditions involving the CNS, present new opportunities to use glibenclamide, a well-known, safe pharmaceutical agent, for medical conditions that heretofore had few or no treatment options. Glyburide 141-154 ATP binding cassette subfamily C member 8 Homo sapiens 39-43 23907487-0 2013 Effects of selected OATP and/or ABC transporter inhibitors on the brain and whole-body distribution of glyburide. Glyburide 103-112 solute carrier organic anion transporter family, member 1a6 Mus musculus 20-24 24130952-0 2013 Changing the Treatment of Permanent Neonatal Diabetes Mellitus from Insulin to Glibenclamide in a 4-Month-Old Infant with KCNJ11 Activating Mutation. Glyburide 79-92 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 122-128 23806476-5 2013 We found that glibenclamide pharmacokinetics could be adequately modeled if next to CYP metabolism an active hepatic uptake process was assumed. Glyburide 14-27 peptidylprolyl isomerase G Homo sapiens 84-87 23628292-3 2013 RESULTS: ACE inhibition and/or HS diet eliminated endothelium-dependent arteriolar dilation to acetylcholine, endothelium-independent dilation to the NO donor sodium nitroprusside, the prostacyclin analogs carbacyclin and iloprost, and the KATP channel opener cromakalim; and eliminated arteriolar constriction during KATP channel blockade with glibenclamide. Glyburide 345-358 angiotensin I converting enzyme Homo sapiens 9-12 23806476-13 2013 In conclusion, glibenclamide pharmacokinetics and its CYP-mediated DDIs can be simulated via PBPK-modeling. Glyburide 15-28 peptidylprolyl isomerase G Homo sapiens 54-57 24834370-10 2013 The potential advantage of inhibiting Sur1-Trpm4 channels using glibenclamide is a highly promising strategy for ameliorating the devastating sequelae of spinal cord trauma in humans. Glyburide 64-77 ATP binding cassette subfamily C member 8 Homo sapiens 38-42 24834370-10 2013 The potential advantage of inhibiting Sur1-Trpm4 channels using glibenclamide is a highly promising strategy for ameliorating the devastating sequelae of spinal cord trauma in humans. Glyburide 64-77 transient receptor potential cation channel subfamily M member 4 Homo sapiens 43-48 23785074-7 2013 This effect was reduced by glibenclamide (KATP channels blocker), NG-monomethyl-L-arginine (NOS inhibitor), 1H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one (guanylyl cyclase inhibitor), KT5823 (PKG inhibitor), and it was blocked by Akt1/2 (Akt inhibitor) and by detergent Triton X-100. Glyburide 27-40 AKT serine/threonine kinase 1 Rattus norvegicus 230-236 23785074-7 2013 This effect was reduced by glibenclamide (KATP channels blocker), NG-monomethyl-L-arginine (NOS inhibitor), 1H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one (guanylyl cyclase inhibitor), KT5823 (PKG inhibitor), and it was blocked by Akt1/2 (Akt inhibitor) and by detergent Triton X-100. Glyburide 27-40 AKT serine/threonine kinase 1 Rattus norvegicus 230-233 23488724-12 2013 Clotrimazole and glibenclamide each reversed hyperpolarizations to adiponectin and A-769662, suggesting the involvement of myocyte TRPM4 channels in the ADHF-induced myocyte electrical changes mediated via the opening of BKCa channels. Glyburide 17-30 adiponectin, C1Q and collagen domain containing Rattus norvegicus 67-78 23488724-12 2013 Clotrimazole and glibenclamide each reversed hyperpolarizations to adiponectin and A-769662, suggesting the involvement of myocyte TRPM4 channels in the ADHF-induced myocyte electrical changes mediated via the opening of BKCa channels. Glyburide 17-30 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 131-136 23488724-12 2013 Clotrimazole and glibenclamide each reversed hyperpolarizations to adiponectin and A-769662, suggesting the involvement of myocyte TRPM4 channels in the ADHF-induced myocyte electrical changes mediated via the opening of BKCa channels. Glyburide 17-30 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 221-225 23462667-5 2013 RESEARCH DESIGN AND METHODS: To localize and quantify the effect of glibenclamide administration, we performed single-photon emission computed tomography in seven patients with different mutations in KCNJ11. Glyburide 68-81 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 200-206 23494827-6 2013 Functional impairment of the channel activity, using a SUR blocker (glibenclamide 10 or 20 nM), reduced the protein levels of GLUT-1 and GLUT-3 by approximately 30% in normal chondrocytes, while in cells from cartilage with increasing osteoarthritic (OA) grade no changes were observed. Glyburide 68-81 ATP binding cassette subfamily C member 8 Homo sapiens 55-58 23494827-6 2013 Functional impairment of the channel activity, using a SUR blocker (glibenclamide 10 or 20 nM), reduced the protein levels of GLUT-1 and GLUT-3 by approximately 30% in normal chondrocytes, while in cells from cartilage with increasing osteoarthritic (OA) grade no changes were observed. Glyburide 68-81 solute carrier family 2 member 1 Homo sapiens 126-132 23494827-6 2013 Functional impairment of the channel activity, using a SUR blocker (glibenclamide 10 or 20 nM), reduced the protein levels of GLUT-1 and GLUT-3 by approximately 30% in normal chondrocytes, while in cells from cartilage with increasing osteoarthritic (OA) grade no changes were observed. Glyburide 68-81 solute carrier family 2 member 3 Homo sapiens 137-143 23686859-10 2013 Finally, both LXA4 and pinacidil stimulated ERK-MAP kinase phosphorylation, whereas the effect of LXA4 on ERK phosphorylation was inhibited by glibenclamide. Glyburide 143-156 mitogen-activated protein kinase 1 Homo sapiens 106-109 23545333-0 2013 Pharmacophore modeling, homology modeling, and in silico screening reveal mammalian target of rapamycin inhibitory activities for sotalol, glyburide, metipranolol, sulfamethizole, glipizide, and pioglitazone. Glyburide 139-148 mechanistic target of rapamycin kinase Homo sapiens 74-103 23714264-0 2013 Combined treatment of glibenclamide and CoCl2 decreases MMP9 expression and inhibits growth in highly metastatic breast cancer. Glyburide 22-35 matrix metallopeptidase 9 Mus musculus 56-60 23714264-11 2013 The mean percentage of cells expressing MMP9 and PCNA was the lowest in the CoCl(2) + glibenclamide group (P < 0.05). Glyburide 86-99 matrix metallopeptidase 9 Mus musculus 40-44 23714264-11 2013 The mean percentage of cells expressing MMP9 and PCNA was the lowest in the CoCl(2) + glibenclamide group (P < 0.05). Glyburide 86-99 proliferating cell nuclear antigen Mus musculus 49-53 23714264-13 2013 CONCLUSIONS: Combined treatment with glibenclamide and CoCl(2) inhibits TA2 spontaneous breast cancer growth and invasiveness with effects similar to paclitaxel. Glyburide 37-50 transforming growth factor alpha regulated gene 1 Mus musculus 72-75 23413771-4 2013 Fasting plasma insulin and homeostasis model assessment of insulin resistance were significantly increased by triple therapy with glibenclamide and decreased by that with sitagliptin. Glyburide 130-143 insulin Homo sapiens 15-22 23413771-4 2013 Fasting plasma insulin and homeostasis model assessment of insulin resistance were significantly increased by triple therapy with glibenclamide and decreased by that with sitagliptin. Glyburide 130-143 insulin Homo sapiens 59-66 23840624-12 2013 Systemic injection of glibenclamide rapidly released insulin and phosphorylated AKT in NGs. Glyburide 22-35 thymoma viral proto-oncogene 1 Mus musculus 80-83 23543229-8 2013 Glibenclamide did not affect leukocyte infiltration, IL-1beta release and PGE2 production, but only reduced IL-1beta production by MSU-stimulated macrophages at very high concentration (200 muM). Glyburide 0-13 interleukin 1 beta Rattus norvegicus 108-116 23273975-0 2013 The R230C variant of the ATP binding cassette protein A1 (ABCA1) gene is associated with a decreased response to glyburide therapy in patients with type 2 diabetes mellitus. Glyburide 113-122 ATP binding cassette subfamily A member 1 Homo sapiens 58-63 23273975-1 2013 OBJECTIVE: To test the hypothesis that persons with the R230C allele of ABCA1 show a decreased glycemic response to glyburide. Glyburide 116-125 ATP binding cassette subfamily A member 1 Homo sapiens 72-77 23273975-11 2013 CONCLUSIONS: Patients with type 2 diabetes who have the R230C allele of ABCA1 needed a higher dose of glyburide in order to achieve the same glucose lowering effect as that in persons with the wild type variant. Glyburide 102-111 ATP binding cassette subfamily A member 1 Homo sapiens 72-77 23633925-1 2013 Inhibition of sulfonylurea receptor 1 (SUR1) by glyburide has been shown to decrease edema after subarachnoid hemorrhage. Glyburide 48-57 ATP binding cassette subfamily C member 8 Rattus norvegicus 14-37 23633925-1 2013 Inhibition of sulfonylurea receptor 1 (SUR1) by glyburide has been shown to decrease edema after subarachnoid hemorrhage. Glyburide 48-57 ATP binding cassette subfamily C member 8 Rattus norvegicus 39-43 23633925-10 2013 Both glyburide (P < .001) and dexamethasone (P < .01) decreased ZO-1 gap formation. Glyburide 5-14 tight junction protein 1 Rattus norvegicus 70-74 23633925-11 2013 By decreasing ZO-1 gaps, glyburide was at least as effective as dexamethasone at halting increased BTB permeability caused by SCLC and melanoma. Glyburide 25-34 tight junction protein 1 Rattus norvegicus 14-18 23461853-0 2013 The anti-diabetic drug glibenclamide is an agonist of the transient receptor potential Ankyrin 1 (TRPA1) ion channel. Glyburide 23-36 transient receptor potential cation channel subfamily A member 1 Homo sapiens 58-96 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 79-92 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 31-37 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 79-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 158-171 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 31-37 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23470198-8 2013 The inhibitory effect of complex I in the carrageenin-induced hyperalgesia, MPO activity and formalin was prevented by the treatment with ODQ, KT5823 and glybenclamide, indicating that complex I inhibits inflammatory hyperalgesia by activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway. Glyburide 154-167 myeloperoxidase Homo sapiens 76-79 23470198-8 2013 The inhibitory effect of complex I in the carrageenin-induced hyperalgesia, MPO activity and formalin was prevented by the treatment with ODQ, KT5823 and glybenclamide, indicating that complex I inhibits inflammatory hyperalgesia by activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway. Glyburide 154-167 protein kinase cGMP-dependent 1 Homo sapiens 253-256 23470198-8 2013 The inhibitory effect of complex I in the carrageenin-induced hyperalgesia, MPO activity and formalin was prevented by the treatment with ODQ, KT5823 and glybenclamide, indicating that complex I inhibits inflammatory hyperalgesia by activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway. Glyburide 154-167 ATPase phospholipid transporting 8A2 Homo sapiens 257-260 23121773-6 2013 The oral antidiabetic drugs glibenclamide, glimepiride and nateglinide inhibited the transport of the model substrate bromosulfophthalein, particularly the OATP2B1-mediated uptake. Glyburide 28-41 solute carrier organic anion transporter family member 2B1 Homo sapiens 156-163 23121773-8 2013 For glibenclamide, inhibitory constants (Ki values) of 13.6 muM, 8.1 muM and 0.5 muM for OATP1B1-, OATP1B3- and OATP2B1-mediated BSP uptake were determined. Glyburide 4-17 solute carrier organic anion transporter family member 1B1 Homo sapiens 89-96 23121773-8 2013 For glibenclamide, inhibitory constants (Ki values) of 13.6 muM, 8.1 muM and 0.5 muM for OATP1B1-, OATP1B3- and OATP2B1-mediated BSP uptake were determined. Glyburide 4-17 solute carrier organic anion transporter family member 1B3 Homo sapiens 99-106 23121773-8 2013 For glibenclamide, inhibitory constants (Ki values) of 13.6 muM, 8.1 muM and 0.5 muM for OATP1B1-, OATP1B3- and OATP2B1-mediated BSP uptake were determined. Glyburide 4-17 solute carrier organic anion transporter family member 2B1 Homo sapiens 112-119 23461853-0 2013 The anti-diabetic drug glibenclamide is an agonist of the transient receptor potential Ankyrin 1 (TRPA1) ion channel. Glyburide 23-36 transient receptor potential cation channel subfamily A member 1 Homo sapiens 98-103 23461853-3 2013 We report that glibenclamide activates human TRPA1 in a concentration range that is commonly used to induce inhibition of K(ATP) channels in vitro. Glyburide 15-28 transient receptor potential cation channel subfamily A member 1 Homo sapiens 45-50 23461853-4 2013 Glibenclamide generates calcium transients in HEK293t cells transiently transfected with human TRPA1, which are inhibited by the selective TRPA1 antagonist HC030031 and also evokes outwardly rectifying currents mediated by recombinant TRPA1. Glyburide 0-13 transient receptor potential cation channel subfamily A member 1 Homo sapiens 95-100 23461853-4 2013 Glibenclamide generates calcium transients in HEK293t cells transiently transfected with human TRPA1, which are inhibited by the selective TRPA1 antagonist HC030031 and also evokes outwardly rectifying currents mediated by recombinant TRPA1. Glyburide 0-13 transient receptor potential cation channel subfamily A member 1 Homo sapiens 139-144 23461853-4 2013 Glibenclamide generates calcium transients in HEK293t cells transiently transfected with human TRPA1, which are inhibited by the selective TRPA1 antagonist HC030031 and also evokes outwardly rectifying currents mediated by recombinant TRPA1. Glyburide 0-13 transient receptor potential cation channel subfamily A member 1 Homo sapiens 139-144 23461853-5 2013 Glibenclamide activates a subpopulation of mouse primary sensory neurons, most of which are also sensitive to the selective TRPA1 agonist mustard oil. Glyburide 0-13 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 124-129 23461853-6 2013 This glibenclamide sensitivity is completely abolished by genetic ablation of TRPA1. Glyburide 5-18 transient receptor potential cation channel subfamily A member 1 Homo sapiens 78-83 23461853-7 2013 Taken together, our data demonstrate that glibenclamide is an agonist of human TRPA1, which may explain some of the adverse effects of the drug. Glyburide 42-55 transient receptor potential cation channel subfamily A member 1 Homo sapiens 79-84 23427864-6 2013 Fasting plasma insulin level and the homeostasis model assessment insulin resistance index were significantly increased by triple therapy with glibenclamide and decreased by the one with sitagliptin. Glyburide 143-156 insulin Homo sapiens 15-22 23427864-6 2013 Fasting plasma insulin level and the homeostasis model assessment insulin resistance index were significantly increased by triple therapy with glibenclamide and decreased by the one with sitagliptin. Glyburide 143-156 insulin Homo sapiens 66-73 23149556-7 2013 In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. Glyburide 8-21 ATP binding cassette subfamily C member 8 Rattus norvegicus 190-213 23149556-7 2013 In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. Glyburide 8-21 ATP binding cassette subfamily C member 8 Rattus norvegicus 215-219 23149556-7 2013 In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. Glyburide 8-21 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 225-231 23149556-10 2013 Therefore, acute blockade of SUR1 by glibenclamide enhanced long-term brain repair in MCAO rats, which was associated with improved behavioral outcome. Glyburide 37-50 ATP binding cassette subfamily C member 8 Rattus norvegicus 29-33 23218803-7 2013 And the data showed that glibenclamide could ameliorate the progress of atherosclerosis and reduce the production of inflammatory cytokines as well as the phosphorylation of p65 and ERK1/2, while inhibitors of p65 leaded to robust expression of K(ATP) subunits in macrophages. Glyburide 25-38 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 174-177 23218803-7 2013 And the data showed that glibenclamide could ameliorate the progress of atherosclerosis and reduce the production of inflammatory cytokines as well as the phosphorylation of p65 and ERK1/2, while inhibitors of p65 leaded to robust expression of K(ATP) subunits in macrophages. Glyburide 25-38 mitogen-activated protein kinase 3 Mus musculus 182-188 23218803-7 2013 And the data showed that glibenclamide could ameliorate the progress of atherosclerosis and reduce the production of inflammatory cytokines as well as the phosphorylation of p65 and ERK1/2, while inhibitors of p65 leaded to robust expression of K(ATP) subunits in macrophages. Glyburide 25-38 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 210-213 23311706-10 2013 When cell cycle analysis was performed by flow cytometry, Gli induced a significant cell-cycle arrest in G0/G1 phase, together with an up-regulation of p27 levels and a diminution in cyclin E expression, both evaluated by immunoblot. Glyburide 58-61 dynactin subunit 6 Homo sapiens 152-155 23178930-8 2013 This high concentration of glibenclamide had previously been reported to inhibit CFTR. Glyburide 27-40 CF transmembrane conductance regulator Rattus norvegicus 81-85 23178930-10 2013 CONCLUSIONS/INTERPRETATION: Collectively, we demonstrate that two small-molecule inhibitors of the CFTR, glibenclamide and GlyH-101, increase the number of pancreatic endocrine cells by increasing the size of the pool of neurogenin 3-positive endocrine progenitors in the developing pancreas. Glyburide 105-118 CF transmembrane conductance regulator Rattus norvegicus 99-103 23178930-10 2013 CONCLUSIONS/INTERPRETATION: Collectively, we demonstrate that two small-molecule inhibitors of the CFTR, glibenclamide and GlyH-101, increase the number of pancreatic endocrine cells by increasing the size of the pool of neurogenin 3-positive endocrine progenitors in the developing pancreas. Glyburide 105-118 neurogenin 3 Rattus norvegicus 221-233 23179858-7 2013 Drug effects that increased insulin secretion resulted in the best model fit, thus identifying the primary mechanism of action of Gb and metabolites as insulin secretagogues. Glyburide 130-132 insulin Homo sapiens 28-35 23179858-9 2013 The semi-mechanistic IGI model was successfully applied to MTT data and identified the primary mechanism of action for Gb, quantifying its effects on glucose and insulin time profiles. Glyburide 119-121 insulin Homo sapiens 162-169 23148319-6 2013 The suppression of hypoxia sensitivity was attributable to upregulation of K(ATP) current density and the K(ATP) channel subunit Kir6.2, and was reversed by the K(ATP) channel blocker, glibenclamide. Glyburide 185-198 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 129-135 24189413-3 2013 The ATP transport activity of proteoliposomes containing purified human VNUT was blocked by glibenclamide, carbenoxolone, 18 alpha-glycyrrhetinic acid, flufenamic acid, arachidonic acid and A438079 without the formation of Deltapsi (positive inside) as a driving force being affected. Glyburide 92-105 solute carrier family 17 member 9 Homo sapiens 72-76 24266052-0 2013 KCNJ11 in-frame 15-bp deletion leading to glibenclamide-responsive neonatal diabetes mellitus in a Chinese child. Glyburide 42-55 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 0-6 23640936-0 2013 KCNJ11 in-frame 15-bp deletion leading to glibenclamide- responsive neonatal diabetes mellitus in a Chinese child. Glyburide 42-55 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 0-6 24266052-3 2013 To date, more than 30 KCNJ11 mutations have been revealed as related to the onset of neonatal diabetes mellitus (NDM), most of which are responsive to glibenclamide treatment. Glyburide 151-164 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 22-28 23640936-3 2013 To date, more than 30 KCNJ11 mutations have been revealed as related to the onset of neonatal diabetes mellitus (NDM), most of which are responsive to glibenclamide treatment. Glyburide 151-164 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 22-28 23160238-5 2012 Deficiency or pharmacological inhibition of TRPM4 using the antidiabetic drug glibenclamide resulted in reduced axonal and neuronal degeneration and attenuated clinical disease scores in EAE, but this occurred without altering EAE-relevant immune function. Glyburide 78-91 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 44-49 22982177-8 2013 Treatments with GLP-1, exenatide, glyburide, nateglinide and sitagliptin effectively increased plasma human C-peptide levels and improved postprandial glucose concentrations. Glyburide 34-43 insulin Homo sapiens 108-117 23460810-6 2013 Respective mean changes in HbA1c from baseline were -0.70% and -0.66% for Xiaoke Pill and Glibenclamide, with a between-group difference (95% CI) of -0.04% (-0.20, 0.12) in the drug naive group, and those in metformin group were -0.45% and -0.59%, 0.14% (-0.12, 0.39) respectively. Glyburide 90-103 hemoglobin subunit alpha 1 Homo sapiens 27-31 22917079-8 2012 The potassium channel inhibitor glibenclamide partly inhibited IL-1beta induction, suggesting involvement of the inflammasome. Glyburide 32-45 interleukin 1 beta Rattus norvegicus 63-71 22694282-0 2012 Glyburide ameliorates motor coordination and glucose homeostasis in a child with diabetes associated with the KCNJ11/S225T, del226-232 mutation. Glyburide 0-9 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 110-116 23092871-0 2012 Analysis of drug interactions with modified proteins by high-performance affinity chromatography: binding of glibenclamide to normal and glycated human serum albumin. Glyburide 109-122 albumin Homo sapiens 152-165 23092871-1 2012 High-performance affinity chromatography (HPAC) was used to examine the changes in binding that occur for the sulfonylurea drug glibenclamide with human serum albumin (HSA) at various stages of glycation for HSA. Glyburide 128-141 albumin Homo sapiens 153-166 23280795-2 2012 In rat models of stroke, sulfonylurea (SU) drugs such as glibenclamide (adopted US name, glyburide) confer protection against swelling and HT through actions on the novel SUR1-regulated NC(Ca-ATP) channel. Glyburide 57-70 ATP binding cassette subfamily C member 8 Rattus norvegicus 171-175 23280795-2 2012 In rat models of stroke, sulfonylurea (SU) drugs such as glibenclamide (adopted US name, glyburide) confer protection against swelling and HT through actions on the novel SUR1-regulated NC(Ca-ATP) channel. Glyburide 89-98 ATP binding cassette subfamily C member 8 Rattus norvegicus 171-175 22898325-9 2012 Glibenclamide and 4-aminopyridine inhibited the relaxation to ANP, and these inhibitions were lower in diabetic than in control rabbits. Glyburide 0-13 natriuretic peptides A Oryctolagus cuniculus 62-65 22622455-10 2012 Consistently, we found that stimulating SUR2 with nicorandil prevented angiotensin II-mediated upregulation of xanthine oxidase in the cultured macrophage, while xanthine oxidase expression was rather induced by blocking SUR2 with glibenclamide. Glyburide 231-244 ATP binding cassette subfamily C member 9 Rattus norvegicus 40-44 22884808-7 2012 Glibenclamide (a K(ATP) channel blocker) blocked the inhibitory effects of H(2)S on PLB and Akt phosphorylation. Glyburide 0-13 AKT serine/threonine kinase 1 Rattus norvegicus 92-95 22994227-2 2012 Here, we provide a focused review on the involvement of matrix metalloproteinase 9 (MMP-9) in rt-PA-associated HT in cerebral ischemia, and we review emerging evidence that the selective inhibitor of the sulfonylurea receptor 1 (Sur1), glibenclamide (U.S. adopted name, glyburide), may provide protection against rt-PA-associated HT in cerebral ischemia. Glyburide 270-279 ATP binding cassette subfamily C member 8 Homo sapiens 204-227 22994227-2 2012 Here, we provide a focused review on the involvement of matrix metalloproteinase 9 (MMP-9) in rt-PA-associated HT in cerebral ischemia, and we review emerging evidence that the selective inhibitor of the sulfonylurea receptor 1 (Sur1), glibenclamide (U.S. adopted name, glyburide), may provide protection against rt-PA-associated HT in cerebral ischemia. Glyburide 270-279 ATP binding cassette subfamily C member 8 Homo sapiens 229-233 22994227-3 2012 Glyburide inhibits activation of MMP-9, ameliorates edema formation, swelling, and symptomatic hemorrhagic transformation, and improves preclinical outcomes in several clinically relevant models of stroke, both without and with rt-PA treatment. Glyburide 0-9 matrix metallopeptidase 9 Homo sapiens 33-38 22994227-5 2012 Inhibition of Sur1 with injectable glyburide holds promise for ameliorating rt-PA-associated HT in stroke. Glyburide 35-44 ATP binding cassette subfamily C member 8 Homo sapiens 14-18 22853867-4 2012 RESULTS: The AUC and t1/2 of glibenclamide following the microdosing tended to be higher and longer, respectively, in CYP2C9*1/*3 than CYP2C9*1/*1 subjects. Glyburide 29-42 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 118-124 22853867-4 2012 RESULTS: The AUC and t1/2 of glibenclamide following the microdosing tended to be higher and longer, respectively, in CYP2C9*1/*3 than CYP2C9*1/*1 subjects. Glyburide 29-42 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 135-141 22895566-7 2012 Our results showed that treatment of PC12 cells with glibenclamide for 24 h can notably promote TH expression and can also enhance the expression of TH which were reduced by rotenone. Glyburide 53-66 tyrosine hydroxylase Rattus norvegicus 108-110 22895566-7 2012 Our results showed that treatment of PC12 cells with glibenclamide for 24 h can notably promote TH expression and can also enhance the expression of TH which were reduced by rotenone. Glyburide 53-66 tyrosine hydroxylase Rattus norvegicus 173-175 22994227-2 2012 Here, we provide a focused review on the involvement of matrix metalloproteinase 9 (MMP-9) in rt-PA-associated HT in cerebral ischemia, and we review emerging evidence that the selective inhibitor of the sulfonylurea receptor 1 (Sur1), glibenclamide (U.S. adopted name, glyburide), may provide protection against rt-PA-associated HT in cerebral ischemia. Glyburide 236-249 ATP binding cassette subfamily C member 8 Homo sapiens 229-233 22714048-5 2012 In animal models of SCI, pharmacological inhibition of Sur1 by glibenclamide, as well as gene suppression of Abcc8, prevents delayed capillary fragmentation and tissue necrosis. Glyburide 63-76 ATP binding cassette subfamily C member 8 Homo sapiens 55-59 22714048-8 2012 Clinical trials of an intravenous formulation of glibenclamide in TBI and stroke underscore the importance of recent advances in understanding the role of the Sur1-regulated NC(Ca-ATP) channel in acute ischemic, traumatic, and inflammatory injury to the CNS. Glyburide 49-62 ATP binding cassette subfamily C member 8 Homo sapiens 159-163 22252046-5 2012 Furthermore, embelin and glibenclamide treatment increased the pancreatic antioxidant enzyme status (superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, glutathione S-transferase, and ascorbic acid), and also decreased the thiobarbituric acid reactive oxygen species contents (P < 0.001). Glyburide 25-38 catalase Rattus norvegicus 123-131 22252046-5 2012 Furthermore, embelin and glibenclamide treatment increased the pancreatic antioxidant enzyme status (superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, glutathione S-transferase, and ascorbic acid), and also decreased the thiobarbituric acid reactive oxygen species contents (P < 0.001). Glyburide 25-38 hematopoietic prostaglandin D synthase Rattus norvegicus 178-203 22622455-10 2012 Consistently, we found that stimulating SUR2 with nicorandil prevented angiotensin II-mediated upregulation of xanthine oxidase in the cultured macrophage, while xanthine oxidase expression was rather induced by blocking SUR2 with glibenclamide. Glyburide 231-244 angiotensinogen Rattus norvegicus 71-85 23139715-9 2012 Moreover, we also determined the expression of the Kir6.2 subunits of the K(ATP) channel, which increased in response to U50,488H in the presence of phenylephrine, but was suppressed by chelerythrine, glibenclamide and 5-hydroxydecanoic acid. Glyburide 201-214 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 51-57 22613960-6 2012 Moreover, membrane-depolarizing agents, including K+ and ATP-sensitive K+ (KATP) channel inhibitors glibenclamide and U37883A enhanced TRAIL-induced apoptosis. Glyburide 112-125 TNF superfamily member 10 Homo sapiens 159-164 22387180-4 2012 We found in vitro that BV2 cell line showed upregulated expression of K(ATP) channel subunits in response to pro-inflammatory signals and that glibenclamide increases the reactive morphology of microglia, phagocytic capacity and TNFalpha release. Glyburide 143-156 tumor necrosis factor Mus musculus 229-237 22393122-7 2012 GLB metabolism in hepatic microsomes was significantly inhibited by a selective inhibitor (sulfaphenazole) of CYP2C11 and an anti-CYP2C11 antibody. Glyburide 0-3 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 110-117 22393122-7 2012 GLB metabolism in hepatic microsomes was significantly inhibited by a selective inhibitor (sulfaphenazole) of CYP2C11 and an anti-CYP2C11 antibody. Glyburide 0-3 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 130-137 22393122-8 2012 Western blotting further indicated the contribution of impaired CYP2C11 expression to the impairment of GLB metabolism. Glyburide 104-107 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 64-71 22393122-13 2012 All results yielded the conclusion that impaired hepatic CYP2C11 and intestinal BCRP expression and activity induced by diabetes contributed to the increased exposure of orally administered GLB. Glyburide 190-193 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 57-64 22403794-6 2012 In the transverse and proximal colon, the PRL-induced increase in I(sc) was suppressed by DPC, glibenclamide, and bumetanide, but not by NPPB, DIDS, or amiloride. Glyburide 95-108 prolactin Rattus norvegicus 42-45 22561102-11 2012 Both PI-103 and glibenclamide (10 muM, pmK(ATP) inhibitor) abolished EET cytoprotection. Glyburide 16-29 phosphomevalonate kinase Mus musculus 39-42 22474124-7 2012 The ObR-KO islets also showed significantly higher glibenclamide-induced insulin secretion compared with control islets, whereas [Ca(2+)](i) was similar to the controls. Glyburide 51-64 leptin receptor Mus musculus 4-7 22202177-5 2012 Furthermore, the main product of glibenclamide, cis-3-hydroxy-glibenclamide is identical with the phase-1-metabolite of this drug in human. Glyburide 33-46 suppressor of cytokine signaling 3 Homo sapiens 48-53 22056721-7 2012 Whole-cell patch-clamp studies showed a 2-fold gain of function of glibenclamide-sensitive ATP-sensitive potassium channel current when KCNJ8-S422L was coexpressed with SUR2A-wild type. Glyburide 67-80 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 136-141 22415212-6 2012 Conversely, CGRP (10 nM) significantly increased whole-cell K(+) currents and this effect was abolished by preexposure to tetraethylammonium chloride (1 mM) or iberiotoxin (100 nM), inhibitors of large-conductance calcium-dependent K (BK(Ca)) channels but not by glibenclamide (10 muM), an inhibitor of ATP-dependent K channels. Glyburide 263-276 calcitonin-related polypeptide alpha Rattus norvegicus 12-16 22507152-0 2012 Diabetes caused by Kir6.2 mutation: successful treatment with oral glibenclamide switched from continuous subcutaneous insulin infusion in the early phase of the disease. Glyburide 67-80 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 19-25 22086197-8 2012 Sequential gene activation in cerebral ischemia provides a plausible molecular explanation for the prolonged treatment window observed for inhibition of the end-target gene product, SUR1, by glibenclamide. Glyburide 191-204 ATP binding cassette subfamily C member 8 Rattus norvegicus 182-186 22083559-0 2012 Importance of the Kir6.2 N-terminus for the interaction of glibenclamide and repaglinide with the pancreatic K(ATP) channel. Glyburide 59-72 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 18-24 22083559-6 2012 Kir and SUR were transiently coexpressed in HEK cells and [(3)H]glibenclamide binding and patch-clamp experiments were performed in whole cells at 37 C and in isolated inside/out patches at 22 C. Truncation of the first 5 N-terminal amino acids abolished most of the affinity increase for glibenclamide and repaglinide that is produced by the association of Kir6.2 with SUR1. Glyburide 289-302 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 0-3 22557973-10 2012 Finally, combined inhibition of PKC and TK prior to quercetin abolished quercetin-induced effects, decreasing eNOS expression, while blocking ATP-sensitive potassium (K(ATP)) channels by glibenclamide suppressed arteriolar dilation. Glyburide 187-200 protein kinase C, gamma Rattus norvegicus 32-35 22190590-8 2012 As in WT but not in ABCA1-deficient hepatocytes, 7.2 nm-sized particles generated by glyburide treatment were also detected in ABCG1-deficient and SR-BI-deficient hepatocytes. Glyburide 85-94 scavenger receptor class B, member 1 Mus musculus 147-152 22173067-4 2012 Hoechst 33342 and glyburide were used as model ABCG2 substrates for these experiments. Glyburide 18-27 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 47-52 21800153-3 2012 In addition, NaHS up-regulated the expression of Bcl-2 and blocked MPP(+)-induced down-regulation of Bcl-2, and this augmentation of Bcl-2 expression was prevented by both glybenclamide and LY294002. Glyburide 172-185 BCL2, apoptosis regulator Rattus norvegicus 49-54 21145891-3 2012 (2007) showing that glibenclamide, an FDA approved anti-diabetic drug that targets sulfonylurea receptor 1 (SUR1)-regulated Ca(2+) activated, [ATP](i)-sensitive nonspecific cation channels, attenuates secondary intraspinal hemorrhage and secondary neurodegeneration caused by hemicontusion injury in rat cervical spinal cord. Glyburide 20-33 ATP binding cassette subfamily C member 8 Rattus norvegicus 83-106 21145891-3 2012 (2007) showing that glibenclamide, an FDA approved anti-diabetic drug that targets sulfonylurea receptor 1 (SUR1)-regulated Ca(2+) activated, [ATP](i)-sensitive nonspecific cation channels, attenuates secondary intraspinal hemorrhage and secondary neurodegeneration caused by hemicontusion injury in rat cervical spinal cord. Glyburide 20-33 ATP binding cassette subfamily C member 8 Rattus norvegicus 108-112 22197047-1 2012 In spinal cord injury (SCI), block of Sur1-regulated NC(Ca-ATP) channels by glibenclamide protects penumbral capillaries from delayed fragmentation, resulting in reduced secondary hemorrhage, smaller lesions and better neurological function. Glyburide 76-89 ATP binding cassette subfamily C member 8 Rattus norvegicus 38-42 22375259-0 2012 Comparative Effects of Glibenclamide and Metformin on C-Reactive Protein and Oxidant/Antioxidant Status in Patients with Type II Diabetes Mellitus. Glyburide 23-36 C-reactive protein Homo sapiens 54-72 22155000-6 2012 Whole cell currents of HEK cells transfected with Kir6.1 or SUR2B were activated by K(ATP) channel opener pinacidil, inhibited by K(ATP) channel inhibitor glibenclamide or inhibited by 8-HUDE in a concentration-dependent manner with an IC50 value of 40 uM. Glyburide 155-168 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 50-56 22375259-1 2012 OBJECTIVES: This study aimed to compare the effects of metformin and glibenclamide on high sensitivity serum C-reactive protein (hs-CRP) and oxidative stress, represented by serum malondialdehyde (MDA) and total antioxidant status (TAS) in newly-diagnosed patients with Type 2 diabetes mellitus (DM) at baseline and after 2 months of therapy in comparison to controls. Glyburide 69-82 C-reactive protein Homo sapiens 109-127 21940661-0 2012 Divergent CFTR orthologs respond differently to the channel inhibitors CFTRinh-172, glibenclamide, and GlyH-101. Glyburide 84-97 CF transmembrane conductance regulator Sus scrofa 10-14 21940661-9 2012 We believe that the potency of the inhibitors CFTR(inh)-172, glibenclamide, and GlyH-101 on the CFTR chloride channel protein is likely dictated by the local environment and the three-dimensional structure of additional residues that form the vestibules, the chloride pore, and regulatory regions of the channel. Glyburide 61-74 CF transmembrane conductance regulator Sus scrofa 96-100 21615723-6 2011 The PAR2-induced PVAT-dependent relaxation (SLIGRL-NH(2) ) persisted in the presence of apamin plus charybdotoxin, 4-aminopyridine and glibenclamide, but was blocked by catalase, implicating a role for H(2) O(2) . Glyburide 135-148 coagulation factor II (thrombin) receptor-like 1 Mus musculus 4-8 22890360-8 2012 The inhibitory effects of LPS on ICCs were blocked by glibenclamide (an inhibitor of ATP-sensitive K(+) channels), NS-398 (a COX-2 inhibitor), AH6808 [a prostaglandin E(2) (PGE(2))-EP(2) receptor antagonist], ODQ (an inhibitor of guanylate cyclase) and L-NAME [an inhibitor of nitric oxide synthase (NOS)]. Glyburide 54-67 toll-like receptor 4 Mus musculus 26-29 23285278-13 2012 Moreover, glibenclamide inhibited NaHS-induced vasorelaxation in vessels from wild-type animals, but not PKG-I-/-, suggesting that there is a cross-talk between K(ATP) and PKG. Glyburide 10-23 protein kinase cGMP-dependent 1 Homo sapiens 172-175 22745684-8 2012 Levels of miR-34c expression (as well as pro-inflammatory cytokines, IL-1beta and TNFalpha) decreased when PBMC cultures were briefly pre-incubated with the K(+) channel (inflammasome) inhibitor, glybenclamide, suggesting that inflammasome activation is upstream of miR-34c expression in response to DAMPs. Glyburide 196-209 microRNA 34c Homo sapiens 10-17 22177998-3 2012 Glibenclamide is a potent blocker of Sur1-regulated NC(Ca-ATP) channels (IC(50), 6-48 nM). Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 37-41 21311889-6 2012 The ATP-sensitive potassium channel (K(ATP)) blocker glyburide (3 muM) reversed DEA/NO-induced decreases in the resting tension. Glyburide 53-62 latexin Homo sapiens 66-69 24250461-9 2012 Glibenclamide decreased SOD and CAT activity after IR (p < 0.05). Glyburide 0-13 catalase Rattus norvegicus 32-35 22768668-10 2012 At age 3 years 11 months, glyburide was reintroduced at a very low dose and was increased with concomitant weaning of insulin over the following 6 months. Glyburide 26-35 insulin Homo sapiens 118-125 23324250-2 2012 Here, the GLUT1 gene and the protein expression was studied in rats in the course of severe and mild streptozotocin-induced diabetes mellitus and under glibenclamide treatment. Glyburide 152-165 solute carrier family 2 member 1 Rattus norvegicus 10-15 23324250-8 2012 Severe diabetes mellitus provoked an increase in both GLUT1 gene and protein expression in the kidneys and the heart, which was nearly normalized by glibenclamide. Glyburide 149-162 solute carrier family 2 member 1 Rattus norvegicus 54-59 23324250-11 2012 CONCLUSIONS: The GLUT1 expression was found to be affected by the glucose and insulin levels and can be modulated by glibenclamide in severely and mildly diabetic rats. Glyburide 117-130 solute carrier family 2 member 1 Rattus norvegicus 17-22 21864494-7 2011 The CFTR transport inhibitors CFTR(inh)-172 (5 muM) and glibenclamide (100 muM) showed a significant reduction (P<0.05) in CFTR activity. Glyburide 56-69 CF transmembrane conductance regulator Homo sapiens 4-8 21864494-7 2011 The CFTR transport inhibitors CFTR(inh)-172 (5 muM) and glibenclamide (100 muM) showed a significant reduction (P<0.05) in CFTR activity. Glyburide 56-69 latexin Homo sapiens 75-78 21925514-5 2011 KEY FINDINGS: In heparinized blood, glibenclamide reduced LPS-induced release of IL-1 beta and TNF-alpha, tissue factor and PAI-2 mRNA in a concentration-dependent manner. Glyburide 36-49 interleukin 1 beta Homo sapiens 81-90 21925514-5 2011 KEY FINDINGS: In heparinized blood, glibenclamide reduced LPS-induced release of IL-1 beta and TNF-alpha, tissue factor and PAI-2 mRNA in a concentration-dependent manner. Glyburide 36-49 tumor necrosis factor Homo sapiens 95-104 21925514-5 2011 KEY FINDINGS: In heparinized blood, glibenclamide reduced LPS-induced release of IL-1 beta and TNF-alpha, tissue factor and PAI-2 mRNA in a concentration-dependent manner. Glyburide 36-49 coagulation factor III, tissue factor Homo sapiens 106-119 21925514-5 2011 KEY FINDINGS: In heparinized blood, glibenclamide reduced LPS-induced release of IL-1 beta and TNF-alpha, tissue factor and PAI-2 mRNA in a concentration-dependent manner. Glyburide 36-49 serpin family B member 2 Homo sapiens 124-129 21925514-8 2011 IL-1 beta mRNA inhibition by glibenclamide appeared to be dependent on P2X7-receptor activation of monocytes by ATP-releasing erythrocytes during hypoxia. Glyburide 29-42 interleukin 1 beta Homo sapiens 0-9 21925514-8 2011 IL-1 beta mRNA inhibition by glibenclamide appeared to be dependent on P2X7-receptor activation of monocytes by ATP-releasing erythrocytes during hypoxia. Glyburide 29-42 purinergic receptor P2X 7 Homo sapiens 71-84 21925514-9 2011 Cytosolic calcium values as well as the duration of calcium transients elicited by P2X7-receptor stimulation in isolated monocytes were strongly increased during hypoxia, both of which could be abolished by glibenclamide. Glyburide 207-220 purinergic receptor P2X 7 Homo sapiens 83-96 21983290-7 2011 We also show that glyburide is a strong inhibitor of Panx1 channels. Glyburide 18-27 pannexin 1 Mus musculus 53-58 22340158-7 2011 ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide (Gli, 20 micromol/L) partially blocked the effects of NaHS (100 micromol/L) on human atrial fiber cells. Glyburide 44-57 GLI family zinc finger 1 Homo sapiens 59-62 21210267-5 2011 CONCLUSION: The patient with NDM due to mutation L233F (not reported till date) in the KCNJ11 gene can be successfully treated with oral glibenclamide therapy. Glyburide 137-150 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 87-93 21792527-5 2011 Treatment with both creatine and glibenclamide increased insulin and c-peptide concentrations after 120 and 240 min (p<0.05 and p<0.01). Glyburide 33-46 insulin Homo sapiens 57-64 21792527-5 2011 Treatment with both creatine and glibenclamide increased insulin and c-peptide concentrations after 120 and 240 min (p<0.05 and p<0.01). Glyburide 33-46 insulin Homo sapiens 69-78 22111039-8 2011 The expression of phosphorylated eukaryotic initiation factor (eIF-2alpha) was increased and cleaved caspase 3 was decreased by adding GB to a glucolipotoxic condition. Glyburide 135-137 eukaryotic translation initiation factor 2A Rattus norvegicus 63-73 21782857-6 2011 Inhibition of ABCA1 by chemical inhibitor, glyburide, as well as ABCA1 RNA inhibition, reversed the observed PLTP-mediated activation of STAT3. Glyburide 43-52 ATP binding cassette subfamily A member 1 Homo sapiens 14-19 21782857-6 2011 Inhibition of ABCA1 by chemical inhibitor, glyburide, as well as ABCA1 RNA inhibition, reversed the observed PLTP-mediated activation of STAT3. Glyburide 43-52 phospholipid transfer protein Homo sapiens 109-113 21782857-6 2011 Inhibition of ABCA1 by chemical inhibitor, glyburide, as well as ABCA1 RNA inhibition, reversed the observed PLTP-mediated activation of STAT3. Glyburide 43-52 signal transducer and activator of transcription 3 Homo sapiens 137-142 21565835-8 2011 Pharmacological inhibition of TRPM4 with 9-phenanthrol or glibenclamide protects endothelium against LPS exposure for 48 h. Furthermore, TRPM4-like currents increase in cells pre-treated with LPS and inhibited with glibenclamide. Glyburide 215-228 transient receptor potential cation channel subfamily M member 4 Homo sapiens 30-35 21565835-8 2011 Pharmacological inhibition of TRPM4 with 9-phenanthrol or glibenclamide protects endothelium against LPS exposure for 48 h. Furthermore, TRPM4-like currents increase in cells pre-treated with LPS and inhibited with glibenclamide. Glyburide 215-228 transient receptor potential cation channel subfamily M member 4 Homo sapiens 137-142 21477042-14 2011 CONCLUSIONS: In primary human pre-adipocytes, glibenclamide and glimepiride strongly induced differentiation, apparently by activating PPARgamma. Glyburide 46-59 peroxisome proliferator activated receptor gamma Homo sapiens 135-144 21336994-0 2011 Influence of CYP2C9 gene polymorphisms on response to glibenclamide in type 2 diabetes mellitus patients. Glyburide 54-67 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 13-19 21477042-11 2011 In direct comparison, glibenclamide was more potent than glimepiride with respect to the induction of fatty acid binding protein 4 (FABP4) (EC(50) 0.32 vs. 2.8 microM), an important adipocyte marker gene. Glyburide 22-35 fatty acid binding protein 4 Homo sapiens 102-130 21477042-11 2011 In direct comparison, glibenclamide was more potent than glimepiride with respect to the induction of fatty acid binding protein 4 (FABP4) (EC(50) 0.32 vs. 2.8 microM), an important adipocyte marker gene. Glyburide 22-35 fatty acid binding protein 4 Homo sapiens 132-137 21336994-1 2011 PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9. Glyburide 31-44 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 74-93 21336994-1 2011 PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9. Glyburide 31-44 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 95-101 21336994-1 2011 PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9. Glyburide 31-44 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 135-141 21336994-2 2011 Previous studies involving healthy volunteers have shown a significant influence of variant CYP2C9 genotypes on glibenclamide metabolism. Glyburide 112-125 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 92-98 21336994-3 2011 The aim of this study was to investigate the influence of genetic polymorphisms of CYP2C9 on the response to glibenclamide and on glibenclamide plasma levels in type 2 diabetes mellitus patients. Glyburide 109-122 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 83-89 21336994-9 2011 There was a significant association (p < 0.001) between genotype status of CYP2C9 and the control of diabetes in patients receiving treatment with glibenclamide. Glyburide 150-163 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 78-84 21336994-11 2011 CONCLUSION: The type 2 diabetes mellitus patients participating in this study with variant genotypes of CYP2C9 were found to respond better to treatment with glibenclamide than those with the normal genotype. Glyburide 158-171 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 104-110 21135815-7 2011 Furthermore, mite-infested Cftr(+/+) mice orally administered with a chloride channel inhibitor glibenclamide had higher scratching count and increased level of NGF than vehicle-treated mice. Glyburide 96-109 cystic fibrosis transmembrane conductance regulator Mus musculus 27-31 21354174-3 2011 Glibenclamide, an inhibitor of K(ATP) channels, blocked GLUT1 induction. Glyburide 0-13 solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus 56-61 21681337-9 2011 (3) Inhibitory effect of CIHH on ANGII-induced contraction in thoracic aorta rings was endothelium-independent, and was reversed by glibenclamide (Gli), an ATP-sensitive potassium channels (K(ATP)) blocker, and L-NAME, a NO synthase inhibitor, but not by indomethacin (Indo), a cyclooxygenase inhibitor. Glyburide 132-145 angiotensinogen Rattus norvegicus 33-38 21681337-9 2011 (3) Inhibitory effect of CIHH on ANGII-induced contraction in thoracic aorta rings was endothelium-independent, and was reversed by glibenclamide (Gli), an ATP-sensitive potassium channels (K(ATP)) blocker, and L-NAME, a NO synthase inhibitor, but not by indomethacin (Indo), a cyclooxygenase inhibitor. Glyburide 147-150 angiotensinogen Rattus norvegicus 33-38 21154199-5 2011 Administration of bacosine and glibenclamide significantly decreased the levels of malondialdehyde (MDA), and increased the levels of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT) in the liver of diabetic rats. Glyburide 31-44 catalase Rattus norvegicus 213-221 21154199-5 2011 Administration of bacosine and glibenclamide significantly decreased the levels of malondialdehyde (MDA), and increased the levels of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT) in the liver of diabetic rats. Glyburide 31-44 catalase Rattus norvegicus 223-226 21050070-7 2011 Treatment of THP-1-derived macrophages with inhibitors of the membrane transporter ATP-binding cassette A1, such as glyburide or a specific antibody, significantly reduced the export of this fluorescent compound, indicating that ATP-binding cassette A1 represents the primary mediator of its cellular efflux. Glyburide 116-125 GLI family zinc finger 2 Homo sapiens 13-18 21135815-7 2011 Furthermore, mite-infested Cftr(+/+) mice orally administered with a chloride channel inhibitor glibenclamide had higher scratching count and increased level of NGF than vehicle-treated mice. Glyburide 96-109 nerve growth factor Mus musculus 161-164 21308994-7 2011 Electrophysiological recording with sharp electrodes showed that the CFTR blocker glibenclamide increased motoneuron input resistance, suggesting functional CFTR in P1-P8 motoneurons. Glyburide 82-95 CF transmembrane conductance regulator Rattus norvegicus 69-73 21308994-7 2011 Electrophysiological recording with sharp electrodes showed that the CFTR blocker glibenclamide increased motoneuron input resistance, suggesting functional CFTR in P1-P8 motoneurons. Glyburide 82-95 CF transmembrane conductance regulator Rattus norvegicus 157-161 21148625-10 2011 The CGRP-induced vasodilatation was greater in segments from cirrhotic rats, and was inhibited by ODQ or glibenclamide. Glyburide 105-118 calcitonin-related polypeptide alpha Rattus norvegicus 4-8 20178462-8 2011 and was inhibited by glyburide, indicating that this MIF pool was secreted by a non-classical mechanism and originated from pre-formed MIF stores. Glyburide 21-30 macrophage migration inhibitory factor Homo sapiens 53-56 20178462-8 2011 and was inhibited by glyburide, indicating that this MIF pool was secreted by a non-classical mechanism and originated from pre-formed MIF stores. Glyburide 21-30 macrophage migration inhibitory factor Homo sapiens 135-138 21328463-12 2011 Glibenclamide-sensitive and DIDS-insensitive CFTR Cl(-) currents were consistently observed after stimulation with VIP (10(-8) mol/L). Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 45-49 21328463-12 2011 Glibenclamide-sensitive and DIDS-insensitive CFTR Cl(-) currents were consistently observed after stimulation with VIP (10(-8) mol/L). Glyburide 0-13 vasoactive intestinal peptide Homo sapiens 115-118 21122803-8 2011 The inhibition of K(+)(ATP) channels with glibenclamide attenuated the ursolic acid-induced increase in ANP secretion-but not atrial dynamics-in a concentration-dependent manner. Glyburide 42-55 natriuretic peptides A Oryctolagus cuniculus 104-107 21098040-11 2011 Considering the various residues experimentally assigned to be involved in drug binding, we uncovered several hot spots, which organized spatially in two main binding domains, selective for SR47063 and for glibenclamide, in matching regions of both P-gp and SUR. Glyburide 206-219 phosphoglycolate phosphatase Mus musculus 249-253 21098040-11 2011 Considering the various residues experimentally assigned to be involved in drug binding, we uncovered several hot spots, which organized spatially in two main binding domains, selective for SR47063 and for glibenclamide, in matching regions of both P-gp and SUR. Glyburide 206-219 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 258-261 21084384-8 2011 These effects were counteracted by addition of glibenclamide, the action of which was blocked by the mTOR inhibitor rapamycin and the protein kinase A (PKA) inhibitor Rp-8-Br-cAMPs. Glyburide 47-60 mechanistic target of rapamycin kinase Rattus norvegicus 101-105 21459309-8 2011 RESULTS: Incidence rate ratios (IRRs) for glyburide discontinuation in targeted versus nontargeted cohorts were statistically significantly elevated in September (IRR 2.1; 95% CI 1.7-2.5), October (IRR 1.3; 95% CI 1.1-1.6), and November 2007 (IRR 1.4; 95% CI 1.1-1.7). Glyburide 42-51 insulin receptor related receptor Homo sapiens 32-35 21459309-8 2011 RESULTS: Incidence rate ratios (IRRs) for glyburide discontinuation in targeted versus nontargeted cohorts were statistically significantly elevated in September (IRR 2.1; 95% CI 1.7-2.5), October (IRR 1.3; 95% CI 1.1-1.6), and November 2007 (IRR 1.4; 95% CI 1.1-1.7). Glyburide 42-51 insulin receptor related receptor Homo sapiens 163-166 21459309-8 2011 RESULTS: Incidence rate ratios (IRRs) for glyburide discontinuation in targeted versus nontargeted cohorts were statistically significantly elevated in September (IRR 2.1; 95% CI 1.7-2.5), October (IRR 1.3; 95% CI 1.1-1.6), and November 2007 (IRR 1.4; 95% CI 1.1-1.7). Glyburide 42-51 insulin receptor related receptor Homo sapiens 163-166 21084384-10 2011 Glibenclamide antagonizes these metformin effects through activation of mTOR- and PKA-dependent signaling pathways. Glyburide 0-13 mechanistic target of rapamycin kinase Rattus norvegicus 72-76 21084763-1 2011 The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa. Glyburide 131-140 dipeptidyl peptidase 4 Homo sapiens 59-81 21340016-5 2011 CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or glibenclamide. Glyburide 128-141 catalase Rattus norvegicus 0-3 21340016-5 2011 CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or glibenclamide. Glyburide 128-141 glutathione-disulfide reductase Rattus norvegicus 5-26 21340016-5 2011 CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or glibenclamide. Glyburide 128-141 glutathione-disulfide reductase Rattus norvegicus 28-30 21340016-6 2011 In contrast, metformin or glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH. Glyburide 26-39 catalase Rattus norvegicus 84-87 21340016-6 2011 In contrast, metformin or glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH. Glyburide 26-39 glutathione-disulfide reductase Rattus norvegicus 89-91 21175273-5 2011 RESULTS: the 0-30 min area under the curve (AUC) for insulin was higher (glyburide, 294 +- 37 pM; repaglinide, 382 +- 39 pM) (P < 0.01), and the 180-240 min AUC for insulin was lower (glyburide, 325 +- 50 pM; repaglinide, 196 +- 20 pM) (P < 0.01) with repaglinide. Glyburide 73-82 insulin Homo sapiens 53-60 21175273-5 2011 RESULTS: the 0-30 min area under the curve (AUC) for insulin was higher (glyburide, 294 +- 37 pM; repaglinide, 382 +- 39 pM) (P < 0.01), and the 180-240 min AUC for insulin was lower (glyburide, 325 +- 50 pM; repaglinide, 196 +- 20 pM) (P < 0.01) with repaglinide. Glyburide 191-200 insulin Homo sapiens 53-60 21084763-1 2011 The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa. Glyburide 131-140 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 144-150 21084763-1 2011 The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa. Glyburide 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 21636950-3 2011 We therefore investigated how the SUAs glibenclamide and glimepiride affected the functionality of ABCA1/ABCG1 and scavenger receptor class B type I (SR-BI) expression in macrophages in vitro and overall RCT in vivo. Glyburide 39-52 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 99-104 21636950-3 2011 We therefore investigated how the SUAs glibenclamide and glimepiride affected the functionality of ABCA1/ABCG1 and scavenger receptor class B type I (SR-BI) expression in macrophages in vitro and overall RCT in vivo. Glyburide 39-52 scavenger receptor class B, member 1 Mus musculus 115-148 21636950-3 2011 We therefore investigated how the SUAs glibenclamide and glimepiride affected the functionality of ABCA1/ABCG1 and scavenger receptor class B type I (SR-BI) expression in macrophages in vitro and overall RCT in vivo. Glyburide 39-52 scavenger receptor class B, member 1 Mus musculus 150-155 21636950-6 2011 RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression. Glyburide 34-47 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 58-63 21636950-6 2011 RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression. Glyburide 34-47 apolipoprotein A-I Mus musculus 77-95 21636950-6 2011 RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression. Glyburide 34-47 apolipoprotein A-I Mus musculus 97-103 21636950-6 2011 RESULTS: High dose (500microM) of glibenclamide inhibited ABCA1 function and apolipoprotein A-I (apoA-I)-mediated cholesterol efflux, and attenuated ABCA1 expression. Glyburide 34-47 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 149-154 20724526-7 2010 Whole-cell patch-clamp recordings demonstrated a glibenclamide-sensitive current in the presence of barium chloride, consistent with functional CFTR channels, in control NHBEs and hMSC/NHBE heterokaryons. Glyburide 49-62 CF transmembrane conductance regulator Homo sapiens 144-148 21824448-12 2011 Both the P-gp inhibitor, verapamil, and the MRP2 inhibitor, glibenclamide, didn"t affect the efflux transport of tryptanthrin. Glyburide 60-73 ATP binding cassette subfamily C member 2 Homo sapiens 44-48 21346392-7 2011 RESULTS: Nicorandil (0.1-10 mumol/l) caused a concentration-dependent inhibition of Ang-II-increased cell proliferation and ET-1 expression which were prevented by the K(ATP) channel blocker glibenclamide (1 mumol/l). Glyburide 191-204 angiotensinogen Rattus norvegicus 84-90 20890228-2 2010 We found that insulin-producing cells (IPCs) of adult Drosophila respond to glucose and glibenclamide with a burst-like pattern of activity. Glyburide 88-101 Insulin-like receptor Drosophila melanogaster 14-21 20977577-9 2010 Beneficial effects of metformin were also observed in cells exposed to glibenclamide for 18 h with significant improvements in the insulin secretory responsiveness to alanine, GLP-1 and sulphonylureas. Glyburide 71-84 glucagon Rattus norvegicus 176-181 21107131-7 2010 At 2 weeks, the increase in activated caspase-3 in the hilus of glibenclamide-treated rats was half of that in vehicle-treated rats. Glyburide 64-77 caspase 3 Rattus norvegicus 38-47 20855438-2 2010 During FAT1, both tetanic [Ca(2+)](i)/force decreased; however, they decreased to significantly lower levels when FAT1 was carried out in the presence of glibenclamide, a sarcolemmal K(ATP) (sK(ATP)) channel blocker. Glyburide 154-167 FAT atypical cadherin 1 Mus musculus 7-11 20855438-2 2010 During FAT1, both tetanic [Ca(2+)](i)/force decreased; however, they decreased to significantly lower levels when FAT1 was carried out in the presence of glibenclamide, a sarcolemmal K(ATP) (sK(ATP)) channel blocker. Glyburide 154-167 FAT atypical cadherin 1 Mus musculus 114-118 20855438-3 2010 Glibenclamide also elicited greater increases in unstimulated [Ca(2+)](i)/force, which occurred when fibres failed to fully relax between contractions during FAT1. Glyburide 0-13 FAT atypical cadherin 1 Mus musculus 158-162 20855438-4 2010 Finally, glibenclamide impaired force recovery after FAT1. Glyburide 9-22 FAT atypical cadherin 1 Mus musculus 53-57 20855438-7 2010 In the presence of glibenclamide, on the other hand, the differences between FAT1 and FAT2 were very large. Glyburide 19-32 FAT atypical cadherin 1 Mus musculus 77-81 20855438-7 2010 In the presence of glibenclamide, on the other hand, the differences between FAT1 and FAT2 were very large. Glyburide 19-32 FAT atypical cadherin 2 Mus musculus 86-90 20855438-8 2010 Unexpectedly, the differences in unstimulated and tetanic [Ca(2+)](i)/force between control and glibenclamide conditions observed during FAT1 were no longer observed during FAT2. Glyburide 96-109 FAT atypical cadherin 1 Mus musculus 137-141 20937249-9 2010 In conclusion, the GPR119 agonist AS1535907 induces a more rapid and physiological pattern of insulin release than glibenclamide, and represents a novel strategy for the treatment of type 2 diabetes. Glyburide 115-128 G protein-coupled receptor 119 Rattus norvegicus 19-25 20694540-9 2010 In ED rings, the PKA inhibitor H-89 and K(ATP) channel inhibitor glibenclamide almost totally abolished the vasodilatation effect of VIP. Glyburide 65-78 vasoactive intestinal peptide Rattus norvegicus 133-136 20540932-10 2010 Molecules known to interact with OATPs, including cyclosporin A, rifampicin, and glibenclamide, each demonstrated concentration-dependent inhibition of 8-FcA transport by OATP1B1 and OATP1B3. Glyburide 81-94 solute carrier organic anion transporter family member 1B1 Homo sapiens 171-178 21335294-6 2010 These publications described studies of DPP-4 inhibitors administered as monotherapy or in combination with metformin, a thiazolidinedione, glimepiride, glibenclamide, or insulin. Glyburide 153-166 dipeptidyl peptidase 4 Homo sapiens 40-45 20540932-10 2010 Molecules known to interact with OATPs, including cyclosporin A, rifampicin, and glibenclamide, each demonstrated concentration-dependent inhibition of 8-FcA transport by OATP1B1 and OATP1B3. Glyburide 81-94 solute carrier organic anion transporter family member 1B3 Homo sapiens 183-190 20656890-2 2010 Mice deleted for the first nucleotide binding region of sulfonylurea receptor 2 (SUR2) are referred to as SUR2 null since they lack full-length SUR2 and glibenclamide-responsive K(ATP) channels in cardiac, skeletal, and smooth muscle. Glyburide 153-166 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 56-79 20656890-2 2010 Mice deleted for the first nucleotide binding region of sulfonylurea receptor 2 (SUR2) are referred to as SUR2 null since they lack full-length SUR2 and glibenclamide-responsive K(ATP) channels in cardiac, skeletal, and smooth muscle. Glyburide 153-166 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 106-110 20656890-2 2010 Mice deleted for the first nucleotide binding region of sulfonylurea receptor 2 (SUR2) are referred to as SUR2 null since they lack full-length SUR2 and glibenclamide-responsive K(ATP) channels in cardiac, skeletal, and smooth muscle. Glyburide 153-166 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 106-110 20860660-8 2010 KEY RESULTS Quercetin (20 micromol L(-1)) potentiated both glucose (8.3 mmol L(-1))- and glibenclamide (0.01 micromol L(-1))-induced insulin secretion and ERK1/2 phosphorylation. Glyburide 89-102 mitogen activated protein kinase 3 Rattus norvegicus 155-161 20698928-0 2010 Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide. Glyburide 131-144 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 10-16 20698928-2 2010 Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor. Glyburide 157-170 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 83-89 20698928-2 2010 Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor. Glyburide 157-170 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 230-236 20698928-2 2010 Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor. Glyburide 157-170 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 230-236 20698928-10 2010 CONCLUSIONS: Concomitant use of a CYP2C9 inhibitor results in exaggerated pharmacodynamic effects of sulphonylureas and increases the risk of hypoglycaemia in T2DM patients receiving glibenclamide, glimepiride or glipizide. Glyburide 183-196 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 34-40 20804735-7 2010 This contrasted with the action of the sulfonylurea glibenclamide, which also induced insulin secretion under low-glucose conditions (2.8mM). Glyburide 52-65 insulin Homo sapiens 86-93 21264098-1 2010 The everted gut sac method was used to assess the role of the P-glycoprotein (P-gp) on the intestinal secretion of glibenclamide, a prototype of drug used to treat diabetic mellitus. Glyburide 115-128 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 62-76 21264098-1 2010 The everted gut sac method was used to assess the role of the P-glycoprotein (P-gp) on the intestinal secretion of glibenclamide, a prototype of drug used to treat diabetic mellitus. Glyburide 115-128 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 78-82 21264098-10 2010 The results obtained in this study, both under in vivo and in vitro conditions confirm the relevance of P-gp-mediated transport to the intestinal secretion of glibenclamide. Glyburide 159-172 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 104-108 20535530-8 2010 Furthermore, the study of the effect of inhibitors of lipid efflux showed that glyburide and brefeldin A, which affect ABCA1 function, exerted strong and similar inhibitory effects on lipid efflux from both adipocytes and macrophages, whereas BLT1, an SRB-I inhibitor, only exerted a moderate inhibition. Glyburide 79-88 ATP binding cassette subfamily A member 1 Homo sapiens 119-124 20535530-8 2010 Furthermore, the study of the effect of inhibitors of lipid efflux showed that glyburide and brefeldin A, which affect ABCA1 function, exerted strong and similar inhibitory effects on lipid efflux from both adipocytes and macrophages, whereas BLT1, an SRB-I inhibitor, only exerted a moderate inhibition. Glyburide 79-88 leukotriene B4 receptor Homo sapiens 243-247 20835230-3 2010 One therapy for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1beta production in vitro. Glyburide 33-42 islet amyloid polypeptide Homo sapiens 55-59 20835230-3 2010 One therapy for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1beta production in vitro. Glyburide 33-42 interleukin 1 beta Homo sapiens 69-77 21409314-9 2010 The IAPP response to glucagon declined in the glibenclamide group (p < 0.001), but not in insulin-treated subjects (p = 0.05 for difference between groups). Glyburide 46-59 islet amyloid polypeptide Homo sapiens 4-8 20638992-6 2010 In non-diabetic rats after either GM or GB administration the decreased PON1 activity in the plasma was observed (GM: P < 0.001, GB: P < 0.05), but plasma PAF-AH activity remained unchanged. Glyburide 132-134 paraoxonase 1 Rattus norvegicus 72-76 20367258-6 2010 Pharmacological inhibitors directed toward PI3K (wortmannin and LY294002), or the mito-K(ATP) channel (glybenclamide) inhibited the H(2)O(2)-mediated increase in ATP in cells overexpressing human Ngb and consequently cell viability decreased. Glyburide 103-116 neuroglobin Homo sapiens 196-199 20638992-0 2010 The differentiating effect of glimepiride and glibenclamide on paraoxonase 1 and platelet-activating factor acetylohydrolase activity. Glyburide 46-59 paraoxonase 1 Rattus norvegicus 63-76 20638992-1 2010 AIMS: The present study was designed to examine the effect of sulphonylureas, glimepiride (GM) and glibenclamide (GB), on paraoxonase 1 (PON1) and platelet activating factor acetylohydrolase (PAF-AH) activity in normal and streptozotocin (STZ)-induced (50 mg/kg) diabetic rats. Glyburide 99-112 paraoxonase 1 Rattus norvegicus 122-135 20638992-1 2010 AIMS: The present study was designed to examine the effect of sulphonylureas, glimepiride (GM) and glibenclamide (GB), on paraoxonase 1 (PON1) and platelet activating factor acetylohydrolase (PAF-AH) activity in normal and streptozotocin (STZ)-induced (50 mg/kg) diabetic rats. Glyburide 99-112 paraoxonase 1 Rattus norvegicus 137-141 20638992-1 2010 AIMS: The present study was designed to examine the effect of sulphonylureas, glimepiride (GM) and glibenclamide (GB), on paraoxonase 1 (PON1) and platelet activating factor acetylohydrolase (PAF-AH) activity in normal and streptozotocin (STZ)-induced (50 mg/kg) diabetic rats. Glyburide 114-116 paraoxonase 1 Rattus norvegicus 122-135 20812902-3 2010 BCRP is capable of transporting non-chemotherapy drugs and xenobiotiocs as well, including nitrofurantoin, prazosin, glyburide, and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. Glyburide 117-126 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-4 20538722-8 2010 The canalicular secretion of TA-0201CA was inhibited by the bile salt export pump (Bsep) inhibitor glibenclamide and by the Mrp2 inhibitor 3-[[3-[2-(7-chloroquinolin-2-yl)vinyl]phenyl]-(2-dimethylcarbamoylethylsulfanyl)methylsulfanyl] propionic acid (MK-571) in SCRH from SDR and EHBR. Glyburide 99-112 ATP binding cassette subfamily B member 11 Rattus norvegicus 60-81 20538722-8 2010 The canalicular secretion of TA-0201CA was inhibited by the bile salt export pump (Bsep) inhibitor glibenclamide and by the Mrp2 inhibitor 3-[[3-[2-(7-chloroquinolin-2-yl)vinyl]phenyl]-(2-dimethylcarbamoylethylsulfanyl)methylsulfanyl] propionic acid (MK-571) in SCRH from SDR and EHBR. Glyburide 99-112 ATP binding cassette subfamily B member 11 Rattus norvegicus 83-87 20558597-8 2010 Moreover, GLB depletion was markedly inhibited by ketoconazole, a potent inhibitor of mouse Cyp3a, suggesting that GLB metabolism in mice is primarily mediated by hepatic Cyp3a. Glyburide 10-13 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 92-97 20558597-8 2010 Moreover, GLB depletion was markedly inhibited by ketoconazole, a potent inhibitor of mouse Cyp3a, suggesting that GLB metabolism in mice is primarily mediated by hepatic Cyp3a. Glyburide 10-13 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 171-176 20558597-8 2010 Moreover, GLB depletion was markedly inhibited by ketoconazole, a potent inhibitor of mouse Cyp3a, suggesting that GLB metabolism in mice is primarily mediated by hepatic Cyp3a. Glyburide 115-118 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 92-97 20558597-9 2010 These data suggest that the increased systemic clearance of GLB in pregnant mice is likely caused by an increase in hepatic Cyp3a activity during pregnancy, and they provide a basis for further mechanistic understanding and analysis of pregnancy-induced alterations in the disposition of GLB and drugs that are predominantly and extensively metabolized by CYP3A/Cyp3a. Glyburide 60-63 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 124-129 20558597-9 2010 These data suggest that the increased systemic clearance of GLB in pregnant mice is likely caused by an increase in hepatic Cyp3a activity during pregnancy, and they provide a basis for further mechanistic understanding and analysis of pregnancy-induced alterations in the disposition of GLB and drugs that are predominantly and extensively metabolized by CYP3A/Cyp3a. Glyburide 60-63 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 356-361 20558597-9 2010 These data suggest that the increased systemic clearance of GLB in pregnant mice is likely caused by an increase in hepatic Cyp3a activity during pregnancy, and they provide a basis for further mechanistic understanding and analysis of pregnancy-induced alterations in the disposition of GLB and drugs that are predominantly and extensively metabolized by CYP3A/Cyp3a. Glyburide 60-63 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 362-367 20357193-9 2010 The aortic relaxations induced by RRF and exogenous PAME were inhibited by 4-aminopyridine (2 mM) and tetraethylammonium (TEA, 10 mM) but were not affected by TEA at 1 mM or 3 mM, glibenclamide (3 microM), or iberiotoxin (100 nM). Glyburide 180-193 mitochondrial ribosome recycling factor Rattus norvegicus 34-37 20035575-7 2010 Bumetanide and glibenclamide are 2 well-characterized, safe, FDA-approved drugs that inhibit NKCC1 and the SUR1/TRPM4 channel, respectively. Glyburide 15-28 solute carrier family 12 member 2 Rattus norvegicus 93-98 20035575-7 2010 Bumetanide and glibenclamide are 2 well-characterized, safe, FDA-approved drugs that inhibit NKCC1 and the SUR1/TRPM4 channel, respectively. Glyburide 15-28 ATP binding cassette subfamily C member 8 Rattus norvegicus 107-111 20035575-7 2010 Bumetanide and glibenclamide are 2 well-characterized, safe, FDA-approved drugs that inhibit NKCC1 and the SUR1/TRPM4 channel, respectively. Glyburide 15-28 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 112-117 20035575-9 2010 Given the mechanistic and temporal differences by which NKCC1 and the SUR1/TRPM4 channel contribute to the pathophysiological mechanisms of these events, combination therapy with bumetanide and glibenclamide may yield critical synergy in preventing injury-associated capillary failure. Glyburide 194-207 solute carrier family 12 member 2 Rattus norvegicus 56-61 20035575-9 2010 Given the mechanistic and temporal differences by which NKCC1 and the SUR1/TRPM4 channel contribute to the pathophysiological mechanisms of these events, combination therapy with bumetanide and glibenclamide may yield critical synergy in preventing injury-associated capillary failure. Glyburide 194-207 ATP binding cassette subfamily C member 8 Rattus norvegicus 70-74 20035575-9 2010 Given the mechanistic and temporal differences by which NKCC1 and the SUR1/TRPM4 channel contribute to the pathophysiological mechanisms of these events, combination therapy with bumetanide and glibenclamide may yield critical synergy in preventing injury-associated capillary failure. Glyburide 194-207 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 75-80 20655424-8 2010 Because the effect of insulin could be abolished by barium, glybenclamide, or ouabain, the underlying mechanisms of the insulin action could be an increased K(+) conductance or an increased Na/K-ATPase activity or both. Glyburide 60-73 insulin Bos taurus 22-29 20655424-8 2010 Because the effect of insulin could be abolished by barium, glybenclamide, or ouabain, the underlying mechanisms of the insulin action could be an increased K(+) conductance or an increased Na/K-ATPase activity or both. Glyburide 60-73 insulin Bos taurus 120-127 20421591-9 2010 ApoA-I removal of microdomains was blocked by glyburide and inhibitor of ATP-binding cassette transporter A1 (ABCA1) function. Glyburide 46-55 apolipoprotein A1 Homo sapiens 0-6 20638992-6 2010 In non-diabetic rats after either GM or GB administration the decreased PON1 activity in the plasma was observed (GM: P < 0.001, GB: P < 0.05), but plasma PAF-AH activity remained unchanged. Glyburide 40-42 paraoxonase 1 Rattus norvegicus 72-76 20638992-8 2010 Additionally, both drugs increased PON1 activity toward phenyl acetate in the liver, in diabetic rats (GM: P < 0.05, GB:ns) as well as in non-diabetic rats (GM: P < 0.001, GB: P < 0.001), and reduced lipid peroxidation in the liver. Glyburide 120-122 paraoxonase 1 Rattus norvegicus 35-39 20559501-6 2010 In contrast, the combination of glibenclamide, metformin and honey significantly up-regulated CAT activity and down-regulated GPx activity while TBARS levels were significantly reduced. Glyburide 32-45 catalase Rattus norvegicus 94-97 20386871-5 2010 The TRAP effect was blocked by 4 mg/kg glibenclamide and 4 mg/kg HMR1098 and partially blocked by 3 mg/kg 5HD. Glyburide 39-52 TRAP Homo sapiens 4-8 19656320-5 2010 A K(ATP) mutation (R201H; KCNJ11) was detected in the infant, the mother, and 6-yr-old sister with PNDM; both were also subsequently transitioned off insulin onto glyburide. Glyburide 163-172 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 26-32 19656320-8 2010 Pancreatic insulin disappears in an animal model of K(ATP)-induced NDM, unless glycemia is well controlled, thus, a dramatically lower glyburide requirement in the infant may reflect preserved insulin content because of early sulfonylurea intervention. Glyburide 135-144 insulin Homo sapiens 11-18 20437462-0 2010 Contributions of human cytochrome P450 enzymes to glyburide metabolism. Glyburide 50-59 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 23-38 20437462-3 2010 Therefore, there has been a continued interest in identifying human cytochrome P450 (CYP) isoforms that play a major role in the metabolism of GLB. Glyburide 143-146 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 68-83 20437462-3 2010 Therefore, there has been a continued interest in identifying human cytochrome P450 (CYP) isoforms that play a major role in the metabolism of GLB. Glyburide 143-146 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 85-88 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 81-84 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 103-109 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 111-117 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 119-125 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 130-137 20437462-6 2010 GLB depletion and metabolite formation in human liver microsomes were most significantly inhibited by the CYP3A inhibitor ketoconazole compared with the inhibitors of other CYP isoforms. Glyburide 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 20437462-6 2010 GLB depletion and metabolite formation in human liver microsomes were most significantly inhibited by the CYP3A inhibitor ketoconazole compared with the inhibitors of other CYP isoforms. Glyburide 0-3 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 106-109 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 80-83 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 80-83 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 96-99 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 64-67 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 96-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 96-99 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 195-198 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 206-209 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 64-67 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 206-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 206-209 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 195-198 20437462-9 2010 These results confirm that human CYP3A4 is the major enzyme involved in the in vitro metabolism of GLB. Glyburide 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20159988-0 2010 Breast cancer resistance protein (BCRP)-mediated glyburide transport: effect of the C421A/Q141K BCRP single-nucleotide polymorphism. Glyburide 49-58 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-32 20159988-0 2010 Breast cancer resistance protein (BCRP)-mediated glyburide transport: effect of the C421A/Q141K BCRP single-nucleotide polymorphism. Glyburide 49-58 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 34-38 20159988-0 2010 Breast cancer resistance protein (BCRP)-mediated glyburide transport: effect of the C421A/Q141K BCRP single-nucleotide polymorphism. Glyburide 49-58 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 96-100 20159988-2 2010 Evidence suggests that breast cancer resistance protein/ATP-binding cassette, subfamily G, member 2 (ABCG2) expressed in the placenta protects the fetus against the accumulation of glyburide. Glyburide 181-190 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 23-55 20159988-2 2010 Evidence suggests that breast cancer resistance protein/ATP-binding cassette, subfamily G, member 2 (ABCG2) expressed in the placenta protects the fetus against the accumulation of glyburide. Glyburide 181-190 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 101-106 20159988-6 2010 The purpose of this study is to investigate whether the Q141K SNP causes alterations in ABCG2-mediated glyburide transport. Glyburide 103-112 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 88-93 20159988-7 2010 Glyburide accumulation assays were carried out with stably transfected human embryonic kidney (HEK)-293 cells expressing wild-type ABCG2 (Arg482) and polymorphic ABCG2 (Q141K). Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 162-167 20159988-8 2010 Glyburide kinetic parameters were determined for comparison of wild-type and SNP ABCG2 activity by simultaneously fitting data for ABCG2-expressing cells (saturable transport) and empty vector-expressing cells (nonsaturable transport) by nonlinear regression analysis. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 81-86 20159988-8 2010 Glyburide kinetic parameters were determined for comparison of wild-type and SNP ABCG2 activity by simultaneously fitting data for ABCG2-expressing cells (saturable transport) and empty vector-expressing cells (nonsaturable transport) by nonlinear regression analysis. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 131-136 20159988-10 2010 Our results indicate that the Q141K variant of ABCG2 may have the potential to alter the placental pharmacokinetics of glyburide used in pregnancy. Glyburide 119-128 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 47-52 19686306-5 2010 We describe the response to glyburide in a 15-yr-old boy with severe global developmental delays resulting from the KCNJ11 mutation V59M. Glyburide 28-37 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 116-122 20350646-4 2010 RESULTS: Glyburide was transported by multidrug resistance protein (43 +/- 4%); breast cancer resistance protein (25 +/- 5%); and P-glycoprotein (9 +/- 5%). Glyburide 9-18 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 80-112 21426008-1 2010 BACKGROUND: The sulfonylureas glibenclamide and glimepiride are oral antidiabetic drugs that stimulate insulin secretion by closing pancreatic ATP-dependent potassium channels. Glyburide 30-43 insulin Homo sapiens 103-110 21426008-4 2010 RESULTS: We demonstrate that glibenclamide and glimepiride modulate FXR activation in a reporter-gene assay and induce FXR target genes in HepG2 cells. Glyburide 29-42 nuclear receptor subfamily 1 group H member 4 Homo sapiens 68-71 21426008-4 2010 RESULTS: We demonstrate that glibenclamide and glimepiride modulate FXR activation in a reporter-gene assay and induce FXR target genes in HepG2 cells. Glyburide 29-42 nuclear receptor subfamily 1 group H member 4 Homo sapiens 119-122 21426008-5 2010 Within the docking experiments and molecular dynamics simulation, we found glibenclamide interacting with the ligand-binding domain of FXR and with helix 12. Glyburide 75-88 nuclear receptor subfamily 1 group H member 4 Homo sapiens 135-138 21426008-6 2010 CONCLUSION: Glibenclamide and glimepiride are potential ligands of FXR and modulate activation and signaling. Glyburide 12-25 nuclear receptor subfamily 1 group H member 4 Homo sapiens 67-70 19805629-0 2009 Glyburide inhibits the Cryopyrin/Nalp3 inflammasome. Glyburide 0-9 NLR family pyrin domain containing 3 Homo sapiens 23-32 20151774-9 2010 Resistin and RBP-4 decreased with exenatide and increased with glibenclamide. Glyburide 63-76 retinol binding protein 4 Homo sapiens 13-18 20064105-6 2010 Glyburide"s limited fetal transfer has been attributed to its high protein binding, rapid clearance rate and the role of placental efflux transporters such as the breast cancer resistance protein. Glyburide 0-9 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 163-195 20093633-3 2010 Using a rat model of severe ischemia/reperfusion with very high mortality due to malignant cerebral edema, we tested the hypothesis that blocking of sulfonylurea receptor 1-regulated NC(Ca-ATP) channels with glibenclamide would compare favorably to DC when reperfusion and treatment were begun 6 hours after onset of ischemia. Glyburide 208-221 ATP binding cassette subfamily C member 8 Rattus norvegicus 149-172 20102598-8 2010 KATP current recorded in excised patches was blocked by glybenclamide, but preincubation with antibody against SUR1 abolished this blocking effect of glybenclamide, confirming that the antibody targets the SUR1 protein in the neuronal plasmalemmal membrane. Glyburide 150-163 ATP binding cassette subfamily C member 8 Rattus norvegicus 111-115 19808911-5 2010 CRP reduction was greater in the rosiglitazone group by -47.6% relative to glyburide and by -30.5% relative to metformin at 48 months. Glyburide 75-84 C-reactive protein Homo sapiens 0-3 19808911-7 2010 The change in CRP from baseline to 12 months was correlated positively with change in BMI in glyburide (r = 0.18) and metformin (r = 0.20) groups but not in the rosiglitazone (r = -0.05, NS) group. Glyburide 93-102 C-reactive protein Homo sapiens 14-17 19808911-10 2010 CRP in the glyburide and metformin groups was positively associated with changes in weight, but this was not the case with rosiglitazone. Glyburide 11-20 C-reactive protein Homo sapiens 0-3 20137495-11 2009 CFTR mRNA in MG + glibenclamide were much lower than those in MG (P < 0.05). Glyburide 18-31 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 0-4 20137495-12 2009 RANTES and CFTR mRNA treated with glibenclamide in AHATG were significantly lower than those in the AHATG (P < 0.01). Glyburide 34-47 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 11-15 20137495-13 2009 Minimal changes in the secretions of MCP-1 in the epithelial cells were detected between AHATG and AHATG + glibenclamide (P > 0.05). Glyburide 107-120 chemokine (C-C motif) ligand 2 Mus musculus 37-42 20137495-16 2009 Glibenclamide can inhibit the CFTR secretion in mucosal epithelial cells, in particular during AR process. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 30-34 20042732-7 2010 The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine. Glyburide 233-246 nitric oxide synthase 3 Homo sapiens 39-44 20220270-4 2010 We describe a 3-year-old girl with permanent neonatal diabetes mellitus with a mutation in the KCNJ11 gene (R201H), who was successfully transferred from subcutaneous insulin to oral glibenclamide, with a marked improvement in glycemic control. Glyburide 183-196 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 95-101 20151774-8 2010 A decrease of PPr was reported in both groups, but only glibenclamide decreased the PPr/FPI ratio. Glyburide 56-69 PPR1 Homo sapiens 84-87 20540435-6 2010 Insulin therapy was successfully switched to low doses of oral glibenclamide. Glyburide 63-76 insulin Homo sapiens 0-7 20139897-0 2010 Repurposing an old drug for a new use: glybenclamide exerts antiplatelet activity by interacting with the thromboxane A(2) receptor. Glyburide 39-52 thromboxane A2 receptor Homo sapiens 106-131 20139897-1 2010 AIM: To investigate the potential antagonistic activity of the antidiabetic agent glybenclamide for the human platelet thromboxane A(2) receptor (abbreviated as TPR). Glyburide 82-95 thromboxane A2 receptor Homo sapiens 119-144 20139897-1 2010 AIM: To investigate the potential antagonistic activity of the antidiabetic agent glybenclamide for the human platelet thromboxane A(2) receptor (abbreviated as TPR). Glyburide 82-95 translocated promoter region, nuclear basket protein Homo sapiens 161-164 20139897-6 2010 CONCLUSION: The findings indicate that glybenclamide exerts inhibitory effects on platelets by interacting with TPR. Glyburide 39-52 translocated promoter region, nuclear basket protein Homo sapiens 112-115 19896519-4 2010 Among the five fractions (A1, B1, C1, A2 and B2) obtained, of an initial chromatographic separation of the ethanolic extract, fraction A2 (100 mg/kg bw) showed the maximum antihyperglycemic activity which is significantly higher than that of the reference drug glibenclamide (20 mg/kg bw). Glyburide 261-274 UDP glucuronosyltransferase 1 family, polypeptide A7C Rattus norvegicus 34-47 19912999-6 2010 Vasorelaxant activity of NOX-1 was not abolished by pretreatment of aortic rings with L-NNA, 1H-[1,2,4] oxadiazolo [4,3-A] quinoxalin-1-one (ODQ), indomethacin or glibenclamide. Glyburide 163-176 NADPH oxidase 1 Rattus norvegicus 25-30 19926919-11 2010 In conclusion, suppression of AMPK activity in beta-cells inhibited insulin secretion in response to glucose, potassium chloride or glibenclamide without altering insulin content. Glyburide 132-145 protein kinase AMP-activated catalytic subunit alpha 1 Rattus norvegicus 30-34 20814548-8 2010 Glibenclamide also eliminated the insulin-induced changes. Glyburide 0-13 insulin Homo sapiens 34-41 19955410-6 2009 Since glibenclamide inhibited H(2)S-triggered p38 phosphorylation, we propose that K(ATP) channels lay upstream of p38 in this process. Glyburide 6-19 mitogen-activated protein kinase 14 Mus musculus 46-49 19955410-6 2009 Since glibenclamide inhibited H(2)S-triggered p38 phosphorylation, we propose that K(ATP) channels lay upstream of p38 in this process. Glyburide 6-19 mitogen-activated protein kinase 14 Mus musculus 115-118 19679108-8 2009 Human placental microsomal CYP19/aromatase was the major isozyme responsible for the biotransformation of glyburide to predominantly M5. Glyburide 106-115 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 27-32 20050194-7 2009 Membrane hyperpolarization induced by CGRP or cAMP stimulators was blocked by glibenclamide, while their negative chronotropic effects were less affected. Glyburide 78-91 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 38-42 19604096-7 2009 Block of SUR1 using low-dose (non-hypoglycemogenic) glibenclamide largely eliminated PSH and capillary fragmentation, and was associated with a significant reduction in the size of the necrotic lesion and in preservation of neurobehavioral function. Glyburide 52-65 ATP binding cassette subfamily C member 8 Rattus norvegicus 9-13 19805629-0 2009 Glyburide inhibits the Cryopyrin/Nalp3 inflammasome. Glyburide 0-9 NLR family pyrin domain containing 3 Homo sapiens 33-38 19805629-5 2009 In this study, we show that the type 2 diabetes drug glyburide prevented activation of the Cryopyrin inflammasome. Glyburide 53-62 NLR family pyrin domain containing 3 Homo sapiens 91-100 19805629-8 2009 Glyburide analogues inhibit ATP- but not hypothermia-induced IL-1beta secretion from human monocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations, thus suggesting that inhibition occurs upstream of Cryopyrin. Glyburide 0-9 NLR family pyrin domain containing 3 Homo sapiens 174-183 19805629-8 2009 Glyburide analogues inhibit ATP- but not hypothermia-induced IL-1beta secretion from human monocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations, thus suggesting that inhibition occurs upstream of Cryopyrin. Glyburide 0-9 NLR family pyrin domain containing 3 Homo sapiens 246-255 19805629-10 2009 Therefore, glyburide is the first identified compound to prevent Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion. Glyburide 11-20 NLR family pyrin domain containing 3 Homo sapiens 65-74 19805629-10 2009 Therefore, glyburide is the first identified compound to prevent Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion. Glyburide 11-20 interleukin 1 beta Homo sapiens 136-144 19619327-18 2009 Current data indicate that the combined glibenclamide/metformin therapy seems to present special risk and should be avoided in the long-term management of T2DM with proven CAD; 4. Glyburide 40-53 cadherin 4 Homo sapiens 172-178 19520776-9 2009 Troglitazone and glibenclamide inhibited the BSEP/Bsep-mediated transport of different bile salts with similar affinities, whereas the potential of cyclosporine A to inhibit bile salt transport showed species- and bile salt-specific variations. Glyburide 17-30 ATP binding cassette subfamily B member 11 Rattus norvegicus 45-49 19520776-9 2009 Troglitazone and glibenclamide inhibited the BSEP/Bsep-mediated transport of different bile salts with similar affinities, whereas the potential of cyclosporine A to inhibit bile salt transport showed species- and bile salt-specific variations. Glyburide 17-30 ATP binding cassette subfamily B member 11 Rattus norvegicus 50-54 19688040-7 2009 CAPN10 SNP-43 and SNP-44 were genotyped and related to gene expression and insulin release in response to glucose, arginine and glibenclamide. Glyburide 128-141 calpain 10 Homo sapiens 0-6 19688040-7 2009 CAPN10 SNP-43 and SNP-44 were genotyped and related to gene expression and insulin release in response to glucose, arginine and glibenclamide. Glyburide 128-141 insulin Homo sapiens 75-82 19531471-6 2009 The S1P release was reduced by an ABCA1 transporter inhibitor, glyburide, but not by a multidrug resistance-associated protein inhibitor, MK571, or a multidrug resistance protein inhibitor, cyclosporine A. Glyburide 63-72 ATP binding cassette subfamily A member 1 Rattus norvegicus 34-39 19717637-5 2009 In addition, treatment of HepG2 cells with the ABC transporter inhibitor, glyburide, stimulated the apoA-I secretory effects of both DLPC and clofibrate. Glyburide 74-83 apolipoprotein A1 Homo sapiens 100-106 19502091-5 2009 RESULTS: Insulin secretion differed significantly between study groups, with marked decreases in the presence of HG plus glibenclamide. Glyburide 121-134 insulin Homo sapiens 9-16 19502091-6 2009 Compared with NG, insulin expression decreased significantly with HG, and increased similarly with gliclazide as with glibenclamide. Glyburide 118-131 insulin Homo sapiens 18-25 19706871-4 2009 Commonly used sulfonylureas such as tolbutamide and glibenclamide induced Epac2 activation with distinct kinetic profiles. Glyburide 52-65 Rap guanine nucleotide exchange factor (GEF) 4 Mus musculus 74-79 19304587-8 2009 The ABCA1 and SR-BI inhibitor glyburide (also known as glibenclamide) abolished basal transport of POS-derived lipids in RPE cells in the presence of high-density lipoprotein. Glyburide 30-39 scavenger receptor class B, member 1 Mus musculus 14-19 19304587-8 2009 The ABCA1 and SR-BI inhibitor glyburide (also known as glibenclamide) abolished basal transport of POS-derived lipids in RPE cells in the presence of high-density lipoprotein. Glyburide 55-68 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 4-9 19304587-8 2009 The ABCA1 and SR-BI inhibitor glyburide (also known as glibenclamide) abolished basal transport of POS-derived lipids in RPE cells in the presence of high-density lipoprotein. Glyburide 55-68 scavenger receptor class B, member 1 Mus musculus 14-19 19696956-0 2009 Role of the C-terminal part of the extracellular domain of the alpha-ENaC in activation by sulfonylurea glibenclamide. Glyburide 104-117 sodium channel epithelial 1 subunit alpha Rattus norvegicus 63-73 19696956-3 2009 The activator effect of glibenclamide is fast and reversible and was observed in Xenopus oocytes coexpressing the alpha subunit from human, Xenopus, or guinea pig (but not rat) with betagamma-rat ENaC subunits. Glyburide 24-37 sodium channel epithelial 1 subunit gamma Rattus norvegicus 196-200 19696956-7 2009 The effect of glibenclamide on ENaC activity was measured using two-electrode voltage-clamp technique. Glyburide 14-27 sodium channel epithelial 1 subunit gamma Rattus norvegicus 31-35 19696956-8 2009 The alpha-rat ENaC chimera containing the C-terminal part of the extracellular loop of the alpha-guinea pig ENaC was significantly stimulated by glibenclamide (1.26-fold), whereas the rat-alpha combination was not activated by this sulfonylurea. Glyburide 145-158 sodium channel epithelial 1 subunit gamma Rattus norvegicus 14-18 19696956-8 2009 The alpha-rat ENaC chimera containing the C-terminal part of the extracellular loop of the alpha-guinea pig ENaC was significantly stimulated by glibenclamide (1.26-fold), whereas the rat-alpha combination was not activated by this sulfonylurea. Glyburide 145-158 amiloride-sensitive sodium channel subunit alpha Cavia porcellus 108-112 19607676-12 2009 Pretreatment of RIN-m cells with AL-1 prevented H2O2-induced cellular damage, quenched glucose and glibenclamide-stimulated reactive oxidative species production, and inhibited cytokine-stimulated NF-kappaB activation. Glyburide 99-112 ephrin A5 Rattus norvegicus 33-37 19336274-7 2009 Similarly, activation of PI3K/Akt occurred in the presence of the KATP channel blocker glibenclamide. Glyburide 87-100 thymoma viral proto-oncogene 1 Mus musculus 30-33 19345438-1 2009 A girl with celiac disease and KCNJ11 mutation was transferred to glibenclamide when 19.8 years old. Glyburide 66-79 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 31-37 19295505-7 2009 Despite comparable beta-cell responsivity indices, the average beta-cell function corrected for insulin resistance was more than 3.5-fold lower in women with glyburide-treated GDM than in healthy pregnant women. Glyburide 158-167 insulin Homo sapiens 96-103 18512251-8 2008 The stimulatory effect of Abeta(25-35) on endozepine release was blocked by the adenylyl cyclase inhibitor somatostatin, the protein kinase A (PKA) inhibitor H89, the phospholipase C inhibitor U73122, the protein kinase C (PKC) inhibitor chelerythrine and the ATP binding cassette transporter blocker glyburide. Glyburide 301-310 amyloid beta precursor protein Rattus norvegicus 26-31 19306849-2 2009 Block of SUR 1 with sulfonylurea such as glibenclamide has been shown to be highly effective in reducing cerebral edema, infarct volume and mortality in adult rat models of ischemic stroke. Glyburide 41-54 ATP binding cassette subfamily C member 8 Rattus norvegicus 9-14 19166858-5 2009 These had properties similar to those reported for SUR2/Kir6.1 channels, i.e. activation by pinacidil, inhibition by glibenclamide and activation by intracellular UDP. Glyburide 117-130 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 51-55 19166858-5 2009 These had properties similar to those reported for SUR2/Kir6.1 channels, i.e. activation by pinacidil, inhibition by glibenclamide and activation by intracellular UDP. Glyburide 117-130 potassium inwardly-rectifying channel, subfamily J, member 8 Mus musculus 56-62 19019741-5 2009 CFTR-mediated HCO(3)(-) currents were inhibited by open channel blockers DNDS, glibenclamide and suramin, and these inhibitions were affected by mutations within the channel pore. Glyburide 79-92 CF transmembrane conductance regulator Homo sapiens 0-4 18757309-9 2009 The CFTR pharmacological blockers, glibenclamide and N-phenyl anthranilic acid, significantly reduced histamine-induced Ca(2+) release in non-CF cells, and similar results were obtained when CFTR expression was varied using antisense oligonucleotides. Glyburide 35-48 CF transmembrane conductance regulator Homo sapiens 4-8 18757309-9 2009 The CFTR pharmacological blockers, glibenclamide and N-phenyl anthranilic acid, significantly reduced histamine-induced Ca(2+) release in non-CF cells, and similar results were obtained when CFTR expression was varied using antisense oligonucleotides. Glyburide 35-48 CF transmembrane conductance regulator Homo sapiens 191-195 18854840-0 2009 Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage. Glyburide 0-13 caspase 3 Rattus norvegicus 57-66 18854840-8 2009 In addition, SAH caused large increases in markers of inflammation, including TNFalpha and NFkappaB, and markers of cell injury or cell death, including IgG endocytosis and caspase-3 activation, with glibenclamide significantly reducing these effects. Glyburide 200-213 tumor necrosis factor Rattus norvegicus 78-86 18854840-8 2009 In addition, SAH caused large increases in markers of inflammation, including TNFalpha and NFkappaB, and markers of cell injury or cell death, including IgG endocytosis and caspase-3 activation, with glibenclamide significantly reducing these effects. Glyburide 200-213 caspase 3 Rattus norvegicus 173-182 18854840-9 2009 We conclude that block of SUR1 by glibenclamide may ameliorate several pathologic effects associated with inflammation that lead to cortical dysfunction after SAH. Glyburide 34-47 ATP binding cassette subfamily C member 8 Rattus norvegicus 26-30 19125899-12 2009 In the glibenclamide group, we found significant changes in HbA(1c) (P < 0.05 vs. baseline), FPG (P < 0.01 vs. baseline), PPG (P < 0.05 vs. baseline), and HOMA index (P < 0.05 vs. baseline). Glyburide 7-20 serglycin Homo sapiens 128-131 19125899-16 2009 Although both nateglinide and glibenclamide attenuated PPG and HOMA index, they did not have significant effects on lipid metabolism, as already shown in subjects with type 2 diabetes and good glycemic control. Glyburide 30-43 serglycin Homo sapiens 55-58 19224154-3 2009 The expression of P21 and P27 in preadipocytes treated with diazoxide or glibenclamide was assayed by Western blot. Glyburide 73-86 KRAS proto-oncogene, GTPase Rattus norvegicus 18-21 19224154-3 2009 The expression of P21 and P27 in preadipocytes treated with diazoxide or glibenclamide was assayed by Western blot. Glyburide 73-86 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 26-29 19224154-5 2009 After treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than those in control group, but the expression levels of P21 and P27 in glibenclamide-treated group were lower than those in control group. Glyburide 181-194 KRAS proto-oncogene, GTPase Rattus norvegicus 166-169 19224154-5 2009 After treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than those in control group, but the expression levels of P21 and P27 in glibenclamide-treated group were lower than those in control group. Glyburide 181-194 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 174-177 19224154-6 2009 During the process of inducing differentiation, the expression of leptin mRNA in preadipocytes treated with diazoxide was increased greatly, but the expression of leptin mRNA in glibenclamide-treated group decreased obviously. Glyburide 178-191 leptin Rattus norvegicus 163-169 19023097-7 2009 RESULTS: Glibenclamide reduced total lesion volume by 53% in the thromboembolic MCAo model at 6 hours, reduced corrected cortical lesion volume by 51% in the permanent MCAo model at 4 hours, and reduced corrected cortical lesion volume by 41% in the temporary MCAo model at 5.75 hours (P<0.05 for all 3). Glyburide 9-22 paired box 5 Homo sapiens 300-305 19629706-2 2009 The formulation TDP1 having a drug-polymer ratio 1:1 showed comparatively higher GL release and better permeation across mice skin (p < 0.05). Glyburide 81-83 tyrosyl-DNA phosphodiesterase 1 Mus musculus 16-20 19154434-1 2009 BACKGROUND AND PURPOSE: The antidiabetic sulphonylurea, glibenclamide, acts by inhibiting the pancreatic ATP-sensitive K(+) (K(ATP)) channel, a tetradimeric complex of K(IR)6.2 and sulphonylurea receptor 1 (K(IR)6.2/SUR1)(4). Glyburide 56-69 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 168-205 19154434-1 2009 BACKGROUND AND PURPOSE: The antidiabetic sulphonylurea, glibenclamide, acts by inhibiting the pancreatic ATP-sensitive K(+) (K(ATP)) channel, a tetradimeric complex of K(IR)6.2 and sulphonylurea receptor 1 (K(IR)6.2/SUR1)(4). Glyburide 56-69 ATP binding cassette subfamily C member 8 Homo sapiens 216-220 19154434-3 2009 This study investigates the relation between the recovery of channel activity from glibenclamide inhibition and the dissociation rate of [(3)H]-glibenclamide from the channel at 37 degrees C. EXPERIMENTAL APPROACH: K(IR)6.2, K(IR)6.2DeltaN5 or K(IR)6.2DeltaN10 (the latter lacking amino-terminal residues 2-5 or 2-10 respectively) were coexpressed with SUR1 in HEK cells. Glyburide 144-157 ATP binding cassette subfamily C member 8 Homo sapiens 353-357 19515014-2 2009 CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin). Glyburide 75-84 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 19922361-10 2009 Western blot analysis showed that diazoxide and glibenclamide inhibited and enhanced Bax protein expression respectively. Glyburide 48-61 BCL2 associated X, apoptosis regulator Rattus norvegicus 85-88 18840412-0 2008 Glibenclamide exerts an antitumor activity through reactive oxygen species-c-jun NH2-terminal kinase pathway in human gastric cancer cell line MGC-803. Glyburide 0-13 mitogen-activated protein kinase 8 Homo sapiens 75-100 18840412-5 2008 Glibenclamide could also lead to loss of mitochondrial membrane potential, release of cytochrome c and apoptosis-inducing factor (AIF), and activation of c-jun NH2-terminal kinase (JNK) in MGC-803 cells. Glyburide 0-13 cytochrome c, somatic Homo sapiens 86-98 18840412-5 2008 Glibenclamide could also lead to loss of mitochondrial membrane potential, release of cytochrome c and apoptosis-inducing factor (AIF), and activation of c-jun NH2-terminal kinase (JNK) in MGC-803 cells. Glyburide 0-13 mitogen-activated protein kinase 8 Homo sapiens 154-179 18840412-5 2008 Glibenclamide could also lead to loss of mitochondrial membrane potential, release of cytochrome c and apoptosis-inducing factor (AIF), and activation of c-jun NH2-terminal kinase (JNK) in MGC-803 cells. Glyburide 0-13 mitogen-activated protein kinase 8 Homo sapiens 181-184 18840412-6 2008 Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline. Glyburide 66-79 X-linked Kx blood group Homo sapiens 51-54 18840412-6 2008 Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline. Glyburide 66-79 mitogen-activated protein kinase 8 Homo sapiens 88-91 18840412-7 2008 Furthermore, glibenclamide greatly decreased the cellular viability, induced apoptosis and inhibited Akt activation in wild-type mouse embryonic fibroblast (MEF) cells but not in JNK1-/- or JNK2-/- MEF cells. Glyburide 13-26 thymoma viral proto-oncogene 1 Mus musculus 101-104 18840412-8 2008 Taken together, our study reveals that glibenclamide exerts an antitumor activity in MGC-803 cells by activating ROS-dependent, JNK-driven cell apoptosis. Glyburide 39-52 mitogen-activated protein kinase 8 Homo sapiens 128-131 19128771-8 2008 Treatment with glibenclamide was started at a dose of 2.5 mg/day in order to reduce the risk of microvascular disease, as this as high in MODY 3 type diabetes as in type 1 diabetes mellitus. Glyburide 15-28 HNF1 homeobox A Homo sapiens 138-144 18658272-6 2008 Flagellin-, IL-1beta-, ATP-, and forskolin-stimulated I(Cl) were inhibited by cystic fibrosis transmembrane conductance regulator (CFTR) blockers GlyH101, CFTRinh172, and glibenclamide. Glyburide 171-184 interleukin 1 beta Homo sapiens 12-20 19646201-0 2009 Glibenclamide treatment in relapsed transient neonatal diabetes as a result of a KCNJ11 activating mutation (N48D). Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 81-87 18413155-6 2009 GLY treatment of 4 weeks had restored the SOD and CAT enzyme activities in diabetic rat brain (P<.05). Glyburide 0-3 catalase Rattus norvegicus 50-53 18413155-8 2009 Administration of GLY to diabetic rats restored the diabetes-induced changes, suggesting that GLY could restore the brain SOD and CAT activities. Glyburide 18-21 catalase Rattus norvegicus 130-133 18413155-8 2009 Administration of GLY to diabetic rats restored the diabetes-induced changes, suggesting that GLY could restore the brain SOD and CAT activities. Glyburide 94-97 catalase Rattus norvegicus 130-133 19262486-3 2009 In vehicle-treated normal Brown- Norway-Kitasato (nBN-Ki) rats, the administration of glibenclamide increased urinary kallikrein secretion, but changed neither the systolic blood pressure nor the urinary sodium on low (0.3%) NaCl diets. Glyburide 86-99 nibrin Rattus norvegicus 50-53 19262486-4 2009 Although on high (8%) NaCl diets, the systolic blood pressure of the nBN-Ki rats administrated glibenclamide was significantly lower (P<0.05). Glyburide 95-108 nibrin Rattus norvegicus 69-72 19262486-5 2009 The urinary levels of kallikrein and sodium of the nBN-Ki rats administrated glibenclamide were significantly increased (P<0.05, glibenclamide vs. vehicle). Glyburide 77-90 nibrin Rattus norvegicus 51-54 19262486-5 2009 The urinary levels of kallikrein and sodium of the nBN-Ki rats administrated glibenclamide were significantly increased (P<0.05, glibenclamide vs. vehicle). Glyburide 132-145 nibrin Rattus norvegicus 51-54 19169493-0 2008 Glibenclamide unresponsiveness in a Brazilian child with permanent neonatal diabetes mellitus and DEND syndrome due to a C166Y mutation in KCNJ11 (Kir6.2) gene. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 139-145 19169493-0 2008 Glibenclamide unresponsiveness in a Brazilian child with permanent neonatal diabetes mellitus and DEND syndrome due to a C166Y mutation in KCNJ11 (Kir6.2) gene. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 147-153 19169493-2 2008 We report on the attempted transfer of insulin therapy to glibenclamide in a 4-year old child with PNDM and DEND syndrome, bearing a C166Y mutation in KCNJ11. Glyburide 58-71 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 151-157 18985798-5 2008 The uptake of [(3)H]taurocholic acid by all three transporters was significantly inhibited by troglitazone, glibenclamide, and other several inhibitors, while pravastatin inhibited dog Bsep and human BSEP, but not rat Bsep at 100 microM. Glyburide 108-121 ATP binding cassette subfamily B member 11 Homo sapiens 200-204 18985798-5 2008 The uptake of [(3)H]taurocholic acid by all three transporters was significantly inhibited by troglitazone, glibenclamide, and other several inhibitors, while pravastatin inhibited dog Bsep and human BSEP, but not rat Bsep at 100 microM. Glyburide 108-121 ATP binding cassette subfamily B member 11 Rattus norvegicus 218-222 19160144-6 2008 Renal TNF-alpha and caspase-3 levels were decreased in both glibenclamide and EPO-treated IR rats compared to untreated rats. Glyburide 60-73 tumor necrosis factor Rattus norvegicus 6-15 19160144-6 2008 Renal TNF-alpha and caspase-3 levels were decreased in both glibenclamide and EPO-treated IR rats compared to untreated rats. Glyburide 60-73 caspase 3 Rattus norvegicus 20-29 19160144-7 2008 The protection afforded by the pretreatment with EPO alone was greater than that of administering glibenclamide alone. Glyburide 98-111 erythropoietin Rattus norvegicus 49-52 19160144-8 2008 Application of glibenclamide at the same time partly abolished the cytoprotective effect of EPO treatment. Glyburide 15-28 erythropoietin Rattus norvegicus 92-95 18658272-6 2008 Flagellin-, IL-1beta-, ATP-, and forskolin-stimulated I(Cl) were inhibited by cystic fibrosis transmembrane conductance regulator (CFTR) blockers GlyH101, CFTRinh172, and glibenclamide. Glyburide 171-184 CF transmembrane conductance regulator Homo sapiens 131-135 18512251-8 2008 The stimulatory effect of Abeta(25-35) on endozepine release was blocked by the adenylyl cyclase inhibitor somatostatin, the protein kinase A (PKA) inhibitor H89, the phospholipase C inhibitor U73122, the protein kinase C (PKC) inhibitor chelerythrine and the ATP binding cassette transporter blocker glyburide. Glyburide 301-310 somatostatin Rattus norvegicus 107-119 18768887-11 2008 The effects of NaHS on neutrophil migration both in vivo and in vitro, together with CXCR2 internalization and G protein-coupled receptor kinase 2 expression were prevented by the ATP-sensitive potassium (K(ATP)(+)) channel blocker, glybenclamide. Glyburide 233-246 chemokine (C-X-C motif) receptor 2 Mus musculus 85-90 18625211-6 2008 Pharmacological experiments revealed that glibenclamide (500 nM), an ATP-sensitive potassium conductance antagonist, prevented nesfatin-1-induced hyperpolarization. Glyburide 42-55 nucleobindin 2 Homo sapiens 127-137 18768887-11 2008 The effects of NaHS on neutrophil migration both in vivo and in vitro, together with CXCR2 internalization and G protein-coupled receptor kinase 2 expression were prevented by the ATP-sensitive potassium (K(ATP)(+)) channel blocker, glybenclamide. Glyburide 233-246 G protein-coupled receptor kinase 2 Mus musculus 111-146 18558430-0 2008 The role of placental breast cancer resistance protein in the efflux of glyburide across the human placenta. Glyburide 72-81 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 22-54 18647185-7 2008 METHODS: We examined the effects of the K(ATP) channel inhibitor glibenclamide on dural and pial vasodilatation induced by CGRP, NO, and endogenously released CGRP by TES. Glyburide 65-78 calcitonin-related polypeptide alpha Rattus norvegicus 123-127 18647185-12 2008 In anesthetized rats glibenclamide significantly attenuated CGRP induced dural and TES induced dural/pial artery dilatation (P = .001; P = .001; P = .005), but had no effect on dural/pial vasodilatation induced by GTN. Glyburide 21-34 calcitonin-related polypeptide alpha Rattus norvegicus 60-64 18924582-8 2008 The range of HbA1c improved significantly from 8-12% on insulin to 4.7-6% on glyburide. Glyburide 77-86 hemoglobin subunit alpha 1 Homo sapiens 13-17 18677097-4 2008 During current clamping, CGRP hyperpolarized the membrane and this effect was antagonized by glibenclamide. Glyburide 93-106 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 25-29 18625248-5 2008 ET-1 also induced an increase in ()O(2)(-) production that was inhibited by the NADPH oxidase blocker, apocynin, and by the blockers of mitochondrial ATP-sensitive K(+) channels (mK(ATP)), glibenclamide and 5 hydroxydecanoic acid. Glyburide 189-202 endothelin 1 Homo sapiens 0-4 18625248-6 2008 The ET-1-induced positive inotropic effect was inhibited by apocynin (0.3 mM; 6.3+/-6.6%, n=13), glibenclamide (50 microM; 8.8+/-3.5%, n=6), 5 hydroxydecanoic acid (500 microM; 14.1+/-8.1, n=9), and by scavenging ROS with MPG (2 mM; 0.92+/-5.6%, n=8). Glyburide 97-110 endothelin 1 Homo sapiens 4-8 18558430-5 2008 The objective of the present study was to determine whether BCRP participates in the transport of glyburide across the human placenta. Glyburide 98-107 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 60-64 18558430-9 2008 Results obtained from perfusions (n=4) in the presence of the BCRP inhibitor show a significant increase in the mean fetal-to-maternal concentration ratio of glyburide determined at 180 min, 0.56+/-0.06, when compared to the mean ratio obtained in the absence of inhibitor, 0.32+/-0.06 (p=0.04). Glyburide 158-167 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 62-66 18558430-10 2008 These data indicate that nicardipine partially blocked the transfer of glyburide across the whole placenta through its inhibition of BCRP. Glyburide 71-80 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 133-137 18558430-11 2008 This is the first ex vivo evidence that BCRP actively transports glyburide. Glyburide 65-74 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 40-44 18503607-3 2008 Glyburide, a sulphonylurea, is an insulin sensitizer and mainly metabolized by CYP2C9. Glyburide 0-9 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 79-85 18493247-0 2008 alpha2A-adrenoceptor antagonism increases insulin secretion and synergistically augments the insulinotropic effect of glibenclamide in mice. Glyburide 118-131 adrenergic receptor, alpha 2a Mus musculus 0-20 18493739-0 2008 Glibenclamide activates translation in rat pancreatic beta cells through calcium-dependent mTOR, PKA and MEK signalling pathways. Glyburide 0-13 mechanistic target of rapamycin kinase Rattus norvegicus 91-95 18493739-0 2008 Glibenclamide activates translation in rat pancreatic beta cells through calcium-dependent mTOR, PKA and MEK signalling pathways. Glyburide 0-13 mitogen-activated protein kinase kinase 7 Homo sapiens 105-108 18493739-5 2008 RESULTS: A 24 h exposure to glibenclamide induced activation of four translation factors, i.e. phosphorylation of eukaryotic initiation factor (eIF) 4e binding protein 1 and ribosomal protein S6 (rpS6), and dephosphorylation of eIF-2alpha and eukaryotic elongation factor 2. Glyburide 28-41 eukaryotic translation initiation factor 4E binding protein 1 Rattus norvegicus 114-169 18493739-5 2008 RESULTS: A 24 h exposure to glibenclamide induced activation of four translation factors, i.e. phosphorylation of eukaryotic initiation factor (eIF) 4e binding protein 1 and ribosomal protein S6 (rpS6), and dephosphorylation of eIF-2alpha and eukaryotic elongation factor 2. Glyburide 28-41 ribosomal protein S6 Rattus norvegicus 174-194 18493739-5 2008 RESULTS: A 24 h exposure to glibenclamide induced activation of four translation factors, i.e. phosphorylation of eukaryotic initiation factor (eIF) 4e binding protein 1 and ribosomal protein S6 (rpS6), and dephosphorylation of eIF-2alpha and eukaryotic elongation factor 2. Glyburide 28-41 ribosomal protein S6 Rattus norvegicus 196-200 18493739-5 2008 RESULTS: A 24 h exposure to glibenclamide induced activation of four translation factors, i.e. phosphorylation of eukaryotic initiation factor (eIF) 4e binding protein 1 and ribosomal protein S6 (rpS6), and dephosphorylation of eIF-2alpha and eukaryotic elongation factor 2. Glyburide 28-41 eukaryotic translation initiation factor 2A Rattus norvegicus 228-238 18493739-8 2008 CONCLUSIONS/INTERPRETATION: Prolonged exposure to glibenclamide activates protein translation in pancreatic beta cells through the calcium-regulated mTOR, PKA and MEK signalling pathways. Glyburide 50-63 mechanistic target of rapamycin kinase Rattus norvegicus 149-153 18493739-8 2008 CONCLUSIONS/INTERPRETATION: Prolonged exposure to glibenclamide activates protein translation in pancreatic beta cells through the calcium-regulated mTOR, PKA and MEK signalling pathways. Glyburide 50-63 mitogen-activated protein kinase kinase 7 Homo sapiens 163-166 18850420-0 2008 Investigating the potential role of multi-drug resistance protein (MRP) transporters in fetal to maternal glyburide efflux in the human placenta. Glyburide 106-115 ATP binding cassette subfamily C member 1 Homo sapiens 36-65 18793589-12 2008 Vildagliptin/glyburide coadministration significantly reduced the area under the plasma glucose-time curve compared with glyburide alone (AUE0-5h reduced by 12% (p = 0.005) and AUE0-15h by 13% (p = 0.003)), and increased the area under the plasma insulin-time curve (AUE0-15h increased by 12% (p = 0.041)). Glyburide 13-22 insulin Homo sapiens 247-254 18850420-0 2008 Investigating the potential role of multi-drug resistance protein (MRP) transporters in fetal to maternal glyburide efflux in the human placenta. Glyburide 106-115 ATP binding cassette subfamily C member 1 Homo sapiens 67-70 18850420-2 2008 The objective of the study is to determine whether indomethacin, an inhibitor of the multi-drug resistance family (MRP) of transporters is involved in the active efflux of glyburide from the fetus to the mother. Glyburide 172-181 ATP binding cassette subfamily C member 1 Homo sapiens 115-118 18850420-5 2008 Furthermore, our study suggests that MRP1, 2 or 3 may be only minimally involved in the transport of glyburide across the human placenta. Glyburide 101-110 ATP binding cassette subfamily C member 1 Homo sapiens 37-49 18551039-8 2008 CONCLUSION: In participants with the TG or GG genotype at rs10494366 in the NOS1AP gene, glibenclamide is less effective in reducing glucose levels and mortality rates were higher compared with glibenclamide users with the TT genotype. Glyburide 89-102 nitric oxide synthase 1 adaptor protein Homo sapiens 76-82 18551039-8 2008 CONCLUSION: In participants with the TG or GG genotype at rs10494366 in the NOS1AP gene, glibenclamide is less effective in reducing glucose levels and mortality rates were higher compared with glibenclamide users with the TT genotype. Glyburide 194-207 nitric oxide synthase 1 adaptor protein Homo sapiens 76-82 18462715-5 2008 The activities of hepatic CYP3A and the markers of liver injury, plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), were significantly decreased in rats treated with 18alpha-GL alone and in combination with glibenclamide. Glyburide 232-245 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 26-31 18445600-6 2008 Glutaminolysis stimulated by the leucine analogue d,l-beta-2-amino-2-norbornane-carboxylic acid was, however, enhanced in SUR1(-/-) and glyburide-treated SUR1(+/+) islets. Glyburide 136-145 hemoglobin, beta adult minor chain Mus musculus 54-60 18445600-6 2008 Glutaminolysis stimulated by the leucine analogue d,l-beta-2-amino-2-norbornane-carboxylic acid was, however, enhanced in SUR1(-/-) and glyburide-treated SUR1(+/+) islets. Glyburide 136-145 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 154-158 18462715-5 2008 The activities of hepatic CYP3A and the markers of liver injury, plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), were significantly decreased in rats treated with 18alpha-GL alone and in combination with glibenclamide. Glyburide 232-245 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 107-133 18462715-7 2008 Our results revealed that 18alpha-GL led to the enhancement of the hypoglycemic effect of glibenclamide by inhibiting the activity of CYP3A; on the other hand, 18alpha-GL protected the pancreatic islet beta cells and liver from damage in diabetes which suggested that 18alpha-GL might be beneficial as an adjuvant drug of glibenclamide in a proper dose, especially to the diabetic patients associated with liver dysfunction. Glyburide 90-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 18221420-0 2008 Outpatient transition of an infant with permanent neonatal diabetes due to a KCNJ11 activating mutation from subcutaneous insulin to oral glyburide. Glyburide 138-147 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 77-83 17980009-12 2008 Glibenclamide increased fasting insulin and the postprandial insulin AUC but had no effect on the PI and SPI AUCs. Glyburide 0-13 insulin Homo sapiens 32-39 19099789-5 2008 (5) Control + Ouabain + CRK + glibenclamide (GLB). Glyburide 30-43 L-xylulose reductase Cavia porcellus 45-48 19099789-15 2008 ATP-sensitive potassium channel blocker glibenclamide (10 micromol/L) could antagonize the effects of CRK on APD and I(ti) currents. Glyburide 40-53 adapter molecule crk Cavia porcellus 102-105 18211896-8 2008 Surface expression of annexin 2 was reduced in cells treated with glyburide, an ABCA1 inhibitor, whereas inhibition of calpain abrogated IFNgamma-induced annexin 2 down-regulation and suppression of Matrigel invasion. Glyburide 66-75 annexin A2 Homo sapiens 22-31 18211896-8 2008 Surface expression of annexin 2 was reduced in cells treated with glyburide, an ABCA1 inhibitor, whereas inhibition of calpain abrogated IFNgamma-induced annexin 2 down-regulation and suppression of Matrigel invasion. Glyburide 66-75 ATP binding cassette subfamily A member 1 Homo sapiens 80-85 18211896-8 2008 Surface expression of annexin 2 was reduced in cells treated with glyburide, an ABCA1 inhibitor, whereas inhibition of calpain abrogated IFNgamma-induced annexin 2 down-regulation and suppression of Matrigel invasion. Glyburide 66-75 interferon gamma Homo sapiens 137-145 18211896-8 2008 Surface expression of annexin 2 was reduced in cells treated with glyburide, an ABCA1 inhibitor, whereas inhibition of calpain abrogated IFNgamma-induced annexin 2 down-regulation and suppression of Matrigel invasion. Glyburide 66-75 annexin A2 Homo sapiens 154-163 17980009-12 2008 Glibenclamide increased fasting insulin and the postprandial insulin AUC but had no effect on the PI and SPI AUCs. Glyburide 0-13 insulin Homo sapiens 61-68 18032480-5 2008 Inhibitors of PKA (H-89) and CFTR (glibenclamide) also significantly reduced PAR-2-stimulated Cl(-) transport. Glyburide 35-48 CF transmembrane conductance regulator Homo sapiens 29-33 17394534-9 2008 HbA1c improved identical during the first year but thereafter deteriorated in the glibenclamide group (p < 0.005 for difference at year 4). Glyburide 82-95 hemoglobin subunit alpha 1 Homo sapiens 0-4 17394534-10 2008 Ratios of proinsulin to insulin were higher during treatment in glibenclamide- vs. insulin-treated patients after year 2. Glyburide 64-77 insulin Homo sapiens 10-20 17394534-10 2008 Ratios of proinsulin to insulin were higher during treatment in glibenclamide- vs. insulin-treated patients after year 2. Glyburide 64-77 insulin Homo sapiens 13-20 17394534-10 2008 Ratios of proinsulin to insulin were higher during treatment in glibenclamide- vs. insulin-treated patients after year 2. Glyburide 64-77 insulin Homo sapiens 24-31 17394534-13 2008 However, deterioration occurred faster in the glibenclamide group, indicating that alleviating demands on secretion by insulin treatment is beneficial. Glyburide 46-59 insulin Homo sapiens 119-126 18096816-10 2008 Uroguanylin- and guanylin-stimulated DBS were significantly inhibited by glibenclamide, but not by 4,4"-diisothiocyanato-stilbene-2,2"-disulfonic acid (DIDS). Glyburide 73-86 guanylate cyclase activator 2b (retina) Mus musculus 0-12 18297105-4 2008 TRPM4 is inhibited by glibenclamide, a modulator of ATP binding cassette proteins (ABC transporters), such as the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 22-35 transient receptor potential cation channel subfamily M member 4 Homo sapiens 0-5 18297105-4 2008 TRPM4 is inhibited by glibenclamide, a modulator of ATP binding cassette proteins (ABC transporters), such as the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 22-35 CF transmembrane conductance regulator Homo sapiens 114-165 18297105-4 2008 TRPM4 is inhibited by glibenclamide, a modulator of ATP binding cassette proteins (ABC transporters), such as the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 22-35 CF transmembrane conductance regulator Homo sapiens 167-171 18622055-6 2008 It has also been demonstrated that glyburide is effluxed from the fetal to the maternal circulation by the breast cancer resistance protein (BRCP) and the human multidrug resistance protein 3 (MRP3). Glyburide 35-44 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 107-139 18622055-6 2008 It has also been demonstrated that glyburide is effluxed from the fetal to the maternal circulation by the breast cancer resistance protein (BRCP) and the human multidrug resistance protein 3 (MRP3). Glyburide 35-44 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 141-145 18622055-6 2008 It has also been demonstrated that glyburide is effluxed from the fetal to the maternal circulation by the breast cancer resistance protein (BRCP) and the human multidrug resistance protein 3 (MRP3). Glyburide 35-44 ATP binding cassette subfamily B member 4 Homo sapiens 161-191 18622055-6 2008 It has also been demonstrated that glyburide is effluxed from the fetal to the maternal circulation by the breast cancer resistance protein (BRCP) and the human multidrug resistance protein 3 (MRP3). Glyburide 35-44 ATP binding cassette subfamily B member 4 Homo sapiens 193-197 18246324-1 2008 In many countries, first- or second-line pharmacological treatment of patients with type 2 diabetes consists of sulfonylureas (such as glibenclamide [known as glyburide in the USA and Canada]), which stimulate the beta cell to secrete insulin. Glyburide 135-148 insulin Homo sapiens 235-242 18246324-1 2008 In many countries, first- or second-line pharmacological treatment of patients with type 2 diabetes consists of sulfonylureas (such as glibenclamide [known as glyburide in the USA and Canada]), which stimulate the beta cell to secrete insulin. Glyburide 159-168 insulin Homo sapiens 235-242 18395553-8 2008 Fibrinogen vasorelaxations were completely inhibited by abciximab and diminished by endothelial denudation and treatment with the nitric oxide synthase inhibitor L-nitroargininemethylester and glibenclamide (P < .01). Glyburide 193-206 fibrinogen beta chain Homo sapiens 0-10 19787078-7 2008 Cell growth assay shows that when each of calcitriol and 5 alpha-dihydrotestosterone (DHT) was co-treated with ABCA1 blocker, glybenclamide, cell-growth is significantly decreased compared to their own treatments respectively. Glyburide 126-139 ATP binding cassette subfamily A member 1 Homo sapiens 111-116 18307455-7 2008 Identification of a Kir6.2 mutation allowed insulin injections to be replaced by glibenclamide tablets. Glyburide 81-94 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 20-26 18457474-13 2008 Average infant birth weight may be lower in mothers treated with insulin than with glyburide. Glyburide 83-92 insulin Homo sapiens 65-72 18073297-13 2008 High-affinity block by glibenclamide is present in G53D channels coexpressed with either SUR1 or SUR2A. Glyburide 23-36 ATP binding cassette subfamily C member 8 Homo sapiens 89-93 18079276-0 2008 The breast cancer resistance protein (Bcrp1/Abcg2) limits fetal distribution of glyburide in the pregnant mouse: an Obstetric-Fetal Pharmacology Research Unit Network and University of Washington Specialized Center of Research Study. Glyburide 80-89 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 4-36 18079276-0 2008 The breast cancer resistance protein (Bcrp1/Abcg2) limits fetal distribution of glyburide in the pregnant mouse: an Obstetric-Fetal Pharmacology Research Unit Network and University of Washington Specialized Center of Research Study. Glyburide 80-89 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 38-43 18079276-0 2008 The breast cancer resistance protein (Bcrp1/Abcg2) limits fetal distribution of glyburide in the pregnant mouse: an Obstetric-Fetal Pharmacology Research Unit Network and University of Washington Specialized Center of Research Study. Glyburide 80-89 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 44-49 18079276-4 2008 The intracellular [(3)H]GLB concentrations in Madin-Darby canine kidney (MDCK)/BCRP cells were significantly lower than those in MDCK/vector cells. Glyburide 24-27 ATP binding cassette subfamily G member 2 Canis lupus familiaris 79-83 18079276-9 2008 GLB was administered by retro-orbital injection to the wild-type and Bcrp1(-/-) pregnant mice. Glyburide 0-3 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 69-74 17901979-7 2008 These effects were significantly attenuated by glibenclamide, an ATP-sensitive K(+) channel (K(ATP)) blocker, and chelerythrine, a selective protein kinase C (PKC) inhibitor, suggesting that activation of both K(ATP) and PKC is required for the stimulation of COX-2. Glyburide 47-60 protein kinase C, gamma Rattus norvegicus 221-224 17901979-7 2008 These effects were significantly attenuated by glibenclamide, an ATP-sensitive K(+) channel (K(ATP)) blocker, and chelerythrine, a selective protein kinase C (PKC) inhibitor, suggesting that activation of both K(ATP) and PKC is required for the stimulation of COX-2. Glyburide 47-60 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 260-265 18032480-5 2008 Inhibitors of PKA (H-89) and CFTR (glibenclamide) also significantly reduced PAR-2-stimulated Cl(-) transport. Glyburide 35-48 F2R like trypsin receptor 1 Homo sapiens 77-82 18047834-4 2008 Inhibition of CFTR chloride transport activity by using glibenclamide (50muM, 24h) or CFTR(inh)-172 (5muM, 24h), resulted in the down-regulation of CISD1 mRNA, and CFTR stimulation with cAMP/isoproterenol/IBMX upregulated its expression. Glyburide 56-69 CDGSH iron sulfur domain 1 Homo sapiens 148-153 18047834-4 2008 Inhibition of CFTR chloride transport activity by using glibenclamide (50muM, 24h) or CFTR(inh)-172 (5muM, 24h), resulted in the down-regulation of CISD1 mRNA, and CFTR stimulation with cAMP/isoproterenol/IBMX upregulated its expression. Glyburide 56-69 CF transmembrane conductance regulator Homo sapiens 14-18 18276195-4 2008 Furthermore, we found that the inhibition of iptakalim and pinacidil on the ET-1-induced proliferation of human PASMCs was blocked by glyburide, a selective K(ATP) channel antagonist. Glyburide 134-143 endothelin 1 Homo sapiens 76-80 17674030-7 2008 The phosphorylation of ERK1/2 induced by SP was attenuated by either glibenclamide, an ATP-sensitive K(+) channel (K(ATP)) blocker, or chelerythrine, a specific protein kinase C (PKC) blocker. Glyburide 69-82 mitogen activated protein kinase 3 Rattus norvegicus 23-29 17942071-13 2008 In endothelium-free mesenteric artery rings, VIP produced concentration-dependent vasorelaxation that was attenuated by glibenclamide. Glyburide 120-133 vasoactive intestinal peptide Homo sapiens 45-48 18831351-0 2008 Relationship between plasma leptin and plasma insulin levels in type-2 diabetic patients before and after treatment with glibenclamide and glimepiride. Glyburide 121-134 leptin Homo sapiens 28-34 18831351-0 2008 Relationship between plasma leptin and plasma insulin levels in type-2 diabetic patients before and after treatment with glibenclamide and glimepiride. Glyburide 121-134 insulin Homo sapiens 46-53 18001767-3 2008 An SUR2 mutant mouse was previously generated by disrupting the first nucleotide-binding domain (NBD1), where a glibenclamide action site was located. Glyburide 112-125 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 3-7 18831351-11 2008 Glibenclamide increased leptin levels but they remained unaltered with glimepiride. Glyburide 0-13 leptin Homo sapiens 24-30 17675187-7 2008 Glibenclamide also significantly reduced the relative area under the LD flux curve during the PRH response 14551+/-2508 PU*s vs. 6402+/-1476 PU*s (paired t-test, p=0.01) and increased the principal frequency of postocclusive PRH oscillations 0.0931+/-0.01 Hz vs. 0.1309+/-0.02 Hz (p=0.01). Glyburide 0-13 prolactin releasing hormone Homo sapiens 94-97 17675187-7 2008 Glibenclamide also significantly reduced the relative area under the LD flux curve during the PRH response 14551+/-2508 PU*s vs. 6402+/-1476 PU*s (paired t-test, p=0.01) and increased the principal frequency of postocclusive PRH oscillations 0.0931+/-0.01 Hz vs. 0.1309+/-0.02 Hz (p=0.01). Glyburide 0-13 prolactin releasing hormone Homo sapiens 225-228 18091586-6 2007 RESULTS: PGE1 significantly decreased the isometric tension in a concentration-dependent manner, which was partially inhibited by pretreating with a KATP channel inhibitor, glibenclamide (1 microM), or an inhibitor of protein kinase A (PKA), Rp-cAMPS (100 microM). Glyburide 173-186 calmodulin 2, pseudogene 1 Rattus norvegicus 245-250 17980680-1 2007 Glyburide (glibenclamide, INN), a second generation sulfonylurea is widely used in the treatment of gestational diabetes mellitus (GDM). Glyburide 0-9 growth hormone releasing hormone Homo sapiens 26-29 17923155-0 2008 Breast cancer resistance protein: mediating the trans-placental transfer of glyburide across the human placenta. Glyburide 76-85 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-32 17923155-9 2008 This is the first evidence to clearly indicate that glyburide is preferentially transported by BCRP, in the brush border of the human placenta. Glyburide 52-61 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 95-99 17631610-11 2007 K(ATP) or KvLQT1 inhibitors (glibenclamide, clofilium) reduced EGF-stimulated wound healing, cell migration, and proliferation. Glyburide 29-42 potassium voltage-gated channel subfamily Q member 1 Rattus norvegicus 10-16 17931360-5 2007 S1P release from astrocytes was inhibited by the treatment of the cells with glybenclamide or small interfering RNAs specific to ATP-binding cassette transporter A1 (ABCA1). Glyburide 77-90 sphingosine-1-phosphate receptor 1 Mus musculus 0-3 18080920-11 2007 The K channel inhibitor glibenclamide decreased the cytoproliferative and cytoprotective effect of erythropoietin during H2O2 toxicity of Hep3B cells. Glyburide 24-37 erythropoietin Homo sapiens 99-113 18080920-12 2007 CONCLUSIONS: Erythropoietin treatment may be considered as a therapeutic agent during oxidative injuries of hepatocytes and its cytoprotective effect is abolished by glibenclamide. Glyburide 166-179 erythropoietin Homo sapiens 13-27 17828386-5 2007 RESULTS: We found that (1) Cx36 channels favour the exchange of cations and larger positively charged molecules between beta cells at the expense of anionic molecules; (2) this exchange occurs across sizable portions of pancreatic islets; and (3) during glibenclamide (known as glyburide in the USA and Canada) stimulation beta cell coupling increases to an extent that varies for different gap junction-permeant molecules. Glyburide 254-267 gap junction protein, delta 2 Mus musculus 27-31 17828386-5 2007 RESULTS: We found that (1) Cx36 channels favour the exchange of cations and larger positively charged molecules between beta cells at the expense of anionic molecules; (2) this exchange occurs across sizable portions of pancreatic islets; and (3) during glibenclamide (known as glyburide in the USA and Canada) stimulation beta cell coupling increases to an extent that varies for different gap junction-permeant molecules. Glyburide 278-287 gap junction protein, delta 2 Mus musculus 27-31 17596272-8 2007 Furthermore, the following effects were found: 1) inhibition of forskolin/genistein-activated iodide efflux by glibenclamide, diphenylamine-2-carboxylic acid and CFTR-specific inhibitor (CFTR(inh))-172; 2) activation of iodide efflux by the benzoquinolizinium derivative CFTR activators MPB-07 and MPB-91; and 3) inhibition of MPB-dependent efflux by CFTR(inh)-172. Glyburide 111-124 CF transmembrane conductance regulator Rattus norvegicus 187-191 17596272-8 2007 Furthermore, the following effects were found: 1) inhibition of forskolin/genistein-activated iodide efflux by glibenclamide, diphenylamine-2-carboxylic acid and CFTR-specific inhibitor (CFTR(inh))-172; 2) activation of iodide efflux by the benzoquinolizinium derivative CFTR activators MPB-07 and MPB-91; and 3) inhibition of MPB-dependent efflux by CFTR(inh)-172. Glyburide 111-124 CF transmembrane conductance regulator Rattus norvegicus 187-191 17596272-8 2007 Furthermore, the following effects were found: 1) inhibition of forskolin/genistein-activated iodide efflux by glibenclamide, diphenylamine-2-carboxylic acid and CFTR-specific inhibitor (CFTR(inh))-172; 2) activation of iodide efflux by the benzoquinolizinium derivative CFTR activators MPB-07 and MPB-91; and 3) inhibition of MPB-dependent efflux by CFTR(inh)-172. Glyburide 111-124 CF transmembrane conductance regulator Rattus norvegicus 187-191 17656736-5 2007 Glyburide drastically reduced (125)I-apoA-I binding to the HCBS, whereas (125)I-apoA-I showed no significant binding to the HCBS in ABCA1 mutant (Q597R) fibroblasts. Glyburide 0-9 apolipoprotein A1 Homo sapiens 37-43 18004211-7 2007 Sequencing of SCNN1B in 207 Caucasian participants receiving farglitazar plus insulin or glyburide combination therapies, identified additional polymorphisms that were also significantly associated with oedema (P<0.0005) and maintained the treatment-regional associations. Glyburide 89-98 sodium channel epithelial 1 subunit beta Homo sapiens 14-20 17711996-0 2007 Beneficial effects of GLP-1 on endothelial function in humans: dampening by glyburide but not by glimepiride. Glyburide 76-85 glucagon Homo sapiens 22-27 17711996-8 2007 However, in contrast, glyburide abolished GLP-1-induced Ach-mediated vasodilatation (Delta+11.7 +/- 2.0 vs. Delta+11.7 +/- 2.5 ml.100 ml(-1).min(-1)). Glyburide 22-31 glucagon Homo sapiens 42-47 17698900-8 2007 The integrated incremental responses of total GLP-1 were reduced by vildagliptin by 72% (with glibenclamide) and 48% (without glibenclamide) (effect of vildagliptin: P < 0.0001; glibenclamide: P = 0.31; interaction: P = 0.26). Glyburide 94-107 glucagon Homo sapiens 46-51 17698900-9 2007 Similarly, integrated incremental responses of total GIP were reduced by vildagliptin by 26 and 21%, with and without glibenclamide, respectively (vildagliptin: P = 0.017; glibenclamide: P = 0.44; interaction: P = 0.69). Glyburide 118-131 gastric inhibitory polypeptide Homo sapiens 53-56 17823205-8 2007 Angiotensin II at a dose that mimics the SFR (1 nmol l(-1)) induced an increase in .O(2)(-) production of approximately 30-40% detected by lucigenin in cardiac slices, an effect that was blunted by losartan, MPG, apocynin, 5HD and glybenclamide. Glyburide 231-244 angiotensinogen Homo sapiens 0-14 17991617-8 2007 Pharmcological antagonists of ABC transporters, glyburide and MK-571 attenuated endogenous S1P release. Glyburide 48-57 sphingosine-1-phosphate receptor 1 Mus musculus 91-94 17582383-0 2007 CFTR inhibition by glibenclamide requires a positive charge in cytoplasmic loop three. Glyburide 19-32 CF transmembrane conductance regulator Homo sapiens 0-4 17582383-3 2007 Charge-neutralizing mutations K978A, K978Q, K978S abolished the inhibition of forskolin-activated CFTR chloride current by glibenclamide but not by CFTR(inh)-172. Glyburide 123-136 CF transmembrane conductance regulator Homo sapiens 98-102 17901525-0 2007 Early glibenclamide treatment in a clinical newborn with KCNJ11 gene mutation. Glyburide 6-19 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 57-63 17911402-2 2007 Anti-diabetic drugs (e.g. glibenclamide) block K(ATP) channels and abrogate H(2)S-mediated physiological responses which suggest that H(2)S may also regulate insulin secretion by pancreatic beta-cells. Glyburide 26-39 insulin Mesocricetus auratus 158-165 17911402-4 2007 The concentration of insulin released from HIT-T15 cells decreased significantly after NaHS exposure and this effect was reversed by the addition of glibenclamide (10 microM). Glyburide 149-162 insulin Mesocricetus auratus 21-28 17652641-10 2007 Treatment of the patient with the sulfonylurea glibenclamide not only enabled insulin therapy to be stopped, but also resulted in improvement in epilepsy and psychomotor abilities. Glyburide 47-60 insulin Homo sapiens 78-85 17316868-3 2007 Chronic exposure of pancreatic beta-cells to sulfonylureas (glibenclamide or tolbutamide) and glinide (nateglinide) similarly impaired their acute effectiveness by reducing the insulin content and the number of functional K(ATP) channels on the plasma membrane. Glyburide 60-73 insulin Homo sapiens 177-184 17673715-1 2007 BACKGROUND AND PURPOSE: The sulfonylurea receptor 1-regulated NC(Ca-ATP) channel is upregulated in rodent models of stroke with block of the channel by the sulfonylurea, glibenclamide (glyburide), significantly reducing mortality, cerebral edema, and infarct volume. Glyburide 170-183 ATP binding cassette subfamily C member 8 Homo sapiens 28-51 17385195-7 2007 At Cox regression, after adjustment for potential confounders, including comorbidity, glibenclamide treatment was associated with a significant increase in all-cause mortality [OR 2.1(1.2;2.7), p < 0.05], while the difference in cardiovascular mortality was not statistically significant after adjustment for age and sex. Glyburide 86-99 cytochrome c oxidase subunit 8A Homo sapiens 3-6 17385195-8 2007 Mortality for malignancies was significantly higher in patients treated with glibenclamide after adjustment for age, sex, BMI, and insulin and metformin treatment, [OR 3.6(1.1;11.9); p < 0.05]. Glyburide 77-90 insulin Homo sapiens 131-138 17593344-6 2007 In rat beta cells degranulated by in vivo treatment with glibenclamide (known as glyburide in the USA and Canada), the insulin and SUR1 staining intensity was similarly decreased by approximately 45%, whereas SUR1 staining was not changed in non-beta cells. Glyburide 57-70 ATP binding cassette subfamily C member 8 Rattus norvegicus 131-135 17593344-6 2007 In rat beta cells degranulated by in vivo treatment with glibenclamide (known as glyburide in the USA and Canada), the insulin and SUR1 staining intensity was similarly decreased by approximately 45%, whereas SUR1 staining was not changed in non-beta cells. Glyburide 57-70 ATP binding cassette subfamily C member 8 Rattus norvegicus 209-213 17593344-6 2007 In rat beta cells degranulated by in vivo treatment with glibenclamide (known as glyburide in the USA and Canada), the insulin and SUR1 staining intensity was similarly decreased by approximately 45%, whereas SUR1 staining was not changed in non-beta cells. Glyburide 81-90 ATP binding cassette subfamily C member 8 Rattus norvegicus 131-135 17593344-6 2007 In rat beta cells degranulated by in vivo treatment with glibenclamide (known as glyburide in the USA and Canada), the insulin and SUR1 staining intensity was similarly decreased by approximately 45%, whereas SUR1 staining was not changed in non-beta cells. Glyburide 81-90 ATP binding cassette subfamily C member 8 Rattus norvegicus 209-213 17673715-1 2007 BACKGROUND AND PURPOSE: The sulfonylurea receptor 1-regulated NC(Ca-ATP) channel is upregulated in rodent models of stroke with block of the channel by the sulfonylurea, glibenclamide (glyburide), significantly reducing mortality, cerebral edema, and infarct volume. Glyburide 185-194 ATP binding cassette subfamily C member 8 Homo sapiens 28-51 17596474-3 2007 A single randomized controlled trial of glyburide versus insulin indicates that glyburide treatment can provide a relatively safe alternative to insulin therapy. Glyburide 80-89 insulin Homo sapiens 57-64 17558440-10 2007 Carbenoxolone, a gap junction inhibitor that inhibits ATP release, and glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR), which is required for ATP release, inhibited the spontaneous and stimulated EET release from RBCs. Glyburide 71-84 CF transmembrane conductance regulator Rattus norvegicus 106-157 17558440-10 2007 Carbenoxolone, a gap junction inhibitor that inhibits ATP release, and glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR), which is required for ATP release, inhibited the spontaneous and stimulated EET release from RBCs. Glyburide 71-84 CF transmembrane conductance regulator Rattus norvegicus 159-163 17524375-8 2007 This effect was abolished by an inhibitor of ABCA1-mediated lipid efflux (glyburide) and was absent in Tangier fibroblasts. Glyburide 74-83 ATP binding cassette subfamily A member 1 Homo sapiens 45-50 17728498-6 2007 Their basal c-peptide levels increased after one week of glibenclamide therapy, and one month later, the insulin and c-peptide levels were in the normal ranges without any episodes of hyper- or hypoglycemia. Glyburide 57-70 insulin Homo sapiens 12-21 17659066-0 2007 Transition from insulin to glyburide in a 4-month-old girl with neonatal diabetes mellitus caused by a mutation in KCNJ11. Glyburide 27-36 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 115-121 17659066-3 2007 We report on the transition from insulin to glyburide (glibenclamide) therapy in a 4-month-old girl with neonatal diabetes mellitus caused by a mutation in KCNJ11. Glyburide 44-53 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 156-162 17659066-3 2007 We report on the transition from insulin to glyburide (glibenclamide) therapy in a 4-month-old girl with neonatal diabetes mellitus caused by a mutation in KCNJ11. Glyburide 55-68 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 156-162 17592198-4 2007 However, glibenclamide, a nonselective SUR blocker, attenuates this beneficial effect. Glyburide 9-22 ATP binding cassette subfamily C member 8 Rattus norvegicus 39-42 17301957-5 2007 The protective effects were abolished by both non-selective K(ATP) channel blocker glibenclamide and selective mitoK(ATP) channel blocker 5-hydroxydecanoate (5-HD). Glyburide 83-96 ATPase phospholipid transporting 8A2 Homo sapiens 62-65 17382898-7 2007 In addition, the CFTR chloride transport inhibitors glibenclamide and CFTR(inh)-172 also reduced MT-ND4 expression in CFDE cells ectopically expressing wt CFTR. Glyburide 52-65 CF transmembrane conductance regulator Homo sapiens 17-21 17382898-7 2007 In addition, the CFTR chloride transport inhibitors glibenclamide and CFTR(inh)-172 also reduced MT-ND4 expression in CFDE cells ectopically expressing wt CFTR. Glyburide 52-65 mitochondrially encoded NADH dehydrogenase 4 Homo sapiens 97-103 17395634-8 2007 The cAMP-stimulated Isc component was sensitive to glibenclamide but not to DIDS, suggesting that a cystic fibrosis transmembrane conductance regulator (Cftr)-mediated anion conductance was responsible. Glyburide 51-64 cystic fibrosis transmembrane conductance regulator Mus musculus 100-151 17395634-8 2007 The cAMP-stimulated Isc component was sensitive to glibenclamide but not to DIDS, suggesting that a cystic fibrosis transmembrane conductance regulator (Cftr)-mediated anion conductance was responsible. Glyburide 51-64 cystic fibrosis transmembrane conductance regulator Mus musculus 153-157 17223797-7 2007 Pre-treatment of cells with glyburide, an inhibitor of the lipid-export pump, ABCA1 (ATP-binding cassette transporter A1), attenuated Ps. Glyburide 28-37 ATP binding cassette subfamily A member 1 Homo sapiens 78-83 17363911-9 2007 Women in the insulin group were younger (31.5+/-5.8 vs 35.2+/-4.7 years, P<0.001) and had a higher mean BMI (32.4+/-6.4 vs 29.1+/-5.8 kg/m(2), P=0.003) compared to glyburide group. Glyburide 167-176 insulin Homo sapiens 13-20 17182029-7 2007 In the severe injury model, glibenclamide inhibited inflammatory parameters, as assessed by Evans blue extravasation, neutrophil influx and haemoglobin content, and the increase in TNF-alpha (tumor necrose factor-alpha) and IL (interleukin)-6 levels in the intestine and lung. Glyburide 28-41 tumor necrosis factor Rattus norvegicus 181-190 17373390-6 2007 The ADOPT study shows the benefits of rosiglitazone over glyburide in de novo DM2. Glyburide 57-66 immunoglobulin heavy diversity 1-14 (non-functional) Homo sapiens 78-81 17222470-1 2007 The search for novel SUR1-ligands originates from the idea to influence the in vivo behaviour by adding new structural moieties to the glibenclamide structure while preserving its binding affinity. Glyburide 135-148 ATP binding cassette subfamily C member 8 Homo sapiens 21-25 17294036-6 2007 Glibenclamide inhibited the expression of SUR2 mRNA in preadipocyte, promoted preadipocyte proliferation in a dose-dependent manner, increased the cell percentages in G(2)/M + S phase, increased lipid content, augmented adipocyte diameter, and promoted the expression of PPAR-gamma mRNA. Glyburide 0-13 ATP binding cassette subfamily C member 9 Rattus norvegicus 42-46 17294036-6 2007 Glibenclamide inhibited the expression of SUR2 mRNA in preadipocyte, promoted preadipocyte proliferation in a dose-dependent manner, increased the cell percentages in G(2)/M + S phase, increased lipid content, augmented adipocyte diameter, and promoted the expression of PPAR-gamma mRNA. Glyburide 0-13 peroxisome proliferator-activated receptor gamma Rattus norvegicus 271-281 17182029-7 2007 In the severe injury model, glibenclamide inhibited inflammatory parameters, as assessed by Evans blue extravasation, neutrophil influx and haemoglobin content, and the increase in TNF-alpha (tumor necrose factor-alpha) and IL (interleukin)-6 levels in the intestine and lung. Glyburide 28-41 interleukin 6 Rattus norvegicus 224-242 17138562-2 2007 SUR binds nucleotides and synthetic K(ATP) channel modulators, e.g. the antidiabetic sulfonylurea glibenclamide, which acts as a channel blocker. Glyburide 98-111 ATP binding cassette subfamily C member 8 Homo sapiens 0-3 17138562-10 2007 Resveratrol was much more potent than glibenclamide in inducing SUR1-specific apoptosis. Glyburide 38-51 ATP binding cassette subfamily C member 8 Homo sapiens 64-68 17174222-11 2007 However, rosiglitazone reduced insulin resistance and proinsulin levels whereas glibenclamide use was associated with an increase in fasting insulin and proinsulin. Glyburide 80-93 insulin Homo sapiens 153-163 17970197-3 2007 Preliminary blockade of protein kinase C with chelerythrine or inhibition of ATP-dependent K+ channels (K(ATP) channels) with glybenclamide abolished the antiarrhythmic effect of kappa-opioid receptor activation. Glyburide 126-139 opioid receptor kappa 1 Homo sapiens 179-200 17188667-15 2007 We confirm the expression of this TRP channel on SAN cells by Western blotting and RT-PCR and validate that TRPM4 is glibenclamide sensitive. Glyburide 117-130 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 108-113 17064967-8 2007 This effect was abolished with pretreatment of iNOS inhibitors, l-canavanine and dexamethasone and perfusion of glibenclamide, but not with TEA and non-sulfonylurea drug, nateglinide. Glyburide 112-125 nitric oxide synthase 2 Rattus norvegicus 47-51 17097222-7 2007 The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. Glyburide 85-98 tumor necrosis factor Homo sapiens 195-204 17097222-7 2007 The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. Glyburide 85-98 interleukin 6 Homo sapiens 206-210 17097222-7 2007 The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. Glyburide 85-98 C-X-C motif chemokine ligand 8 Homo sapiens 216-220 17128288-5 2007 The action of glibenclamide was mimicked by tolbutamide (500 microM) or the CFTR blocker diphenylamine-2,2-dicarboxylic acid (500 microM). Glyburide 14-27 CF transmembrane conductance regulator Rattus norvegicus 76-80 18025765-6 2007 Moreover, the HbA1c difference value from baseline observed in the nateglinide-treated group was significantly higher than that observed in the glibenclamide group. Glyburide 144-157 hemoglobin subunit alpha 1 Homo sapiens 14-18 17012605-4 2007 Glibenclamide, a nonselective K(ATP) channel blocker reversed the antihypertrophic effect of all three AR agonists as determined by cell size and atrial natriuretic peptide expression and early c-fos up-regulation. Glyburide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 194-199 17963417-7 2007 Supporting this, one study reported an increased insulin secretion in CYP2C9*3 allele carriers when using the sulfonylurea agent glyburide. Glyburide 129-138 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 70-76 17003337-5 2006 Moreover, Foxa1-/- beta-cells exhibit attenuated calcium influx in response to glucose and glyburide, suggesting an insulin secretion defect either at the level or upstream of the ATP-sensitive K+ channel. Glyburide 91-100 forkhead box A1 Mus musculus 10-15 17150215-8 2006 Moreover, Sb(III) transport was sensitive to classical inhibitors of the human MRP1, such as MK571 or glibenclamide. Glyburide 102-115 ATP binding cassette subfamily C member 1 Homo sapiens 79-83 16824503-9 2006 L-NMMA and glibenclamide abrogated the effects of nicorandil on ventricular function, coronary blood flow volume, area of no-reflow, necrosis area and cNOS activity, but not iNOS activity. Glyburide 11-24 nitric oxide synthase 3 Homo sapiens 151-155 17178262-8 2006 Furthermore, estrone-3-sulfate transport into OATP2B1-overexpressing Madin-Darby canine kidney II cells was inhibited by various drugs, including atorvastatin, simvastatin, cerivastatin, glyburide (INN, glibenclamide), and gemfibrozil, with the most pronounced effect being found for atorvastatin (inhibition constant, 0.7 +/- 0.4 micromol/L). Glyburide 187-196 solute carrier organic anion transporter family member 2B1 Homo sapiens 46-53 17178262-8 2006 Furthermore, estrone-3-sulfate transport into OATP2B1-overexpressing Madin-Darby canine kidney II cells was inhibited by various drugs, including atorvastatin, simvastatin, cerivastatin, glyburide (INN, glibenclamide), and gemfibrozil, with the most pronounced effect being found for atorvastatin (inhibition constant, 0.7 +/- 0.4 micromol/L). Glyburide 203-216 solute carrier organic anion transporter family member 2B1 Homo sapiens 46-53 17047922-6 2006 RESULTS: Glibenclamide (glyburide) treatment was started at 23 months and resulted in insulin being discontinued, lower overall glycaemia, reduced glucose fluctuations and reduced hypoglycaemia. Glyburide 9-22 insulin Homo sapiens 86-93 17047922-6 2006 RESULTS: Glibenclamide (glyburide) treatment was started at 23 months and resulted in insulin being discontinued, lower overall glycaemia, reduced glucose fluctuations and reduced hypoglycaemia. Glyburide 24-33 insulin Homo sapiens 86-93 16460798-4 2006 Thus, [(3)H]-glyburide transport was examined in BCRP, PGP, MRP1, MRP2 and MRP3 over-expressing cell lines in the presence or absence of specific inhibitors. Glyburide 13-22 ATP binding cassette subfamily C member 3 Homo sapiens 75-79 16460798-7 2006 On the other hand, glyburide was found to significantly inhibit MRP1-, MRP2- and MRP3-mediated efflux of 5-carboxyfluorescein diacetate and PGP-mediated transport of rhodamine 123. Glyburide 19-28 ATP binding cassette subfamily C member 1 Homo sapiens 64-68 16460798-7 2006 On the other hand, glyburide was found to significantly inhibit MRP1-, MRP2- and MRP3-mediated efflux of 5-carboxyfluorescein diacetate and PGP-mediated transport of rhodamine 123. Glyburide 19-28 ATP binding cassette subfamily C member 2 Homo sapiens 71-75 16460798-7 2006 On the other hand, glyburide was found to significantly inhibit MRP1-, MRP2- and MRP3-mediated efflux of 5-carboxyfluorescein diacetate and PGP-mediated transport of rhodamine 123. Glyburide 19-28 ATP binding cassette subfamily C member 3 Homo sapiens 81-85 16460798-7 2006 On the other hand, glyburide was found to significantly inhibit MRP1-, MRP2- and MRP3-mediated efflux of 5-carboxyfluorescein diacetate and PGP-mediated transport of rhodamine 123. Glyburide 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 140-143 16460798-8 2006 Our evidence is the first to clearly indicate that glyburide is preferentially transported by BCRP and MRP3. Glyburide 51-60 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 94-98 16460798-8 2006 Our evidence is the first to clearly indicate that glyburide is preferentially transported by BCRP and MRP3. Glyburide 51-60 ATP binding cassette subfamily C member 3 Homo sapiens 103-107 17211564-0 2006 The effect of the sulfonylurea glyburide on glutathione-S-transferase and glucose-6-phosphate dehydrogenase in streptozotocin-induced diabetic rat liver. Glyburide 31-40 hematopoietic prostaglandin D synthase Rattus norvegicus 44-69 17211564-0 2006 The effect of the sulfonylurea glyburide on glutathione-S-transferase and glucose-6-phosphate dehydrogenase in streptozotocin-induced diabetic rat liver. Glyburide 31-40 glucose-6-phosphate dehydrogenase Rattus norvegicus 74-107 17211564-8 2006 Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). Glyburide 148-157 hematopoietic prostaglandin D synthase Rattus norvegicus 6-9 17211564-8 2006 Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). Glyburide 148-157 glucose-6-phosphate dehydrogenase Rattus norvegicus 14-19 17211564-8 2006 Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). Glyburide 148-157 hematopoietic prostaglandin D synthase Rattus norvegicus 208-211 17211564-8 2006 Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). Glyburide 148-157 glucose-6-phosphate dehydrogenase Rattus norvegicus 231-236 16891388-8 2006 alpha-ENaC and CFTR proteins also declined after glibenclamide or clofilium treatment. Glyburide 49-62 sodium channel epithelial 1 subunit alpha Homo sapiens 0-10 16891388-8 2006 alpha-ENaC and CFTR proteins also declined after glibenclamide or clofilium treatment. Glyburide 49-62 CF transmembrane conductance regulator Homo sapiens 15-19 17296510-15 2006 The transfer from insulin injections to oral glibenclamide therapy seems highly effective for most patients and safe. Glyburide 45-58 insulin Homo sapiens 18-25 17114456-7 2006 The entry of HSP70 into this secretory compartment appears to involve the ABC family transporter proteins and ABC transporter inhibitor glibenclamide antagonizes secretion. Glyburide 136-149 heat shock protein family A (Hsp70) member 4 Homo sapiens 13-18 17142143-6 2006 We also tested the impact of the incretin glucagon-like peptide-1 (GLP-1) on the GB-induced desensitization. Glyburide 81-83 glucagon Mus musculus 67-72 17142143-11 2006 Interestingly, the GB-induced desensitization of GSIS was counteracted by both SVS (P < .05) and GLP-1 (P < .05). Glyburide 19-21 glucagon Mus musculus 100-105 17030371-7 2006 VIP reduced CVR by -4+/-1% in the presence of the K(ATP) channel blocker glibenclamide (3x10(-6)M; P<0.05 vs control) and by -28+/-2% in the presence of the K(V) channel blocker 4-aminopyridine (3x10(-4)M; P>0.05 vs control). Glyburide 73-86 vasoactive intestinal peptide Rattus norvegicus 0-3 16603689-13 2006 However, ABCA1-mediated cholesterol efflux was clearly more sensitive to the inhibitory effects of glyburide in Cav-1(-/-) MPMs versus WT MPMs. Glyburide 99-108 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 9-14 16847435-6 2006 Inhibition of VIP/PACAP receptors and of voltage-gated K(+) channels reduced PACAP 38 and VIP relaxations, which were not modified by the K(+) channel blockers iberiotoxin, charybdotoxin, apamin or glibenclamide. Glyburide 198-211 vasoactive intestinal peptide Sus scrofa 14-17 16847435-6 2006 Inhibition of VIP/PACAP receptors and of voltage-gated K(+) channels reduced PACAP 38 and VIP relaxations, which were not modified by the K(+) channel blockers iberiotoxin, charybdotoxin, apamin or glibenclamide. Glyburide 198-211 adenylate cyclase activating polypeptide 1 Sus scrofa 18-23 16922806-10 2006 Glibenclamide blunted systemic vasodilation and reduced the mRNA expression of Kir6.2. Glyburide 0-13 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 79-85 16760228-7 2006 The well known cholestatic drugs, rifampicin, rifamycin SV, glibenclamide, and cyclosporin A, reduced the basal-to-apical transport and the apical efflux clearance of taurocholate across NTCP- and BSEP-coexpressing cell monolayers. Glyburide 60-73 solute carrier family 10 member 1 Homo sapiens 187-191 16760228-7 2006 The well known cholestatic drugs, rifampicin, rifamycin SV, glibenclamide, and cyclosporin A, reduced the basal-to-apical transport and the apical efflux clearance of taurocholate across NTCP- and BSEP-coexpressing cell monolayers. Glyburide 60-73 ATP binding cassette subfamily B member 11 Homo sapiens 197-201 16865362-0 2006 Selectivity of repaglinide and glibenclamide for the pancreatic over the cardiovascular K(ATP) channels. Glyburide 31-44 ATPase phospholipid transporting 8A2 Homo sapiens 90-93 16865362-8 2006 CONCLUSIONS/INTERPRETATION: Repaglinide and glibenclamide show higher potency and efficacy in inhibiting the pancreatic than the cardiovascular K(ATP) channels, thus supporting their clinical use. Glyburide 44-57 ATPase phospholipid transporting 8A2 Homo sapiens 146-149 16760362-5 2006 Glutamate-stimulated ATP release was significantly antagonized by the cystic fibrosis transmembrane conductance regulator (CFTR) blockers flufenamic acid and glibenclamide. Glyburide 158-171 cystic fibrosis transmembrane conductance regulator Mus musculus 70-121 16760362-5 2006 Glutamate-stimulated ATP release was significantly antagonized by the cystic fibrosis transmembrane conductance regulator (CFTR) blockers flufenamic acid and glibenclamide. Glyburide 158-171 cystic fibrosis transmembrane conductance regulator Mus musculus 123-127 16861224-4 2006 Moreover, TNF-alpha-mediated MIF release was blocked by glyburide and propenicide, both inhibitors of ATP-binding cassette-type transporters, suggesting that this transporter system is activated during neutrophil apoptosis. Glyburide 56-65 tumor necrosis factor Homo sapiens 10-19 16861224-4 2006 Moreover, TNF-alpha-mediated MIF release was blocked by glyburide and propenicide, both inhibitors of ATP-binding cassette-type transporters, suggesting that this transporter system is activated during neutrophil apoptosis. Glyburide 56-65 macrophage migration inhibitory factor Homo sapiens 29-32 17003289-3 2006 GLP-1 similarly augmented the K(ATP) channel-independent insulin-releasing effects of tolbutamide, glibenclamide or nateglinide. Glyburide 99-112 glucagon Homo sapiens 0-5 17003289-3 2006 GLP-1 similarly augmented the K(ATP) channel-independent insulin-releasing effects of tolbutamide, glibenclamide or nateglinide. Glyburide 99-112 insulin Homo sapiens 57-64 16725203-6 2006 Western blots of striatal dopamine transporter (DAT) and tyrosine hydroxylase (TH) proteins demonstrated that 30 mg/kg of glibenclamide alone did not affect the expression of DAT and TH after two weeks of daily treatments, but it significantly enhanced the reduction of DAT and TH by a single dose of 20 mg/kg of MPTP. Glyburide 122-135 tyrosine hydroxylase Mus musculus 79-81 16828060-0 2006 Effect of human serum albumin on transplacental transfer of glyburide. Glyburide 60-69 albumin Homo sapiens 16-29 16828060-4 2006 Therefore, the goal of the current investigation was to determine the effect of human serum albumin (HSA) on the transfer and distribution of glyburide across the human placenta. Glyburide 142-151 albumin Homo sapiens 86-99 16938132-6 2006 We demonstrated in rat TSMC that it is remarkably similar to that of the epithelial CFTR, both for activation (using three benzo [c]quinolizinium derivatives) and for inhibition (glibenclamide, DPC and CFTRinh-172). Glyburide 179-192 CF transmembrane conductance regulator Rattus norvegicus 84-88 16603689-13 2006 However, ABCA1-mediated cholesterol efflux was clearly more sensitive to the inhibitory effects of glyburide in Cav-1(-/-) MPMs versus WT MPMs. Glyburide 99-108 caveolin 1, caveolae protein Mus musculus 112-117 16729997-5 2006 The effect of KR-31378 on the angiotensin II-induced increase in cell size was reversed by mitochondrial ATP-sensitive potassium channel blockers, 5-hydroxydecanoate or glibenclamide. Glyburide 169-182 angiotensinogen Rattus norvegicus 30-44 16873786-7 2006 In the A1C >9.5% arm, inhaled insulin demonstrated a significantly greater reduction in A1C than glibenclamide, between-treatment difference -0.37% (-0.62 to -0.12; P = 0.004). Glyburide 100-113 insulin Homo sapiens 33-40 16848726-0 2006 Evaluation of mucin as a release enhancer for rectal delivery of glibenclamide. Glyburide 65-78 solute carrier family 13 member 2 Rattus norvegicus 14-19 16848726-1 2006 In this work mucin was evaluated as a release and absorption enhancer for glibenclamide from rectal glycerogelatin suppository. Glyburide 74-87 solute carrier family 13 member 2 Rattus norvegicus 13-18 16845255-10 2006 A combination of fosinopril or valsartan with glibenclamide significantly increased area of no-reflow (P<0.05) and decreased the levels of SUR2 and Kir6.2 (P<0.01). Glyburide 46-59 potassium inwardly rectifying channel subfamily J member 11 Sus scrofa 151-157 16848726-10 2006 All the suppositories containing either S-mucin, I-mucin or sodium salicylate showed better glibenclamide release than the control without any release enhancer (p < 0.05). Glyburide 92-105 solute carrier family 13 member 2 Rattus norvegicus 42-47 16848726-10 2006 All the suppositories containing either S-mucin, I-mucin or sodium salicylate showed better glibenclamide release than the control without any release enhancer (p < 0.05). Glyburide 92-105 solute carrier family 13 member 2 Rattus norvegicus 51-56 16601136-5 2006 We have previously shown that glyburide, an ATP-binding cassette (ABC) transporter inhibitor, inhibits the externalization of ANXA1 from TtT/GF cells and pituitary tissue. Glyburide 30-39 annexin A1 Mus musculus 126-131 16595597-12 2006 After 24-h exposure to high (16.7 mmol/liter) glucose concentration, impairment of glibenclamide-induced insulin release was significantly (P = 0.01) worse with the E23K variant. Glyburide 83-96 insulin Homo sapiens 105-112 16569910-10 2006 Glyburide, an antagonist of ABCA1, partially inhibited its secretion with I-HDL, whereas plasma HDL increased vitamin E efflux. Glyburide 0-9 ATP binding cassette subfamily A member 1 Homo sapiens 28-33 16713429-9 2006 Similarly, treatment with 5 micromol/L gliclazide or 10 mmol/L NAC significantly overcome the reduction in insulin-stimulated GLUT4 translocation by hydrogen peroxide (P<.01), whereas 5 micromol/L glibenclamide did not. Glyburide 200-213 insulin Homo sapiens 107-114 16470247-4 2006 We report here that both ATP and glibenclamide sensitivities of the 30 pS K channel in TAL cells were absent in mice lacking CFTR and in mice homozygous for the deltaF508 mutation. Glyburide 33-46 cystic fibrosis transmembrane conductance regulator Mus musculus 125-129 16500904-10 2006 Glibenclamide suppressed ABCA1 ATPase, suggesting that it inhibits apoA-I-dependent cellular cholesterol efflux by suppressing ABCA1 ATPase activity. Glyburide 0-13 ATP binding cassette subfamily A member 1 Homo sapiens 25-30 16500904-10 2006 Glibenclamide suppressed ABCA1 ATPase, suggesting that it inhibits apoA-I-dependent cellular cholesterol efflux by suppressing ABCA1 ATPase activity. Glyburide 0-13 dynein axonemal heavy chain 8 Homo sapiens 31-37 16500904-10 2006 Glibenclamide suppressed ABCA1 ATPase, suggesting that it inhibits apoA-I-dependent cellular cholesterol efflux by suppressing ABCA1 ATPase activity. Glyburide 0-13 apolipoprotein A1 Homo sapiens 67-73 16500904-10 2006 Glibenclamide suppressed ABCA1 ATPase, suggesting that it inhibits apoA-I-dependent cellular cholesterol efflux by suppressing ABCA1 ATPase activity. Glyburide 0-13 ATP binding cassette subfamily A member 1 Homo sapiens 127-132 16500904-10 2006 Glibenclamide suppressed ABCA1 ATPase, suggesting that it inhibits apoA-I-dependent cellular cholesterol efflux by suppressing ABCA1 ATPase activity. Glyburide 0-13 dynein axonemal heavy chain 8 Homo sapiens 133-139 16289604-6 2006 HAEt and glibenclamide-treated rats also showed decreased lipid peroxidation that is associated with increased activity of superoxide dismutase (SOD) and catalase. Glyburide 9-22 catalase Rattus norvegicus 154-162 16629371-10 2006 MSE pretreatment showed reversal in the levels of all the above parameters better than GLC. Glyburide 87-90 enolase 3 Rattus norvegicus 0-3 16443932-4 2006 ApoA-I-induced signaling was abrogated by glyburide, an inhibitor of the ABC transporter family, and in fibroblasts from patients with Tangier disease, which do not express ABCA1. Glyburide 42-51 apolipoprotein A1 Homo sapiens 0-6 16472777-5 2006 This efflux was fully inhibited by NPPB, DPC, or glibenclamide, suggesting mediation through CFTR. Glyburide 49-62 CF transmembrane conductance regulator Homo sapiens 93-97 16738156-10 2006 CONCLUSION: Glyburide was more likely to fail in women diagnosed earlier in pregnancy, of older age and multiparity, and with higher fasting glucoses, suggesting that earlier glucose intolerance and a reduced capacity to respond to an insulin secretagogue may distinguish this group. Glyburide 12-21 insulin Homo sapiens 235-242 16735966-2 2006 The aim of this study was to assess the effect of the sulfonylurea drugs gliclazide and glibenclamide on lymphocyte ecto-5"-nucleotidase of type 2 diabetic patients. Glyburide 88-101 5'-nucleotidase ecto Homo sapiens 116-136 16550187-6 2006 Block of SUR1 with low-dose glibenclamide reduced cerebral edema, infarct volume and mortality by 50%, with the reduction in infarct volume being associated with cortical sparing. Glyburide 28-41 ATP binding cassette subfamily C member 8 Homo sapiens 9-13 16492219-1 2006 AIMS: The oral hypoglycaemic sulphonylurea glibenclamide stimulates endogenous insulin secretion through blockade of ATP-sensitive potassium (KATP) channels on pancreatic beta cells, but also blocks cardiovascular KATP channels, leading to increased peripheral vascular resistance and reduced peripheral blood flow in non-diabetic subjects. Glyburide 43-56 insulin Homo sapiens 79-86 16492219-11 2006 Glibenclamide produced an 8-fold increase in circulating insulin compared with placebo (P < 0.001). Glyburide 0-13 insulin Homo sapiens 57-64 16302263-3 2006 The selective K(ATP) and large conductance Ca(2+) activated K(+) (BK(Ca)) channel inhibitors, glibenclamide and charybdotoxin, respectively were used to inhibit responses to PKG activators. Glyburide 94-107 protein kinase cGMP-dependent 1 Homo sapiens 174-177 16371645-9 2006 An ATP binding cassette transporter inhibitor, glyburide, prevents ATP- and thrombin-induced S1P release from platelets. Glyburide 47-56 coagulation factor II Rattus norvegicus 76-84 16306272-0 2006 Glibenclamide-induced apoptosis is specifically enhanced by expression of the sulfonylurea receptor isoform SUR1 but not by expression of SUR2B or the mutant SUR1(M1289T). Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 108-112 16306272-6 2006 By analyzing cell detachment, nuclear condensation, DNA fragmentation, and caspase-3-like activity, we observed a SUR1-specific enhancement of glibenclamide-induced apoptosis that was not seen in SUR2B, SUR1(M1289T), or control cells. Glyburide 143-156 ATP binding cassette subfamily C member 8 Homo sapiens 114-118 16306272-8 2006 In conclusion, expression of SUR1, but not of SUR2B or SUR1(M1289T), renders cells more susceptible to glibenclamide-induced apoptosis. Glyburide 103-116 ATP binding cassette subfamily C member 8 Homo sapiens 29-33 16443858-2 2006 RESEARCH DESIGN AND METHODS: We compared the acute effect of nateglinide, glibenclamide, and placebo on prandial plasma glucose and serum insulin, C-peptide, and glucagon excursions in 15 patients with MODY3. Glyburide 74-87 insulin Homo sapiens 138-145 16722160-0 2006 [Glibenclamide instead of insulin: a new chance for MODY 3 type diabetes patients: case report]. Glyburide 1-14 HNF1 homeobox A Homo sapiens 52-58 16344552-2 2006 Since previous studies indicated that glucose-stimulated activation of mammalian target of rapamycin (mTOR) leads to [3H]thymidine incorporation and that mTOR activation is mediated, in part, through the K(ATP) channel and changes in cytosolic Ca2+, we determined whether glyburide, an inhibitor of K(ATP) channels that stimulates Ca2+ influx, modulates [3H]thymidine incorporation. Glyburide 272-281 mechanistic target of rapamycin kinase Homo sapiens 71-100 16344552-2 2006 Since previous studies indicated that glucose-stimulated activation of mammalian target of rapamycin (mTOR) leads to [3H]thymidine incorporation and that mTOR activation is mediated, in part, through the K(ATP) channel and changes in cytosolic Ca2+, we determined whether glyburide, an inhibitor of K(ATP) channels that stimulates Ca2+ influx, modulates [3H]thymidine incorporation. Glyburide 272-281 mechanistic target of rapamycin kinase Homo sapiens 102-106 16344552-2 2006 Since previous studies indicated that glucose-stimulated activation of mammalian target of rapamycin (mTOR) leads to [3H]thymidine incorporation and that mTOR activation is mediated, in part, through the K(ATP) channel and changes in cytosolic Ca2+, we determined whether glyburide, an inhibitor of K(ATP) channels that stimulates Ca2+ influx, modulates [3H]thymidine incorporation. Glyburide 272-281 mechanistic target of rapamycin kinase Homo sapiens 154-158 16433710-8 2006 Plasma concentrations of VWF and ICAM-1 were elevated in patients with Type 2 diabetes compared with control subjects (P < 0.05 for both) and were reduced during treatment with repaglinide (P < 0.01 for both) but did not change during glibenclamide treatment. Glyburide 241-254 von Willebrand factor Homo sapiens 25-28 16433710-8 2006 Plasma concentrations of VWF and ICAM-1 were elevated in patients with Type 2 diabetes compared with control subjects (P < 0.05 for both) and were reduced during treatment with repaglinide (P < 0.01 for both) but did not change during glibenclamide treatment. Glyburide 241-254 intercellular adhesion molecule 1 Homo sapiens 33-39 16290322-8 2006 The terminal 5-HT(1B) autoreceptor-mediated feedback control was involved in the glibenclamide-induced increase in [(3)H]-5-HT release only in mouse neocortical tissue, as evident from the use of the 5-HT(1B) autoreceptor ligands metitepin (1 microM) and cyanopindolol (1 microM). Glyburide 81-94 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 13-20 16495770-6 2006 Preincubation with glibenclamide, an inhibitor of ATP-sensitive potassium (KATP) channels, reversed both responses to methanandamide (P < 0.01) and calcitonin gene related peptide (P < 0.05). Glyburide 19-32 calcitonin-related polypeptide alpha Rattus norvegicus 151-182 16290322-8 2006 The terminal 5-HT(1B) autoreceptor-mediated feedback control was involved in the glibenclamide-induced increase in [(3)H]-5-HT release only in mouse neocortical tissue, as evident from the use of the 5-HT(1B) autoreceptor ligands metitepin (1 microM) and cyanopindolol (1 microM). Glyburide 81-94 5-hydroxytryptamine (serotonin) receptor 1B Mus musculus 200-207 16475928-4 2006 Blockers of Kir6.2/SUR1 channels, e.g. glibenclamide and repaglinide stimulate release of insulin and are used for treatment of type 2 diabetes. Glyburide 39-52 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 12-18 16418275-8 2006 Pharmacological experiments showed that the channel response to the SUR1 agonist diazoxide, SUR2A/B agonist cromakalim, SUR1 antagonist tolbutamide, and the SUR1/SUR2A/B-antagonist glibenclamide matched the SURs expression pattern. Glyburide 181-194 ATP binding cassette subfamily C member 8 Homo sapiens 68-72 16263802-5 2006 On the other hand, transcripts for the alpha4-subunit of Na+-K+-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and Isc was not inhibited by glibenclamide. Glyburide 175-188 potassium inwardly-rectifying channel, subfamily J, member 1 Rattus norvegicus 72-78 16263802-5 2006 On the other hand, transcripts for the alpha4-subunit of Na+-K+-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and Isc was not inhibited by glibenclamide. Glyburide 175-188 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 96-102 16263802-5 2006 On the other hand, transcripts for the alpha4-subunit of Na+-K+-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and Isc was not inhibited by glibenclamide. Glyburide 175-188 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 104-110 16263802-5 2006 On the other hand, transcripts for the alpha4-subunit of Na+-K+-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and Isc was not inhibited by glibenclamide. Glyburide 175-188 ATP binding cassette subfamily C member 9 Rattus norvegicus 116-120 16135545-6 2006 Glibenclamide or NPPB reduced the DCEBIO-stimulated Isc by >80% indicating the participation of CFTR in the DCEBIO-stimulated Isc response. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 99-103 16572919-0 2006 Changes in butyrylcholinesterase activity and serum lipids after oxprenolol and glibenclamide treatments in non-diabetic rats. Glyburide 80-93 butyrylcholinesterase Rattus norvegicus 11-32 16543717-9 2006 In control cultures, the concentrations of Na and Cl in the apical fluid increased if glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR) was added to the apical medium. Glyburide 86-99 CF transmembrane conductance regulator Homo sapiens 121-172 16543717-9 2006 In control cultures, the concentrations of Na and Cl in the apical fluid increased if glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR) was added to the apical medium. Glyburide 86-99 CF transmembrane conductance regulator Homo sapiens 174-178 16256381-5 2006 The effects of glibenclamide on cell viability were partially inhibited after treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), inhibitor more selective for constitutive nitric oxide synthase, and in the presence of D600--a blocker of voltage-gated L-type Ca(2+) channels inhibited Ca(2+) influx into beta cells, whereas aminoguanidine (AG), a preferential inhibitor of inducible NOS, was significantly less effective. Glyburide 15-28 nitric oxide synthase 2 Homo sapiens 180-201 16475928-4 2006 Blockers of Kir6.2/SUR1 channels, e.g. glibenclamide and repaglinide stimulate release of insulin and are used for treatment of type 2 diabetes. Glyburide 39-52 ATP binding cassette subfamily C member 8 Homo sapiens 19-23 16475928-4 2006 Blockers of Kir6.2/SUR1 channels, e.g. glibenclamide and repaglinide stimulate release of insulin and are used for treatment of type 2 diabetes. Glyburide 39-52 insulin Homo sapiens 90-97 16380479-8 2006 In conclusion, chronic exposure to glibenclamide results in degranulation of a subpopulation of beta-cells, which maintain an elevated protein and insulin synthetic activity irrespective of the presence of the drug and of glucose. Glyburide 35-48 insulin Homo sapiens 147-154 16324923-6 2006 Despite lower plasma glucose levels, glyburide stimulated insulin secretion during this period (0.89 +/- 0.13 vs 1.47 +/- 0.15 pmol x kg(-1) x min(-1), control vs glyburide; P = .001), whereas glimepiride did not (P = .08). Glyburide 37-46 insulin Homo sapiens 58-65 16324923-8 2006 In contrast, during recovery from hypoglycemia, glyburide but not glimepiride inappropriately stimulates insulin secretion at low plasma glucose levels. Glyburide 48-57 insulin Homo sapiens 105-112 16324923-9 2006 This differential effect on insulin secretion may be an important factor in explaining why glyburide causes severe hypoglycemia more frequently than glimepiride. Glyburide 91-100 insulin Homo sapiens 28-35 16174808-6 2005 Four loop diuretics, i.e., furosemide, piretanide, azosemide, and torasemide, thiazides, probenecid, glibenclamide, and nateglinide inhibited the MCT6-mediated uptake of [3H]bumetanide. Glyburide 101-114 solute carrier family 16 member 5 Homo sapiens 146-150 16310184-5 2005 Glibenclamide attenuated the nuclear damage, changes in the mitochondrial membrane permeability, caspase-3 activation and formation of reactive oxygen species due to MPP+ in PC12 cells. Glyburide 0-13 caspase 3 Rattus norvegicus 97-106 16310184-6 2005 The results show that glibenclamide may reduce the MPP+-induced viability loss in PC12 cells by suppressing the changes in the mitochondrial membrane permeability, leading to the release of cytochrome c and subsequent activation of caspase-3, which are associated with the increased reactive oxygen species formation and depletion of GSH. Glyburide 22-35 caspase 3 Rattus norvegicus 232-241 16198656-0 2005 CYP2C9, but not CYP2C19, polymorphisms affect the pharmacokinetics and pharmacodynamics of glyburide in Chinese subjects. Glyburide 91-100 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 15859948-11 2005 The acidification and the initial regulatory volume decrease response were inhibited by glibenclamide and BaCl2 only in AQP2 cells. Glyburide 88-101 aquaporin 2 Homo sapiens 120-124 16342679-0 2005 [Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects]. Glyburide 87-100 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 27-33 16342679-0 2005 [Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects]. Glyburide 87-100 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 49-55 16342679-1 2005 AIM: To investigate the impact of CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam. Glyburide 72-85 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 34-40 16342679-5 2005 RESULTS: After a single oral dose of 2.5 mg glibenclamide, C(max) was (70.0 +/- 11.5) microg x L(-1) in CYP2C9 * 1/ * 3 subjects and (51.9 +/- 12.3) microg x L(-1) in * 1/ *1 subjects. Glyburide 44-57 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 104-110 16342679-7 2005 Statistic analysis results indicated that glibenclamide AUC(0-infinity) was significantly higher (1.5-fold) and subsequently CL/F was significantly lower (40%) in CYP2C9 * 1/ * 3 subjects than those in * 1/ * 1 subjects (P < 0.01). Glyburide 42-55 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 163-169 16342679-12 2005 CONCLUSION: CYP2C9 * 3 greatly affects both the pharmacokinetic profiles of glibenclamide and lornoxicam. Glyburide 76-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 12-18 16014619-11 2005 When the cells were pretreated with glibenclamide, an ATP-sensitive potassium channel blocker, the CGRP actions on bradykinin-induced Ca2+ influx were profoundly inhibited. Glyburide 36-49 calcitonin related polypeptide alpha Homo sapiens 99-103 16014619-11 2005 When the cells were pretreated with glibenclamide, an ATP-sensitive potassium channel blocker, the CGRP actions on bradykinin-induced Ca2+ influx were profoundly inhibited. Glyburide 36-49 kininogen 1 Homo sapiens 115-125 15912128-1 2005 Sulfonylurea drugs, like glibenclamide, stimulate insulin secretion by blocking ATP-sensitive potassium channels on pancreatic beta cells. Glyburide 25-38 insulin Homo sapiens 50-57 15900017-9 2005 The uptake of ketoprofen by hepatocytes was significantly inhibited by probenecid and rOat2 inhibitors (indocyanine green, indomethacin, glibenclamide, and salicylate). Glyburide 137-150 solute carrier family 22 member 7 Rattus norvegicus 86-91 16061206-5 2005 Furthermore, UCN could increase the gene expression of ATP-sensitive potassium channels (K(ATP)) and activate sarcolemmal ATP-sensitive potassium current during normal or hypoxia, which could be inhibited by glibenclamide, a specific K(ATP) blocker. Glyburide 208-221 urocortin Mus musculus 13-16 16081479-6 2005 CFTR was activated in myocytes maintained in medium containing either high potassium or 5-hydroxytryptamine (5-HT) and was inhibited by CFTR(inh)-172, glibenclamide and diphenylamine-2,2"-dicarboxylic acid (DPC). Glyburide 151-164 cystic fibrosis transmembrane conductance regulator Mus musculus 0-4 15901241-7 2005 However, the IP-induced attenuation of sCD40L and P-selectin release was abolished by administering glibenclamide. Glyburide 100-113 selectin P Homo sapiens 50-60 16037573-6 2005 This effect was blocked by mitoKATP inhibitors 5-hydroxydecanoate, tetraphenylphosphonium, and glibenclamide, PKG-selective inhibitor KT5823, and protein kinase C (PKC) inhibitors chelerythrine, Ro318220, and PKC-epsilon peptide antagonist epsilonV(1-2). Glyburide 95-108 protein kinase C epsilon Homo sapiens 209-220 16198656-1 2005 BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect. Glyburide 86-95 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 21-46 16198656-1 2005 BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect. Glyburide 86-95 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 169-176 16198656-1 2005 BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect. Glyburide 102-115 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 21-46 16198656-1 2005 BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect. Glyburide 102-115 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 169-176 16198656-11 2005 CONCLUSION: CYP2C9, but not CYP2C19, polymorphism appears to exert a dominant influence on glyburide pharmacokinetics and pharmacodynamics in vivo. Glyburide 91-100 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 12-18 15958287-11 2005 MZ effects on AT II induced contraction was blocked by glybenclamide (a specific K(ATP) blocker, 3 microM, *p < 0.01). Glyburide 55-68 angiotensinogen Rattus norvegicus 14-19 15905177-7 2005 Glyburide raised the level of receptor-mediated endocytosis in the ABCA1-GFP expressing cell to the level of control cells in the absence of glyburide. Glyburide 0-9 ATP binding cassette subfamily A member 1 Canis lupus familiaris 67-72 15949470-6 2005 RESULTS: Exposure to 2,4-dinitrophenol (100 microM) evoked a glibenclamide-sensitive K(ATP) channel current in atrial cells from wild-type (WT) but not Kir6.2 knockout (Kir6.2 KO) mice. Glyburide 61-74 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 169-175 16012949-0 2005 Glibenclamide stimulates fluid secretion in rodent cholangiocytes through a cystic fibrosis transmembrane conductance regulator-independent mechanism. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 76-127 16012949-3 2005 Glibenclamide, a sulfonylurea and a known CFTR inhibitor, paradoxically stimulates cholangiocyte secretion. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 42-46 16012949-8 2005 Glibenclamide, unlike secretin and forskolin, was able to stimulate secretion in Cftr tm1Unc mice, thus indicating that this secretory mechanism was preserved. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 81-85 16012949-9 2005 CONCLUSIONS: The ability of glibenclamide to stimulate secretion in CFTR-defective mice makes sulfonylureas a model class of compounds to design drugs useful in the treatment of cystic fibrosis with liver impairment and possibly of other cholestatic diseases. Glyburide 28-41 cystic fibrosis transmembrane conductance regulator Mus musculus 68-72 15764598-9 2005 These data strongly suggest that glimepiride and glibenclamide, both of which belong to SU agents, should have PPARgamma agonist activity, whose potencies were 16-25% of the maximum level achieved by pioglitazone. Glyburide 49-62 peroxisome proliferator activated receptor gamma Mus musculus 111-120 15764598-10 2005 Our observation that glimepiride and glibenclamide could act not only on SU receptor but also on PPARgamma may give an important clue to the development of novel antidiabetic drugs, which can enhance both insulin secretion from pancreatic beta-cells and peripheral insulin sensitivity. Glyburide 37-50 peroxisome proliferator activated receptor gamma Mus musculus 97-106 15833737-6 2005 Studies with glibenclamide confirmed that chloride efflux was via the cystic fibrosis transmembrane conductance regulator. Glyburide 13-26 CF transmembrane conductance regulator Homo sapiens 70-121 15650130-7 2005 Similarly, treatment of WT epithelium with the CFTR-selective blocker glybenclamide decreased the Cl(-)/HCO(3)(-) exchange rate to the level of CF epithelium. Glyburide 70-83 cystic fibrosis transmembrane conductance regulator Mus musculus 47-51 16054561-3 2005 The permeability was also inhibited reversibly to approximately 55%, by extracellular glibenclamide (1mM), an inhibitor of some ATP-binding cassette (ABC) transporters, including the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 86-99 CF transmembrane conductance regulator Homo sapiens 183-234 16054561-3 2005 The permeability was also inhibited reversibly to approximately 55%, by extracellular glibenclamide (1mM), an inhibitor of some ATP-binding cassette (ABC) transporters, including the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 86-99 CF transmembrane conductance regulator Homo sapiens 236-240 15626748-4 2005 Apical trypsin and human neutrophil elastase, but not agonists of protease activated receptors, increased Na(+) and Cl(-) short-circuit currents (I(sc)) and transepithelial resistance (R(TE)) across human bronchial and nasal epithelial cells and rat alveolar type II cells, mounted in Ussing chambers, for at least 2 h. The increase in I(sc) was fully reversed by amiloride and glibenclamide. Glyburide 378-391 elastase, neutrophil expressed Homo sapiens 25-44 15936204-6 2005 We further show that two cystic fibrosis transmembrane conductance regulator modulators, glibenclamide and bromotetramisole, can regulate anion channel activities and HrpN ea-induced cell death. Glyburide 89-102 cystic fibrosis transmembrane conductance regulator Arabidopsis thaliana 25-76 15840025-9 2005 Glibenclamide (20 mg/kg) significantly inhibited the reperfusion-associated increase in vascular permeability, neutrophil accumulation, increase in TNF-alpha levels and nuclear factor-kappaB (NF-kappaB) translocation. Glyburide 0-13 tumor necrosis factor Rattus norvegicus 148-157 15673303-9 2005 Also, glibenclamide reduced diabetes-induced glomerular overexpression of fibronectin mRNA. Glyburide 6-19 fibronectin 1 Rattus norvegicus 74-85 15787664-1 2005 AIMS: Diabetic subjects with mutations in the gene encoding hepatocyte nuclear factor (HNF)-1alpha (MODY3) are prone to develop hypoglycaemia at low doses of glibenclamide, interpreted as sulphonylurea hypersensitivity. Glyburide 158-171 HNF1 homeobox A Homo sapiens 60-98 15787664-1 2005 AIMS: Diabetic subjects with mutations in the gene encoding hepatocyte nuclear factor (HNF)-1alpha (MODY3) are prone to develop hypoglycaemia at low doses of glibenclamide, interpreted as sulphonylurea hypersensitivity. Glyburide 158-171 HNF1 homeobox A Homo sapiens 100-105 15817827-6 2005 Syncollin expression in isolated rat islets had no effect on basal insulin secretion but significantly inhibited regulated insulin secretion stimulated by glucose (16.7 mM), glucagon-like peptide-1 (GLP-1) (10 nM) and glyburide (5 microM). Glyburide 218-227 syncollin Rattus norvegicus 0-9 15886061-5 2005 However, compared to glibenclamide-sensitive cells, stationary phase resistant parasites display an increased use of amino acids as energy substrate and an increased activity of the enzymes hexokinase, phosphoglucose isomerase, and especially NAD(+)-linked glutamate dehydrogenase. Glyburide 21-34 hexokinase 1 Homo sapiens 190-200 15886061-5 2005 However, compared to glibenclamide-sensitive cells, stationary phase resistant parasites display an increased use of amino acids as energy substrate and an increased activity of the enzymes hexokinase, phosphoglucose isomerase, and especially NAD(+)-linked glutamate dehydrogenase. Glyburide 21-34 glucose-6-phosphate isomerase Homo sapiens 202-226 15578659-6 2005 Glybenclamide and diisothiocyanato-stilbene-disulfonic acid (DIDS), two blockers of chloride fluxes that drive the export activity of ABC1 transporters, inhibited IL-1beta release without altering its intracellular processing. Glyburide 0-13 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 134-138 15655526-17 2005 In protocol II, Glib and 5-HD abolished the cardioprotective effect induced by ET-1 (IS 48+/-7% after Glib+ET-1 and 42+/-5% after ET-1+5-HD vs 18+/-4% after ET-1 alone; P<0.05). Glyburide 16-20 endothelin 1 Rattus norvegicus 79-83 15655526-17 2005 In protocol II, Glib and 5-HD abolished the cardioprotective effect induced by ET-1 (IS 48+/-7% after Glib+ET-1 and 42+/-5% after ET-1+5-HD vs 18+/-4% after ET-1 alone; P<0.05). Glyburide 16-20 endothelin 1 Rattus norvegicus 107-111 15655526-17 2005 In protocol II, Glib and 5-HD abolished the cardioprotective effect induced by ET-1 (IS 48+/-7% after Glib+ET-1 and 42+/-5% after ET-1+5-HD vs 18+/-4% after ET-1 alone; P<0.05). Glyburide 16-20 endothelin 1 Rattus norvegicus 107-111 15655526-17 2005 In protocol II, Glib and 5-HD abolished the cardioprotective effect induced by ET-1 (IS 48+/-7% after Glib+ET-1 and 42+/-5% after ET-1+5-HD vs 18+/-4% after ET-1 alone; P<0.05). Glyburide 16-20 endothelin 1 Rattus norvegicus 107-111 15678092-16 2005 Glibenclamide, tolbutamide and nateglinide binding appear to involve only SUR1. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 74-78 15640378-8 2005 Glibenclamide, a hypoglycemic drug, was identified for the first time as a substrate for OATP-B with a K(t) value of 6.26 microM. Glyburide 0-13 solute carrier organic anion transporter family member 2B1 Homo sapiens 89-95 15640378-9 2005 GFJ and OJ inhibited the OATP-B-mediated uptake of glibenclamide. Glyburide 51-64 solute carrier organic anion transporter family member 2B1 Homo sapiens 25-31 15640378-10 2005 These results suggest that citrus juices may inhibit the intestinal absorption of anionic drugs, such as glibenclamide, via the inhibition of OATP-B. Glyburide 105-118 solute carrier organic anion transporter family member 2B1 Homo sapiens 142-148 16245034-5 2005 This conductance was inhibited by SITS, but was resistant against glibenclamide, a blocker of CFTR. Glyburide 66-79 CF transmembrane conductance regulator Rattus norvegicus 94-98 15735229-0 2005 High-dose glibenclamide can replace insulin therapy despite transitory diarrhea in early-onset diabetes caused by a novel R201L Kir6.2 mutation. Glyburide 10-23 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 128-134 15578659-6 2005 Glybenclamide and diisothiocyanato-stilbene-disulfonic acid (DIDS), two blockers of chloride fluxes that drive the export activity of ABC1 transporters, inhibited IL-1beta release without altering its intracellular processing. Glyburide 0-13 interleukin 1 beta Mus musculus 163-171 15591059-11 2005 The activity of SLC26A7 was inhibited by all inhibitors of anion transporters tested, 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid, diphenylamine-2-carboxylic acid, and glybenclamide. Glyburide 173-186 solute carrier family 26 member 7 Homo sapiens 16-23 15652236-3 2005 Despite their functional differences, the activity of both SUR1/2 and MRP1 can be blocked by glibenclamide, a sulfonylurea used to treat diabetes. Glyburide 93-106 ATP binding cassette subfamily C member 8 Homo sapiens 59-65 15652236-3 2005 Despite their functional differences, the activity of both SUR1/2 and MRP1 can be blocked by glibenclamide, a sulfonylurea used to treat diabetes. Glyburide 93-106 ATP binding cassette subfamily C member 1 Homo sapiens 70-74 15652236-4 2005 Residues in the cytoplasmic loop connecting transmembrane helices 15 and 16 of the SUR proteins have been implicated as molecular determinants of their sensitivity to glibenclamide and other sulfonylureas. Glyburide 167-180 ATP binding cassette subfamily C member 8 Homo sapiens 83-86 15678092-4 2005 In this study, we investigate the interaction of the hypoglycaemic agents repaglinide and glibenclamide with SUR1 and the effect of Kir6.2 on this interaction. Glyburide 90-103 ATP binding cassette subfamily C member 8 Homo sapiens 109-113 15678092-5 2005 We further explore how the binding properties of repaglinide and glibenclamide are affected by functional uncoupling of SUR1 and Kir6.2 in Kir6.2DeltaN14/SUR1 channels. Glyburide 65-78 ATP binding cassette subfamily C member 8 Homo sapiens 120-124 15678092-5 2005 We further explore how the binding properties of repaglinide and glibenclamide are affected by functional uncoupling of SUR1 and Kir6.2 in Kir6.2DeltaN14/SUR1 channels. Glyburide 65-78 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 129-135 15678092-5 2005 We further explore how the binding properties of repaglinide and glibenclamide are affected by functional uncoupling of SUR1 and Kir6.2 in Kir6.2DeltaN14/SUR1 channels. Glyburide 65-78 ATP binding cassette subfamily C member 8 Homo sapiens 154-158 15678092-8 2005 Glibenclamide, tolbutamide and nateglinide all bound with marginally lower affinity to SUR1 than to Kir6.2/SUR1. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 87-91 15678092-8 2005 Glibenclamide, tolbutamide and nateglinide all bound with marginally lower affinity to SUR1 than to Kir6.2/SUR1. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 100-106 15678092-8 2005 Glibenclamide, tolbutamide and nateglinide all bound with marginally lower affinity to SUR1 than to Kir6.2/SUR1. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 107-111 21166163-4 2005 (2) ADP could inhibit the K(ATP) activation by Pin and attenuate the blockade of K(ATP) by Gli. Glyburide 91-94 WD and tetratricopeptide repeats 1 Homo sapiens 4-7 15480750-8 2005 DRA was inhibited by 4 mM DIDS (45+/-11%), by 50 microM tenidap (71+/-8%) and by 100 microM glibenclamide (59+/-22% inhibition of HCO3- transport and 79+/-3% inhibition of Cl- transport). Glyburide 92-105 solute carrier family 26 member 3 Homo sapiens 0-3 15389550-9 2005 These cAMP-activated Cl- currents have properties consistent with cystic fibrosis transmembrane regulator (CFTR) Cl- channels, as the currents were blocked by glibenclamide or NPPB but insensitive to DIDS. Glyburide 159-172 CF transmembrane conductance regulator Rattus norvegicus 66-105 15672015-1 2005 OBJECTIVE: We sought to investigate the association between glyburide dose, degree of severity in gestational diabetes mellitus (GDM), level of glycemic control, and pregnancy outcome in insulin- and glyburide-treated patients. Glyburide 60-69 insulin Homo sapiens 187-194 16372821-6 2005 Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes. Glyburide 65-78 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 155-161 16372821-6 2005 Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes. Glyburide 80-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 155-161 15389550-9 2005 These cAMP-activated Cl- currents have properties consistent with cystic fibrosis transmembrane regulator (CFTR) Cl- channels, as the currents were blocked by glibenclamide or NPPB but insensitive to DIDS. Glyburide 159-172 CF transmembrane conductance regulator Rattus norvegicus 107-111 15642492-9 2005 Quantitative RT-PCR studies showed that, compared with the control islets, cells preincubated with glibenclamide or chlorpropamide had an increased expression of insulin mRNA, with no change in the expression of GLUT-1. Glyburide 99-112 insulin Homo sapiens 162-169 15365090-1 2005 Glibenclamide, a potent cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel blocker, is frequently used to study function and regulation of CFTR Cl(-) channels. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Cavia porcellus 24-75 15365090-1 2005 Glibenclamide, a potent cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel blocker, is frequently used to study function and regulation of CFTR Cl(-) channels. Glyburide 0-13 ATP-binding cassette sub-family C member 7 Cavia porcellus 77-81 15365090-1 2005 Glibenclamide, a potent cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel blocker, is frequently used to study function and regulation of CFTR Cl(-) channels. Glyburide 0-13 ATP-binding cassette sub-family C member 7 Cavia porcellus 161-165 15308466-6 2004 8-Bromo-cAMP induced Cl(-)-independent HCO(3)(-) secretion (and also inhibited Cl(-)-dependent HCO(3)(-) secretion), which was inhibited by NPPB and by glibenclamide, a CFTR blocker, but not by DIDS. Glyburide 152-165 natriuretic peptide B Rattus norvegicus 140-144 15306545-6 2004 Glibenclamide, a blocker of CFTR, eliminated the genistein-stimulated increase of I(sc) and reduced the forskolin-activated I(sc). Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 28-32 15561897-5 2004 Homology modeling of the SUR1 core offers the possibility of defining the glibenclamide/sulfonylurea binding pocket. Glyburide 74-87 ATP binding cassette subfamily C member 8 Homo sapiens 25-29 15561897-7 2004 Elements of the COOH-terminal half of the core recognize a hydrophobic group in glibenclamide, adjacent to the sulfonylurea moiety, to provide selectivity for SUR1, while the benzamido group appears to be in proximity to L0 and the KIR NH2-terminus. Glyburide 80-93 ATP binding cassette subfamily C member 8 Homo sapiens 159-163 15561897-7 2004 Elements of the COOH-terminal half of the core recognize a hydrophobic group in glibenclamide, adjacent to the sulfonylurea moiety, to provide selectivity for SUR1, while the benzamido group appears to be in proximity to L0 and the KIR NH2-terminus. Glyburide 80-93 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 232-235 15561900-4 2004 SUR1, the typical pancreatic SUR isoform, shows much higher affinity for glibenclamide but considerably lower affinity for most openers than SUR2. Glyburide 73-86 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 15561900-4 2004 SUR1, the typical pancreatic SUR isoform, shows much higher affinity for glibenclamide but considerably lower affinity for most openers than SUR2. Glyburide 73-86 ATP binding cassette subfamily C member 8 Homo sapiens 0-3 15561900-11 2004 In conclusion, mutation of two amino acids in TM17 of SUR1, especially of M1289, leads to class-specific effects on opener binding by increasing opener affinity or by changing allosteric coupling between opener and glibenclamide binding. Glyburide 215-228 ATP binding cassette subfamily C member 8 Homo sapiens 54-58 15465654-1 2004 Troglitazone, bosentan and glibenclamide inhibit the bile salt export pump (Bsep) which transports taurocholate into bile. Glyburide 27-40 ATP binding cassette subfamily B member 11 Rattus norvegicus 53-74 15465654-1 2004 Troglitazone, bosentan and glibenclamide inhibit the bile salt export pump (Bsep) which transports taurocholate into bile. Glyburide 27-40 ATP binding cassette subfamily B member 11 Rattus norvegicus 76-80 15561916-10 2004 Glyburide, an inhibitor of ATP-sensitive K+ channels (K(ATP) channels), provided partial activation of mTOR at basal glucose concentrations due to the influx of extracellular Ca2+, and diazoxide, an activator of KATP channels, resulted in partial inhibition of S6K1 phosphorylation by 20 mmol/l glucose. Glyburide 0-9 mechanistic target of rapamycin kinase Homo sapiens 103-107 15561916-10 2004 Glyburide, an inhibitor of ATP-sensitive K+ channels (K(ATP) channels), provided partial activation of mTOR at basal glucose concentrations due to the influx of extracellular Ca2+, and diazoxide, an activator of KATP channels, resulted in partial inhibition of S6K1 phosphorylation by 20 mmol/l glucose. Glyburide 0-9 ribosomal protein S6 kinase B1 Homo sapiens 261-265 15563963-5 2004 These findings suggest that glimepiride improves insulin resistance in hyperinsulinemic patients treated with glibenclamide. Glyburide 110-123 insulin Homo sapiens 49-56 15579757-7 2004 In contrast, glyburide significantly increased both plasma PI (45%; P < 0.001) and the PI:IRI ratio (10%) (P < 0.05 vs. baseline). Glyburide 13-22 insulin Homo sapiens 59-61 15579757-7 2004 In contrast, glyburide significantly increased both plasma PI (45%; P < 0.001) and the PI:IRI ratio (10%) (P < 0.05 vs. baseline). Glyburide 13-22 insulin Homo sapiens 90-92 15579757-8 2004 These results show that rosiglitazone and glyburide have differential effects on absolute PI levels and the PI:IRI ratio in people with type 2 diabetes. Glyburide 42-51 insulin Homo sapiens 90-92 15579757-8 2004 These results show that rosiglitazone and glyburide have differential effects on absolute PI levels and the PI:IRI ratio in people with type 2 diabetes. Glyburide 42-51 insulin Homo sapiens 108-110 15531505-0 2004 Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2. Glyburide 0-13 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 97-103 15711774-0 2004 Time-dependent interactions of glibenclamide with CFTR: kinetically complex block of macroscopic currents. Glyburide 31-44 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 50-54 15711774-1 2004 Blockade of the CFTR chloride channel by glibenclamide was studied in Xenopus oocytes using two-electrode voltage-clamp recordings, macropatch recordings, and summations of single-channel currents, in order to test a kinetic model recently developed by us from single-channel experiments. Glyburide 41-54 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 16-20 15711774-5 2004 The results are consistent with the presence of multiple glibenclamide binding sites in CFTR, with varying affinity and voltage dependence; they support the kinetic model and suggest experimental approaches for identification of those sites by mutagenesis. Glyburide 57-70 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 88-92 15375790-9 2004 Plasma insulin levels were significantly higher from 100 to 240 minutes after clamp termination in patients given glyburide versus nateglinide. Glyburide 114-123 insulin Homo sapiens 7-14 15235914-5 2004 Cl- efflux was also inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) blocker glibenclamide. Glyburide 104-117 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 37-88 15235914-5 2004 Cl- efflux was also inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) blocker glibenclamide. Glyburide 104-117 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 90-94 15538541-7 2004 These results demonstrate that the sulfonylurea glyburide is capable of exerting direct insulin-like effect on heart superoxide dismutase, catalase and glutathione peroxidase activities of diabetic rats in vivo. Glyburide 48-57 catalase Rattus norvegicus 139-147 15294453-5 2004 The binding of glibenclamide to SUR1 was assessed by using a glibenclamide-fluorescent probe. Glyburide 15-28 ATP-binding cassette sub-family C member 8 Xenopus laevis 32-36 15294453-5 2004 The binding of glibenclamide to SUR1 was assessed by using a glibenclamide-fluorescent probe. Glyburide 61-74 ATP-binding cassette sub-family C member 8 Xenopus laevis 32-36 15294453-8 2004 Taurine at the concentration of 10 mM enhanced the high-affinity bindings of glibenclamide and repaglinide on all types of SUR, whereas the low-affinity binding on Kir6.2 was not affected. Glyburide 77-90 ATP binding cassette subfamily C member 8 Rattus norvegicus 123-126 15177944-7 2004 Incubation with either spironolactone (1 microM), glibenclamide (10 microM), RU 486 10 microM, ODQ (10 microM) or cycloheximide (10 microM) significantly reduced the enhancement of CGRP-relaxation produced by aldosterone, while remained unmodified by SQ 22,536. Glyburide 50-63 calcitonin-related polypeptide alpha Rattus norvegicus 181-185 15300895-9 2004 The effect of MP on ZO-1 and ZO-2 was mimicked by Ligustrazine and the ligustrazine-induced ISC was also blocked by basolateral application of bumetanide and apical addition of diphenylamine-2, 2"-dicarboxylic acid or glibenclamide, and reduced by a removal of extracellular Cl-. Glyburide 218-231 tight junction protein 2 Homo sapiens 14-33 15039139-4 2004 CFTR dependence was demonstrated by glybenclamide block of agonist-stimulated currents. Glyburide 36-49 CF transmembrane conductance regulator Homo sapiens 0-4 15039140-7 2004 ABCA1 knockdown studies using ABCA1 siRNA or the ABCA1 inhibitor, glyburide, selectively attenuated 22HC/RA-driven basolateral PtdCho efflux. Glyburide 66-75 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 0-5 15305038-5 2004 Pretreatment with KR-31378 (10 microM) showed a neuroprotective effect in both CA1 and CA3 regions and its effect was attenuated by glibenclamide in a dose dependent manner in both areas. Glyburide 132-145 carbonic anhydrase 3 Mus musculus 87-90 15270789-6 2004 The glibenclamide group had significantly lower HbA1c than the pioglitazone group after 12 weeks of therapy (7.8% vs. 8.3%, P = 0.015), but significantly higher HbA1c after 52 weeks of therapy (7.8% vs. 7.2%, P = 0.001). Glyburide 4-17 hemoglobin subunit alpha 1 Homo sapiens 48-52 15243303-0 2004 Rosiglitazone improves, while Glibenclamide worsens blood pressure control in treated hypertensive diabetic and dyslipidemic subjects via modulation of insulin resistance and sympathetic activity. Glyburide 30-43 insulin Homo sapiens 152-159 15240997-5 2004 Soluble guanylate cyclase inhibitor, ODQ, and ATP-sensitive potassium channel blocker, glibenclamide, inhibited the CGRP-induced maximum responses by 75 and 55%, respectively. Glyburide 87-100 calcitonin-related polypeptide alpha Rattus norvegicus 116-120 15197140-8 2004 CIMT regression, defined as a decrease of >0.020 mm, was observed in 52% of diabetics receiving repaglinide and in 18% of those receiving glyburide (P<0.01). Glyburide 141-150 CIMT Homo sapiens 0-4 15197140-9 2004 Interleukin-6 (P=0.04) and C-reactive protein (P=0.02) decreased more in the repaglinide group than in the glyburide group. Glyburide 107-116 interleukin 6 Homo sapiens 0-13 15366420-0 2004 Steady-state interactions of glibenclamide with CFTR: evidence for multiple sites in the pore. Glyburide 29-42 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 48-52 15215655-1 2004 The effects of orally administered dipeptidyl peptidase IV (DPP-IV) inhibitor on the glucose-lowering effect of glibenclamide are still unknown. Glyburide 112-125 dipeptidylpeptidase 4 Rattus norvegicus 35-58 15215655-1 2004 The effects of orally administered dipeptidyl peptidase IV (DPP-IV) inhibitor on the glucose-lowering effect of glibenclamide are still unknown. Glyburide 112-125 dipeptidylpeptidase 4 Rattus norvegicus 60-66 15020588-7 2004 Smooth muscle CFTR possesses all of the pharmacological attributes of its epithelial homologues: stimulation by the CFTR pharmacological activators MPB-07 (EC(50) = 158 microm) and MPB-91 (EC(50) = 20 microm) and inhibition by glibenclamide and diphenylamine-2-carboxylic acid but not by 5,11,17,23-tetrasulfonato-25,26,27,28-tetramethoxy-calix[4]arene. Glyburide 227-240 CF transmembrane conductance regulator Rattus norvegicus 14-18 15020588-7 2004 Smooth muscle CFTR possesses all of the pharmacological attributes of its epithelial homologues: stimulation by the CFTR pharmacological activators MPB-07 (EC(50) = 158 microm) and MPB-91 (EC(50) = 20 microm) and inhibition by glibenclamide and diphenylamine-2-carboxylic acid but not by 5,11,17,23-tetrasulfonato-25,26,27,28-tetramethoxy-calix[4]arene. Glyburide 227-240 CF transmembrane conductance regulator Rattus norvegicus 116-120 14736703-8 2004 The hypersensitivity to ACh was reproduced in control islets by depolarization with the SUR1 inhibitor glyburide. Glyburide 103-112 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 88-92 15133754-5 2004 Fasting insulin was not significantly increased by any treatment; 24-h insulin was not increased by glipizide GITS AM, but was elevated by glipizide GITS PM (39%, p < 0.05) and glibenclamide (23%, p < 0.05). Glyburide 180-193 insulin Homo sapiens 71-78 15133755-6 2004 RESULTS: Neutrophil-transendothelial migration and PECAM-1 expression were enhanced by insulin (100 micro U/mL, 24 h) and were attenuated by gliclazide (20 micro M), but not by other K(ATP) channel blockers (glibenclamide, nateglinide, and glimepiride). Glyburide 208-221 insulin Homo sapiens 87-94 15102890-0 2004 Cross-inhibition of SR-BI- and ABCA1-mediated cholesterol transport by the small molecules BLT-4 and glyburide. Glyburide 101-110 scavenger receptor class B member 1 Homo sapiens 20-25 15102890-0 2004 Cross-inhibition of SR-BI- and ABCA1-mediated cholesterol transport by the small molecules BLT-4 and glyburide. Glyburide 101-110 ATP binding cassette subfamily A member 1 Homo sapiens 31-36 15102890-4 2004 The activities of ABCA1 and other ATP binding cassette superfamily members are inhibited by the drug glyburide, and SR-BI-mediated lipid transport is blocked by small molecule inhibitors called BLTs. Glyburide 101-110 ATP binding cassette subfamily A member 1 Homo sapiens 18-23 15102890-6 2004 Reciprocally, glyburide blocked SR-BI-mediated selective lipid uptake and efflux at a potency similar to that for its inhibition of ABCA1 (IC(50) approximately 275-300 microM). Glyburide 14-23 scavenger receptor class B member 1 Homo sapiens 32-37 15102890-7 2004 As is the case with BLTs, glyburide increased the apparent affinity of HDL binding to SR-BI. Glyburide 26-35 scavenger receptor class B member 1 Homo sapiens 86-91 15102890-8 2004 The reciprocal inhibition of SR-BI and ABCA1 by BLT-4 and glyburide raises the possibility that these proteins may share similar or common steps in their mechanisms of lipid transport. Glyburide 58-67 scavenger receptor class B member 1 Homo sapiens 29-34 15102890-8 2004 The reciprocal inhibition of SR-BI and ABCA1 by BLT-4 and glyburide raises the possibility that these proteins may share similar or common steps in their mechanisms of lipid transport. Glyburide 58-67 ATP binding cassette subfamily A member 1 Homo sapiens 39-44 15088102-8 2004 The cardioprotective effects of erythropoietin were abolished by the protein kinase inhibitors SB203580 (p38 MAP kinase), PD98059 (p42/44 MAP kinase) and chelerythrine (PKC) as well as the potassium channel blockers glibenclamide, HMR 1098, 5-HD and Paxilline. Glyburide 216-229 erythropoietin Oryctolagus cuniculus 32-46 15366420-1 2004 The objective of the present study was to clarify the mechanism by which the sulfonylurea drug, glibenclamide, inhibits single CFTR channels in excised patches from Xenopus oocytes. Glyburide 96-109 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 127-131 15366420-9 2004 These results indicate that glibenclamide interacts with open CFTR channels in a complex manner, involving interactions with multiple binding sites in the channel pore. Glyburide 28-41 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 62-66 15370958-0 2004 Identification and relative contributions of human cytochrome P450 isoforms involved in the metabolism of glibenclamide and lansoprazole: evaluation of an approach based on the in vitro substrate disappearance rate. Glyburide 106-119 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 51-66 14978203-7 2004 The I(Cl,ATP) persistently activated by GTPgammaS, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pharmacological properties of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels. Glyburide 68-81 cystic fibrosis transmembrane conductance regulator Mus musculus 151-202 14978203-7 2004 The I(Cl,ATP) persistently activated by GTPgammaS, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pharmacological properties of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels. Glyburide 68-81 cystic fibrosis transmembrane conductance regulator Mus musculus 204-208 15370958-2 2004 The identification and relative contributions of human cytochrome P450 (CYP) enzymes involved in the metabolism of glibenclamide and lansoprazole in human liver microsomes were investigated using an approach based on the in vitro disappearance rate of unchanged drug. Glyburide 115-128 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 55-70 15370958-2 2004 The identification and relative contributions of human cytochrome P450 (CYP) enzymes involved in the metabolism of glibenclamide and lansoprazole in human liver microsomes were investigated using an approach based on the in vitro disappearance rate of unchanged drug. Glyburide 115-128 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 72-75 15370958-5 2004 When the contribution of CYPs to the intrinsic clearance (CL(int)) of drugs in pooled human microsomes was estimated by relative activity factors, contributions of CYP2C19 and CYP3A4 were determined to be 4.6 and 96.4% for glibenclamide, and 75.1 and 35.6% for lansoprazole, respectively. Glyburide 223-236 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 164-171 15370958-10 2004 The results suggest that glibenclamide is mainly metabolized by CYP3A4, whereas lansoprazole is metabolized by both CYP2C19 and CYP3A4 in human liver microsomes. Glyburide 25-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 15006554-10 2004 By contrast, annexin 1 secretion is not blocked by other inhibitors of MRP1 (indomethacin, MK571), MRP2 (ochratoxin A1 or MK571), MRP5 (trequinsin or sulfinpyrazone) or by verapamil, cyclosporin A or glyburide. Glyburide 200-209 annexin A1 Rattus norvegicus 13-22 14672537-5 2004 ATP- and glibenclamide-sensitive K+ currents were decreased in HEK-293 cells expressing full-length Kir6 and SUR2 subunits that were transiently transfected with fragments rSUR2A-CTA, rSUR2A-CTC and rSUR2A-CTE (residues 1294-1359) compared with fragment rSUR2A-CTD or mock-transfected cells, suggesting either channel inhibition or a reduction in the number of functional KATP channels at the cell surface. Glyburide 9-22 ATP binding cassette subfamily C member 9 Homo sapiens 109-113 12947021-6 2004 The hIK-1-mediated ATP release was inhibited by a hIK-1 blocker (charybdotoxin), and an Na(+)-K(+)-2Cl(-) cotransport blocker (bumetanide) without interruption by GdCl(3), an inhibitor of stretch-activated nonselective cation (SA) channels, or glybenclamide, a blocker of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 244-257 potassium calcium-activated channel subfamily N member 4 Homo sapiens 4-9 14592811-6 2004 Preincubation of the soleus muscle with glibenclamide (a KATP channel inhibitor) prevented the NKCC activation by hyperosmolarity, PKA inhibition, pinacidil, and glycolysis inhibitors. Glyburide 40-53 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 131-134 15139508-4 2004 Glibenclamide (1 microM) attenuated the relaxations to VIP, nitroglycerin, or 8-bromo cGMP. Glyburide 0-13 VIP peptides Oryctolagus cuniculus 55-58 15096910-5 2004 To investigate the part played by cholinergic systems in the effects of a K(ATP) antagonist (glibenclamide) on morphine St-D, we administered low doses of atropine before glibenclamide administration. Glyburide 93-106 TATA box binding protein-like 1 Mus musculus 120-124 14746575-5 2004 RESULTS: Mean peak serum insulin levels were lower after nateglinide (115 mU/l) than after glibenclamide (145 mU/l.h; p = 0.017) but higher than after placebo (79 mU/l; p = 0.001). Glyburide 91-104 insulin Homo sapiens 25-32 14746575-7 2004 Total insulin exposure over the day was higher after glibenclamide compared with that following nateglinide (1216 vs. 1067 mU/l.h; p = 0.009). Glyburide 53-66 insulin Homo sapiens 6-13 15139508-5 2004 In the presence of tetrodotoxin (TTX), glibenclamide attenuated relaxations to VIP without effect on those to nitroglycerin. Glyburide 39-52 VIP peptides Oryctolagus cuniculus 79-82 14686960-1 2004 AIM: The aim of this study was to compare the effects of glimepiride and glibenclamide on tumour necrosis factor (TNF)-alpha expression and adipocyte cellularity in spontaneously diabetic, obese rats. Glyburide 73-86 tumor necrosis factor Rattus norvegicus 90-124 14725963-0 2004 Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker. Glyburide 141-154 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-68 14725963-2 2004 Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning. Glyburide 97-110 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 38-43 14725963-2 2004 Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning. Glyburide 97-110 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 53-58 14725963-8 2004 However, the level of c-Fos and c-Jun expression in the group administered glibenclamide after EA was significantly lower than in the glibenclamide group (P< or =0.05). Glyburide 75-88 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 22-27 14744818-7 2004 We found that VIP (EC(50) approximately 7.6 nM) and PACAP-27 (EC(50) approximately 10 nM) stimulated glibenclamide-sensitive and DIDS-insensitive iodide efflux in Calu-3 cells. Glyburide 101-114 vasoactive intestinal peptide Homo sapiens 14-17 14684361-5 2004 Furthermore, CGRP-induced relaxation of placental vessels are inhibited by a CGRP receptor antagonist (CGRP8-37), ATP-sensitive potassium (KATP) channel blocker (glybenclamide), and cAMP-dependent protein kinase A inhibitor (Rp-cAMPS) and partially inhibited by a nitric oxide inhibitor (Nomega-nitro-l-arginine methyl ester). Glyburide 162-175 calcitonin related polypeptide alpha Homo sapiens 13-17 14686960-3 2004 RESULTS: TNF-alpha mRNA expression in retroperitoneal fat tissue was significantly greater in the glibenclamide group (2.2 +/- 1.1), compared with the control group (0.9 +/- 0.4; p<0.05) or the glimepiride group (0.9 +/- 0.2; p<0.01). Glyburide 98-111 tumor necrosis factor Rattus norvegicus 9-18 14686960-8 2004 CONCLUSIONS: This study suggests that although both glibenclamide and glimepiride may have a hypertrophisizing effect on fat cells in adipose tissues, this effect is greater with glibenclamide, leading to augmentation of TNF-alpha mRNA expression and possible exacerbation of insulin resistance. Glyburide 52-65 tumor necrosis factor Rattus norvegicus 221-230 15230625-4 2004 OBJECTIVE: To evaluate the effect of glibenclamide on the activities of antioxidant enzymes (CAT and SOD) in liver and kidney tissue of diabetic rats. Glyburide 37-50 catalase Rattus norvegicus 93-96 15230625-13 2004 CONCLUSION: Administration of glibenclamide to diabetic rats reversed diabetes-induced changes, suggesting that glibenclamide may directly increase liver CAT and SOD activity. Glyburide 30-43 catalase Rattus norvegicus 154-157 15230625-13 2004 CONCLUSION: Administration of glibenclamide to diabetic rats reversed diabetes-induced changes, suggesting that glibenclamide may directly increase liver CAT and SOD activity. Glyburide 112-125 catalase Rattus norvegicus 154-157 15230648-14 2004 The reference compound glibenclamide increased insulin and decreased glucose levels as expected. Glyburide 23-36 insulin Homo sapiens 47-54 14715864-0 2004 The insulin secretagogues glibenclamide and repaglinide do not influence growth hormone secretion in humans but stimulate glucagon secretion during profound insulin deficiency. Glyburide 26-39 insulin Homo sapiens 4-11 14709397-7 2004 RESULTS: Both neutrophil adhesion and ICAM-1 expression enhanced by high insulin (100 microU/ml, 48 h) were attenuated by gliclazide (20 microM), but not by other K(ATP) channel blockers (glibenclamide, nateglinide, and glimepiride). Glyburide 188-201 insulin Homo sapiens 73-80 14676579-5 2004 In addition, the channel was found to be regulated in a manner identical to that of SUR1-regulated KATP channels, including high affinity block by glybenclamide and tolbutamide, and opening by diazoxide. Glyburide 147-160 ATP binding cassette subfamily C member 8 Homo sapiens 84-88 14660039-4 2003 Interleukin-18 liberation was likewise inhibited by glyburide, a modulator of ion transport and inhibitor of ATP-binding cassette transporter 1. Glyburide 52-61 interleukin 18 Homo sapiens 0-14 14684837-7 2004 The root growth of the wild-type plant grown in Murashige and Skoog medium supplemented with the MRP inhibitor glibenclamide and NaCl was inhibited to a very similar extent as the root growth of atmrp5-2 grown in NaCl alone. Glyburide 111-124 multidrug resistance-associated protein 5 Arabidopsis thaliana 195-201 14660039-0 2003 Inhibition of lipopolysaccharide/ATP-induced release of interleukin-18 by KN-62 and glyburide. Glyburide 84-93 interleukin 18 Homo sapiens 56-70 14660039-5 2003 The data presented herein indicate that by pharmacologically interfering with the process of cytokine secretion agents such as KN-62 or glyburide have the potential to curb overproduction of interleukin-18 in septic patients. Glyburide 136-145 interleukin 18 Homo sapiens 191-205 12920163-1 2003 The inhibitory effect of glyburide [International Nonproprietary Name (INN), glibenclamide] on CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was evaluated using pooled human liver microsomes. Glyburide 25-34 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 95-101 14600501-6 2003 Glutamate-stimulated ATP release was decreased by inhibition of anion transporter inhibitors by furosemide, cystic fibrosis transmembrane conductance regulator by glibenclamide and exocytosis by botulinum toxin A, indicating that anion transporters and exocytosis provide the main secretion mechanisms for ATP release from the Schwann cells. Glyburide 163-176 CF transmembrane conductance regulator Rattus norvegicus 108-159 12855600-11 2003 CGRP-induced vasorelaxation was significantly (P < 0.05) attenuated by potassium channel blockers KATP (glybenclamide, 10(-5) M) and K(CA) (tetraethylammonium, 10(-3) M). Glyburide 107-120 calcitonin-related polypeptide alpha Rattus norvegicus 0-4 15260389-12 2003 CONCLUSIONS: With proper patient selection, pioglitazone with glibenclamide and metformin can be safely used in patients receiving insulin with good results. Glyburide 62-75 insulin Homo sapiens 131-138 14596908-4 2003 Glibenclamide also inhibits the cystic fibrosis transmembrane conductance regulator, p-glycoprotein in animals and guard cell ion channels in plants. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 32-83 14596908-4 2003 Glibenclamide also inhibits the cystic fibrosis transmembrane conductance regulator, p-glycoprotein in animals and guard cell ion channels in plants. Glyburide 0-13 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 14565810-11 2003 However, the daily insulin dose alone was significantly lower (p < 0.05) with glimepiride (0.49 +/- 0.10; mean +/- SE) than with other sulfonylureas (tolazamide 0.58 +/- 0.12, glyburide 0.59 +/- 0.12, glipizide GITS 0.59 +/- 0.14). Glyburide 179-188 insulin Homo sapiens 19-26 15260389-0 2003 Beneficial effects of triple drug combination of pioglitazone with glibenclamide and metformin in type 2 diabetes mellitus patients on insulin therapy. Glyburide 67-80 insulin Homo sapiens 135-142 15000437-0 2003 The combination metformin/glyburide exerts its hypoglycemic effect mainly by increasing insulin secretion: a controlled, randomized, double-blind, crossover study. Glyburide 26-35 insulin Homo sapiens 88-95 15000437-11 2003 Increased insulin secretion was the explanation for the additive effects of the combination (percentual change in acute insulin response during the minimal model = 5.8 vs 51.5 vs 88.2% for metformin, glyburide and the combination, p < 0.05). Glyburide 200-209 insulin Homo sapiens 10-17 15000437-13 2003 In conclusion, the additive hypoglycemic effects of the combination glyburide/metformin was caused by increased insulin secretion. Glyburide 68-77 insulin Homo sapiens 112-119 12913062-3 2003 The enhanced ET-1 hypotensive effect in L-NAME-treated rats was abolished by the ETB receptor antagonist BQ-788 but was unaltered by the cyclooxygenase inhibitor diclofenac, the cytochrome P450 inhibitor fluconazole, or the potassium channel blockers apamin, glibenclamide, tetraethylammonium, and 4-aminopyridine. Glyburide 259-272 endothelin 1 Rattus norvegicus 13-17 14975182-7 2003 Whole-cell recordings showed that the cardiomyocytes responded to cAMP with an activation of time- and voltage-independent currents that contained an anion-selective component sensitive to CFTR Cl(-) channel blockers (NPPB and glibenclamide) but not to a stilbene-derivative conventional Cl(-) channel blocker (SITS). Glyburide 227-240 CF transmembrane conductance regulator Rattus norvegicus 189-193 14619572-5 2003 RESULTS: At each time-point of reoxygenation, the expression of HSP70 in sevoflurane preconditioning group was significantly higher than that of normal control, anoxia/reoxygenation, glyburide and glyburide plus sevoflurane groups (P < 0.01). Glyburide 183-192 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 64-69 14619572-5 2003 RESULTS: At each time-point of reoxygenation, the expression of HSP70 in sevoflurane preconditioning group was significantly higher than that of normal control, anoxia/reoxygenation, glyburide and glyburide plus sevoflurane groups (P < 0.01). Glyburide 197-206 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 64-69 12965208-4 2003 Glyburide and probenicide but not other typical inhibitors of non-classical protein export strongly block MIF secretion, indicating that the export pathway of MIF involves an ABCA1 transporter. Glyburide 0-9 macrophage migration inhibitory factor Homo sapiens 106-109 12965208-4 2003 Glyburide and probenicide but not other typical inhibitors of non-classical protein export strongly block MIF secretion, indicating that the export pathway of MIF involves an ABCA1 transporter. Glyburide 0-9 macrophage migration inhibitory factor Homo sapiens 159-162 12965208-4 2003 Glyburide and probenicide but not other typical inhibitors of non-classical protein export strongly block MIF secretion, indicating that the export pathway of MIF involves an ABCA1 transporter. Glyburide 0-9 ATP binding cassette subfamily A member 1 Homo sapiens 175-180 12970093-10 2003 The hyperpolarization produced by capsaicin and CGRP was blocked by glibenclamide (10 microm) but was not changed by the CGRP antagonist, CGRP8-37 (0.5 microm). Glyburide 68-81 calcitonin-related polypeptide alpha Rattus norvegicus 48-52 12920163-1 2003 The inhibitory effect of glyburide [International Nonproprietary Name (INN), glibenclamide] on CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was evaluated using pooled human liver microsomes. Glyburide 25-34 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 103-109 12920163-1 2003 The inhibitory effect of glyburide [International Nonproprietary Name (INN), glibenclamide] on CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was evaluated using pooled human liver microsomes. Glyburide 25-34 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 111-117 12920163-1 2003 The inhibitory effect of glyburide [International Nonproprietary Name (INN), glibenclamide] on CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was evaluated using pooled human liver microsomes. Glyburide 25-34 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 128-134 12920163-2 2003 Glyburide strongly inhibited CYP2C9-catalyzed S-warfarin and phenytoin metabolism in a competitive manner, with Ki (IC50) values of 2.4 (11.3) microM and 3.1 (9.4) microM, respectively. Glyburide 0-9 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 29-35 12920163-3 2003 CYP3A4-catalyzed midazolam 1-hydroxylation was inhibited by glyburide with a Ki (IC50) value of 42.5 (90.0) microM. Glyburide 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 12920163-5 2003 In summary, glyburide showed potent inhibition on CYP2C9 and weak inhibition on CYP3A4, whereas it had minimal or no inhibitory effect on the other cytochromes p450 examined. Glyburide 12-21 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 50-56 12920163-5 2003 In summary, glyburide showed potent inhibition on CYP2C9 and weak inhibition on CYP3A4, whereas it had minimal or no inhibitory effect on the other cytochromes p450 examined. Glyburide 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 12920163-6 2003 It is anticipated that clinically significant drug-drug interactions will ensue when glyburide is coadministered with agents that are cleared primarily by the CYP2C9-mediated pathway and those with narrow therapeutic ranges. Glyburide 85-94 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 159-165 12958175-7 2003 Using radioimmunoassay techniques, we report that exposure of the cells to tolbutamide (100 microM) resulted in an increase in insulin secretion from 0.3 +/- 0.05 to 1.8 +/- 0.2 pmol insulin/10(6) cells and glibenclamide (20 microM) from 0.4 +/- 0.06 to 2.1 +/- 0.3 (n=4), similar to what is seen on glucose (20 mM) stimulation. Glyburide 207-220 insulin Homo sapiens 127-134 12958175-12 2003 Furthermore, glibenclamide (20 microM) also stimulated the release of insulin from fluorescently labeled secretion granules, and diazoxide (150 microM) blocked that stimulated release of insulin. Glyburide 13-26 insulin Homo sapiens 70-77 12684219-0 2003 Glibenclamide inhibits islet carnitine palmitoyltransferase 1 activity, leading to PKC-dependent insulin exocytosis. Glyburide 0-13 carnitine palmitoyltransferase 1A Homo sapiens 29-61 12684219-4 2003 However, recent reports show that >90% of glibenclamide-binding sites are localized intracellularly and that the drug can stimulate insulin release independently of changes in KATP channels and cytoplasmic free Ca2+. Glyburide 45-58 insulin Homo sapiens 135-142 12684219-5 2003 Also, glibenclamide specifically and progressively accumulates in islets in association with secretory granules and mitochondria and causes long-lasting insulin secretion. Glyburide 6-19 insulin Homo sapiens 153-160 12684219-7 2003 We show that glibenclamide dose-dependently inhibits beta-cell CPT-1 activity, consequently suppressing FA oxidation to the same extent as glucose in cultured fetal rat islets. Glyburide 13-26 carnitine palmitoyltransferase 1A Homo sapiens 63-68 12684219-10 2003 We propose a mechanism in which inhibition of CPT-1 activity by glibenclamide switches beta-cell FA metabolism to DAG synthesis and subsequent PKC-dependent and KATP-independent insulin exocytosis. Glyburide 64-77 carnitine palmitoyltransferase 1A Homo sapiens 46-51 12684219-11 2003 We suggest that chronic CPT inhibition, through the progressive islet accumulation of glibenclamide, may explain the prolonged stimulation of insulin secretion in some diabetic patients even after drug removal that contributes to the sustained hypoglycemia of the sulfonylurea. Glyburide 86-99 insulin Homo sapiens 142-149 12842835-5 2003 This cAMP-activated channel had a Pgluconate/PCl or PF/PCl perm-selectivity ratio of 0.35 and 0.30, respectively, and was inhibited by the CFTR blocker glibenclamide and the anti-CFTR antibody MAb 13-1, when added to the cytoplasmatic side of the patch. Glyburide 152-165 CF transmembrane conductance regulator Homo sapiens 139-143 12842835-5 2003 This cAMP-activated channel had a Pgluconate/PCl or PF/PCl perm-selectivity ratio of 0.35 and 0.30, respectively, and was inhibited by the CFTR blocker glibenclamide and the anti-CFTR antibody MAb 13-1, when added to the cytoplasmatic side of the patch. Glyburide 152-165 CF transmembrane conductance regulator Homo sapiens 179-183 12907241-7 2003 MPB-91, but not MPB-07, was able to displace binding of glibenclamide to HEK cells expressing recombinant SUR1/Kir6.2 channels. Glyburide 56-69 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 106-110 12907241-7 2003 MPB-91, but not MPB-07, was able to displace binding of glibenclamide to HEK cells expressing recombinant SUR1/Kir6.2 channels. Glyburide 56-69 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 111-117 12934053-12 2003 The increased currents by SIN-1 were inhibited by glibenclamide (10 microM). Glyburide 50-63 MAPK associated protein 1 Homo sapiens 26-31 12882841-5 2003 RESULTS: After 1 year the glucagon-stimulated C-peptide response was increased in the insulin-treated group by 0.14 +/- 0.08 nmol/l, whereas it was decreased by 0.12 +/- 0.08 nmol/l in the glibenclamide group, P < 0.02 for difference between groups. Glyburide 189-202 insulin Homo sapiens 86-93 12882841-6 2003 After 2 years, fasting insulin levels were higher after treatment withdrawal in the insulin-treated versus the glibenclamide-treated group (P = 0.02). Glyburide 111-124 insulin Homo sapiens 23-30 12877648-2 2003 A new single-tablet of glyburide/metformin combination therapy (Glucovance), Bristol-Myers Squibb, Inc.) has recently been developed, which addresses the primary defects of Type 2 diabetes: beta-cell dysfunction and insulin resistance. Glyburide 23-32 insulin Homo sapiens 216-223 12766083-9 2003 These actions of BK and diazoxide were inhibited by the coapplication of 5HD and glibenclamide. Glyburide 81-94 kininogen 1 Homo sapiens 17-19 12754259-7 2003 Pharmacological analysis showed TRESK to be inhibited by previously reported K+ channel inhibitors Ba2+, propafenone, glyburide, lidocaine, quinine, quinidine, and triethanolamine. Glyburide 118-127 potassium two pore domain channel subfamily K member 18 Homo sapiens 32-37 14502435-9 2003 The inhibitory profile of G551D-CFTR channel activity was similar to that of wild type, i.e., inhibition by glibenclamide (100 microM) and DPC (250 microM) but not by DIDS (200 microM) nor calixarene (100 nM). Glyburide 108-121 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 32-36 12795658-12 2003 While in the group of patients only taking glibenclamide plus placebo the NF-kappaB binding activity did not change significantly (p = 0.58), the NF-kappaB binding activity in the group of patients taking glimepiride was reduced from 19.3 relative NF-kappaB-p65-equivalents to 15.5 relative NF-kappaB-p65-equivalents (p = 0.04). Glyburide 43-56 nuclear factor kappa B subunit 1 Homo sapiens 74-83 12521930-7 2003 Protection afforded by BNP was abolished by glibenclamide or 5-HD but not by HMR-1098, suggesting the involvement of putative mitochondrial but not sarcolemmal K(ATP) channel opening. Glyburide 44-57 natriuretic peptide B Rattus norvegicus 23-26 12505864-6 2003 The PTH response was nearly abolished by apical addition of 100 microM EIPA, an inhibitor of Na(+)/H(+) exchangers, and partially blocked by the Cl(-) channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 100 microM) and glibenclamide (300 microM). Glyburide 235-248 parathyroid hormone Gallus gallus 4-7 12803833-0 2003 Urinary PC-1 and N-acetyl-beta-D-glucosaminidase activity in patients with type 2 diabetes treated with metformin, gliclazide or glibenclamide. Glyburide 129-142 polycystin 1, transient receptor potential channel interacting Homo sapiens 8-12 12803833-0 2003 Urinary PC-1 and N-acetyl-beta-D-glucosaminidase activity in patients with type 2 diabetes treated with metformin, gliclazide or glibenclamide. Glyburide 129-142 O-GlcNAcase Homo sapiens 17-48 12803833-3 2003 METHODS: Urinary excretion of PC-1 was determined in 45 newly detected, obese diabetic patients treated with metformin (16 patients), gliclazide (14 patients) or glibenclamide (15 patients). Glyburide 162-175 polycystin 1, transient receptor potential channel interacting Homo sapiens 30-34 12803833-9 2003 However, glibenclamide treatment produced an increased urinary NAGA excretion in the whole group, and in about twice as many patients as in the pre-treatment period. Glyburide 9-22 O-GlcNAcase Homo sapiens 63-67 12663469-6 2003 Elevation of [Ca(2+)](i) by glyburide potentiated Erk-1/2 phosphorylation, which was also inhibited by H89, suggesting increased [Ca(2+)](i) preceded PKA for glucose-induced Erk-1/2 activation. Glyburide 28-37 mitogen activated protein kinase 3 Rattus norvegicus 50-57 12795025-4 2003 Among insulin secretizers repaglinid, glibenclamid and glipizide have an ATP-sensitive potassium channel inhibiting effect in the vascular smooth muscle cells, too, reducing hereby vasodilation. Glyburide 38-50 insulin Homo sapiens 6-13 12663469-6 2003 Elevation of [Ca(2+)](i) by glyburide potentiated Erk-1/2 phosphorylation, which was also inhibited by H89, suggesting increased [Ca(2+)](i) preceded PKA for glucose-induced Erk-1/2 activation. Glyburide 28-37 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 150-153 12663469-6 2003 Elevation of [Ca(2+)](i) by glyburide potentiated Erk-1/2 phosphorylation, which was also inhibited by H89, suggesting increased [Ca(2+)](i) preceded PKA for glucose-induced Erk-1/2 activation. Glyburide 28-37 mitogen activated protein kinase 1 Rattus norvegicus 174-181 12589230-3 2003 Patients on monotherapy might benefit from a combination agent such as glyburide/metformin, which increases insulin secretion and reduces insulin resistance. Glyburide 71-80 insulin Homo sapiens 108-115 12721499-1 2003 The objective of this study was to examine the effect of the antihyperglycemic agents metformin (insulin sensitizer) and glibenclamide (insulin secretory agent) on the serum level of C-reactive protein (CRP) in well-controlled type 2 diabetics with metabolic syndrome. Glyburide 121-134 C-reactive protein Homo sapiens 183-201 12721499-1 2003 The objective of this study was to examine the effect of the antihyperglycemic agents metformin (insulin sensitizer) and glibenclamide (insulin secretory agent) on the serum level of C-reactive protein (CRP) in well-controlled type 2 diabetics with metabolic syndrome. Glyburide 121-134 C-reactive protein Homo sapiens 203-206 12746761-7 2003 LP versus GB induced changes from baseline to endpoint in fasting C-peptide (nmol/L), proinsulin and insulin levels (pmol/L) were - 0.2 +/- 0.4 versus - 0.1 +/- 0.6 (p = 0.04), - 11.2 +/- 26.0 versus - 1.1 +/- 17.3 (p = 0.03), and - 27.8 +/- 147.4 versus + 32.6 +/- 286.2 (not significant), respectively. Glyburide 10-12 insulin Homo sapiens 86-96 12746761-7 2003 LP versus GB induced changes from baseline to endpoint in fasting C-peptide (nmol/L), proinsulin and insulin levels (pmol/L) were - 0.2 +/- 0.4 versus - 0.1 +/- 0.6 (p = 0.04), - 11.2 +/- 26.0 versus - 1.1 +/- 17.3 (p = 0.03), and - 27.8 +/- 147.4 versus + 32.6 +/- 286.2 (not significant), respectively. Glyburide 10-12 insulin Homo sapiens 89-96 12746761-8 2003 HbA 1c at baseline was 7.5 +/- 1.0 % for LP and 7.7 +/- 1.2 % for GB and did not change significantly in either group during the investigation. Glyburide 66-68 hemoglobin subunit alpha 1 Homo sapiens 0-5 12679437-6 2003 Leptin normalized to percent fat was increased by 25% (P < 0.01) as a result of glyburide therapy compared with pretreatment values, but was unchanged by therapy with metformin. Glyburide 83-92 leptin Homo sapiens 0-6 12679437-6 2003 Leptin normalized to percent fat was increased by 25% (P < 0.01) as a result of glyburide therapy compared with pretreatment values, but was unchanged by therapy with metformin. Glyburide 83-92 FAT atypical cadherin 1 Homo sapiens 29-32 12606519-4 2003 The fluorescent glibenclamides colocalize with Ins-C-GFP, a live-cell fluorescent reporter of insulin granules. Glyburide 16-30 insulin Homo sapiens 94-101 12586783-5 2003 Glucocorticoid-induced externalization of ANXA1 from an FS cell line (TtT/GF) and rat anterior pituitary was blocked by glyburide, which inhibits ABC transporters. Glyburide 120-129 annexin A1 Rattus norvegicus 42-47 12586783-6 2003 Glyburide also blocked the glucocorticoid inhibition of forskolin-stimulated ACTH release from pituitary tissue in vitro. Glyburide 0-9 pro-opiomelanocortin-alpha Mus musculus 77-81 12496311-7 2003 The F1388L-SUR1 channel has increased sensitivity to MgADP and metabolic inhibition, decreased sensitivity to glibenclamide, and responds to both diazoxide and pinacidil. Glyburide 110-123 ATP binding cassette subfamily C member 8 Homo sapiens 11-15 12540608-12 2003 A consequence of this is a conformational change in SUR to increase the SUR/glybenclamide binding affinity. Glyburide 76-89 ATP binding cassette subfamily C member 8 Rattus norvegicus 52-55 12540608-12 2003 A consequence of this is a conformational change in SUR to increase the SUR/glybenclamide binding affinity. Glyburide 76-89 ATP binding cassette subfamily C member 8 Rattus norvegicus 72-75 12803736-8 2003 Metformin (an insulin sensitiser) and glibenclamide (an insulin secretagogue) are well supported by decades of clinical evidence, and the pharmacokinetics of these agents support twice-daily co-administration. Glyburide 38-51 insulin Homo sapiens 56-63 12502786-3 2003 beta(2)AR stimulation increases CFTR activity, in airway epithelial cells, that is glybenclamide sensitive. Glyburide 83-96 adrenoceptor beta 2 Homo sapiens 0-9 12502786-3 2003 beta(2)AR stimulation increases CFTR activity, in airway epithelial cells, that is glybenclamide sensitive. Glyburide 83-96 CF transmembrane conductance regulator Homo sapiens 32-36 12604391-3 2003 The present observation reports on a type 2 diabete mellitus patient presenting with a coma while the patient was on metformin and glibenclamide treatment. Glyburide 131-144 COMA Homo sapiens 87-91 12475773-0 2002 Decreased glibenclamide uptake in hepatocytes of hepatocyte nuclear factor-1alpha-deficient mice: a mechanism for hypersensitivity to sulfonylurea therapy in patients with maturity-onset diabetes of the young, type 3 (MODY3). Glyburide 10-23 HNF1 homeobox A Mus musculus 49-81 12542723-0 2003 Influence of treatment with acarbose or glibenclamide on insulin sensitivity in type 2 diabetic patients. Glyburide 40-53 insulin Homo sapiens 57-64 12542723-1 2003 AIM: The aim of our double-blind, placebo-controlled study was to compare the effect of acarbose and glibenclamide on the insulin sensitivity in type 2 diabetes. Glyburide 101-114 insulin Homo sapiens 122-129 12542723-11 2003 The fasting insulin levels remained unchanged in all three groups, whereas postprandial insulin values increased significantly under glibenclamide. Glyburide 133-146 insulin Homo sapiens 88-95 12475773-0 2002 Decreased glibenclamide uptake in hepatocytes of hepatocyte nuclear factor-1alpha-deficient mice: a mechanism for hypersensitivity to sulfonylurea therapy in patients with maturity-onset diabetes of the young, type 3 (MODY3). Glyburide 10-23 HNF1 homeobox A Homo sapiens 218-223 12475773-4 2002 We show that despite a profound defect in glucose-stimulated insulin secretion, diabetic Hnf-1alpha(-/-) mice have a robust glibenclamide-induced insulin secretory response. Glyburide 124-137 HNF1 homeobox A Mus musculus 89-99 12475773-5 2002 We demonstrate that the half-life (t(1/2)) of glibenclamide in the blood is increased in Hnf-1alpha(-/-) mice compared with wild-type littermates (3.9 +/- 1.3 vs. 1.5 +/- 1.8 min, P <or= 0.05). Glyburide 46-59 HNF1 homeobox A Mus musculus 89-99 12475773-6 2002 The clearance of glibenclamide from the blood during the first hours after intravenous administration was reduced approximately fourfold in Hnf-1alpha(-/-) mice compared with Hnf-1alpha(+/+) littermates. Glyburide 17-30 HNF1 homeobox A Mus musculus 140-150 12475773-6 2002 The clearance of glibenclamide from the blood during the first hours after intravenous administration was reduced approximately fourfold in Hnf-1alpha(-/-) mice compared with Hnf-1alpha(+/+) littermates. Glyburide 17-30 HNF1 homeobox A Mus musculus 175-185 12475773-9 2002 We found that the ratio of the concentrations of glibenclamide and its metabolites was moderately increased in livers of Hnf-1alpha(-/-) mice, suggesting that hepatic glibenclamide metabolism was not impaired in animals with Hnf-1alpha deficiency. Glyburide 49-62 HNF1 homeobox A Mus musculus 121-131 12475773-10 2002 Our data demonstrate that high serum glibenclamide concentrations and an increased t(1/2) of glibenclamide in the blood of Hnf-1alpha(-/-) mice are caused by a defect in hepatic uptake of glibenclamide. Glyburide 93-106 HNF1 homeobox A Mus musculus 123-133 12475773-10 2002 Our data demonstrate that high serum glibenclamide concentrations and an increased t(1/2) of glibenclamide in the blood of Hnf-1alpha(-/-) mice are caused by a defect in hepatic uptake of glibenclamide. Glyburide 93-106 HNF1 homeobox A Mus musculus 123-133 12407077-2 2002 We explored the CFTR pore by studying voltage-dependent blockade of the channel by two organic anions: glibenclamide and isethionate. Glyburide 103-116 CF transmembrane conductance regulator Homo sapiens 16-20 12466933-7 2002 Cell proliferation of human embryonic kidney cells (HEK 293) which endogenously express Kir6.1/SUR2 mRNA was stimulated by pinacidil in a dose-dependent manner, an effect that was partially abolished by glibenclamide (3 microM). Glyburide 203-216 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 88-94 12466933-7 2002 Cell proliferation of human embryonic kidney cells (HEK 293) which endogenously express Kir6.1/SUR2 mRNA was stimulated by pinacidil in a dose-dependent manner, an effect that was partially abolished by glibenclamide (3 microM). Glyburide 203-216 ATP binding cassette subfamily C member 9 Homo sapiens 95-99 12213829-10 2002 The L0 linker has been reported to be required for glibenclamide binding, and DeltaNK(IR)6.2/SUR1 channels exhibit reduced labeling of K(IR) with (125)I-azidoglibenclamide, implying that the K(IR) N terminus and L0 of SUR1 are in proximity. Glyburide 51-64 ATP binding cassette subfamily C member 8 Homo sapiens 93-97 12213829-10 2002 The L0 linker has been reported to be required for glibenclamide binding, and DeltaNK(IR)6.2/SUR1 channels exhibit reduced labeling of K(IR) with (125)I-azidoglibenclamide, implying that the K(IR) N terminus and L0 of SUR1 are in proximity. Glyburide 51-64 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 84-89 12421535-7 2002 (ii) The other identified Cl(-) pathway of mr cells is mediated by small-conductance apical CFTR chloride channels as concluded from its activation via beta-adrenergic receptors, ion selectivity, genistein stimulation and inhibition by glibenclamide. Glyburide 236-249 CF transmembrane conductance regulator Homo sapiens 92-96 12427424-10 2002 The inhibitory effect of verapamil and K(ATP) channel inhibitors like glybenclamide on pharmacologic stress using adenosine or adenosine A(2A)-receptor agonists should be evaluated in the clinical setting to determine their potential for reducing the sensitivity of CAD detection with perfusion imaging. Glyburide 70-83 adenosine A2a receptor Canis lupus familiaris 127-151 12426217-8 2002 Maximum relaxation response to CRP (79.5+/-10%) was attenuated by KCl (2.5+/-11.5%, P<0.001), BaCl (24.5+/-7.5%, P<0.001), and tetraethylammonium chloride (34.9+/-8.25%, P<0.01) but not by glibenclamide. Glyburide 198-211 C-reactive protein Homo sapiens 31-34 12406033-7 2002 RESULTS: Both strengths of glyburide/metformin equally reduced mean HbA1c by 1.7% more than did glyburide alone (p < 0.001), and by 1.9% more than did metformin alone (p < 0.001). Glyburide 27-36 hemoglobin subunit alpha 1 Homo sapiens 68-72 12392564-3 2002 Biochemical analyses using coimmunoprecipitation indicate that SUR1 deletion mutants and Kir6.2 assemble and that a SUR1 deletion mutant binds glibenclamide with high affinity. Glyburide 143-156 ATP binding cassette subfamily C member 8 Homo sapiens 116-120 12404239-10 2002 Cyclosporin A, rifampicin, and glibenclamide were proved to be competitive inhibitors of BSEP taurocholate transport, with inhibition constant values of 9.5 micromol/L, 31 micromol/L, and 27.5 micromol/L, respectively. Glyburide 31-44 ATP binding cassette subfamily B member 11 Homo sapiens 89-93 12397031-8 2002 Glibenclamide, an inhibitor of ATP-sensitive K(+) channels and the cystic fibrosis transmembrane conductance regulator (CFTR), modestly inhibited the forskolin-stimulated current when applied to the apical surface of the monolayers, suggesting a relatively weak effect on CFTR. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 120-124 12397031-8 2002 Glibenclamide, an inhibitor of ATP-sensitive K(+) channels and the cystic fibrosis transmembrane conductance regulator (CFTR), modestly inhibited the forskolin-stimulated current when applied to the apical surface of the monolayers, suggesting a relatively weak effect on CFTR. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 272-276 12409977-5 2002 FMLP-induced increase of [Ca2+] in PMNLs was suppressed by nicorandil and diazoxide, and 5 hydroxy-decanoate and glibenclamide reversed this suppression. Glyburide 113-126 formyl peptide receptor 1 Homo sapiens 0-4 12407077-5 2002 Glibenclamide blocks CFTR from the intracellular side of the membrane with slow kinetics. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 21-25 12472202-9 2002 Possible mechanisms are discussed, including glibenclamide inhibition of the cystic fibrosis transmembrane conductance regulator. Glyburide 45-58 CF transmembrane conductance regulator Homo sapiens 77-128 12107069-8 2002 Only SUR1 and SUR1Delta17 showed high-affinity binding of glibenclamide (K(d) approximately 2 nM in the presence of 1 mM ATP) and formed functional K(ATP) channels upon coexpression with Kir6.2. Glyburide 58-71 ATP-binding cassette sub-family C member 8 Cavia porcellus 5-9 12183335-14 2002 These findings confirm that TM16-TM17 of SUR1 are important for high-affinity glibenclamide binding and that their deletion impairs trafficking of the K(ATP) channel to the surface membrane. Glyburide 78-91 ATP binding cassette subfamily C member 8 Homo sapiens 41-45 12235454-1 2002 OBJECTIVES: Our objective was to investigate the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 on the pharmacokinetics of glyburide (INN, glibenclamide) and glimepiride, two widely used sulfonylurea antidiabetic drugs. Glyburide 138-147 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-110 12235454-1 2002 OBJECTIVES: Our objective was to investigate the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 on the pharmacokinetics of glyburide (INN, glibenclamide) and glimepiride, two widely used sulfonylurea antidiabetic drugs. Glyburide 154-167 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-110 12235454-5 2002 However, in individuals heterozygous for the CYP2C9*3 allele, the median total area under the plasma concentration-time curve of glyburide (n = 2) was 280% (P < or = .05) and that of glimepiride (n = 3) was 267% (P < or = .01) of the respective values in subjects with the CYP2C9*1/*1 genotype (n = 5 and n = 12, respectively). Glyburide 129-138 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 45-51 12235454-5 2002 However, in individuals heterozygous for the CYP2C9*3 allele, the median total area under the plasma concentration-time curve of glyburide (n = 2) was 280% (P < or = .05) and that of glimepiride (n = 3) was 267% (P < or = .01) of the respective values in subjects with the CYP2C9*1/*1 genotype (n = 5 and n = 12, respectively). Glyburide 129-138 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 279-285 12235454-7 2002 CONCLUSIONS: Genetic polymorphisms of CYP2C9 markedly affect the pharmacokinetics of both glyburide and glimepiride. Glyburide 90-99 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 38-44 12235454-8 2002 The influence of the CYP2C9*3 variant allele on glyburide and glimepiride pharmacokinetics may be clinically significant. Glyburide 48-57 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 21-27 12380632-3 2002 A previous 32-week, randomized, double-blind, placebo-controlled trial found that treatment with glyburide/metformin tablets was associated with greater reductions in HbA1c values compared with glyburide monotherapy, metformin monotherapy, and placebo. Glyburide 97-106 hemoglobin subunit alpha 1 Homo sapiens 167-171 12193544-7 2002 Islets overexpressing DGAT and cultured in elevated glucose levels for 72 h had markedly impaired insulin secretion in response to glucose, but responded normally to the nonglucose secretagogues glyburide and potassium chloride. Glyburide 195-204 diacylglycerol O-acyltransferase 1 Rattus norvegicus 22-26 12202948-2 2002 Studies using mostly ex vivo systems suggested diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and glybenclamide inhibit CFTR Cl- conductance (CFTR GCl). Glyburide 138-151 CF transmembrane conductance regulator Homo sapiens 160-164 12202948-2 2002 Studies using mostly ex vivo systems suggested diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and glybenclamide inhibit CFTR Cl- conductance (CFTR GCl). Glyburide 138-151 CF transmembrane conductance regulator Homo sapiens 182-186 12202948-8 2002 At a concentration of 10(-4) M, NPPB, DPC, glybenclamide, and DIDS were equipotent and blocked approximately 50% of irreversibly phosphorylated and ATP-activated CFTR GCl (DIDS = 49 +/- 10% > NPPB = 46 +/- 10% > DPC = 38 +/- 7% > glybenclamide = 34 +/- 5%; values are mean +/- SE expressed as % inhibition from the control). Glyburide 43-56 CF transmembrane conductance regulator Homo sapiens 162-166 12050168-9 2002 The ECM-dependent activity was much reduced in the presence of glyburide, indicating participation of ABCA1 (ATP-binding cassette transporter 1) in the efflux mechanism. Glyburide 63-72 ATP binding cassette subfamily A member 1 Homo sapiens 102-107 12050168-9 2002 The ECM-dependent activity was much reduced in the presence of glyburide, indicating participation of ABCA1 (ATP-binding cassette transporter 1) in the efflux mechanism. Glyburide 63-72 ATP binding cassette subfamily A member 1 Homo sapiens 109-143 12206849-2 2002 The aim of the study was to investigate the effect of bosentan, its metabolites and glibenclamide on the activity of the pregnane X receptor, a nuclear receptor that regulates the transcription of CYP3A4. Glyburide 84-97 nuclear receptor subfamily 1 group I member 2 Homo sapiens 121-140 12206849-2 2002 The aim of the study was to investigate the effect of bosentan, its metabolites and glibenclamide on the activity of the pregnane X receptor, a nuclear receptor that regulates the transcription of CYP3A4. Glyburide 84-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 12395287-10 2002 The K+-channel blockers iberiotoxin and glibenclamide partially prevented the CGRP- or forskolin-induced vasodilations but failed to reverse these vasodilations. Glyburide 40-53 calcitonin related polypeptide alpha Homo sapiens 78-82 12145099-1 2002 1: ATP-sensitive K(+) channels are composed of pore-forming subunits Kir6.2 and of sulphonylurea receptors (SURs); the latter are the target of the hypoglycaemic sulphonylureas like glibenclamide. Glyburide 182-195 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 69-75 12145099-2 2002 Here, we report on the negative allosteric modulation by MgATP and MgADP of glibenclamide binding to SUR1 and to SUR2 mutants with high glibenclamide affinity, SUR2A(Y1206S) and SUR2B(Y1206S). Glyburide 76-89 ATP binding cassette subfamily C member 8 Homo sapiens 101-105 12145099-2 2002 Here, we report on the negative allosteric modulation by MgATP and MgADP of glibenclamide binding to SUR1 and to SUR2 mutants with high glibenclamide affinity, SUR2A(Y1206S) and SUR2B(Y1206S). Glyburide 76-89 ATP binding cassette subfamily C member 9 Homo sapiens 113-117 12145099-9 2002 6: The data show (a) that the inhibitory effects of ATP and ADP on glibenclamide binding differ from one another, (b) that they depend on the SUR subtype, and (c) that they are weakened by coexpression with Kir6.2. Glyburide 67-80 ATP binding cassette subfamily C member 8 Homo sapiens 142-145 12145099-9 2002 6: The data show (a) that the inhibitory effects of ATP and ADP on glibenclamide binding differ from one another, (b) that they depend on the SUR subtype, and (c) that they are weakened by coexpression with Kir6.2. Glyburide 67-80 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 207-213 12145099-3 2002 2: ATP, in the presence of an ATP-regenerating system to oppose hydrolysis during incubation, inhibited glibenclamide binding to SUR1 and SUR2B(Y1206S) by approximately 60%, to SUR2A(Y1206S) by 21%). Glyburide 104-117 ATP binding cassette subfamily C member 8 Homo sapiens 129-133 12145099-5 2002 3: Glibenclamide inhibition curves for ADP, performed in the presence of an ATP-consuming system to oppose ATP formation from ADP, were generally shifted rightwards and showed positive cooperativity, in particular with the SUR2(Y1206S) isoforms. Glyburide 3-16 ATP binding cassette subfamily C member 9 Homo sapiens 223-227 12145099-8 2002 5: Coexpression of SUR1 and SUR2B(Y1206S) with Kir6.2 reduced both potency and efficacy of ATP in inhibiting glibenclamide binding; this was particularly marked for Kir6.2/SUR1. Glyburide 109-122 ATP binding cassette subfamily C member 8 Homo sapiens 19-23 12145099-8 2002 5: Coexpression of SUR1 and SUR2B(Y1206S) with Kir6.2 reduced both potency and efficacy of ATP in inhibiting glibenclamide binding; this was particularly marked for Kir6.2/SUR1. Glyburide 109-122 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 47-53 12145099-8 2002 5: Coexpression of SUR1 and SUR2B(Y1206S) with Kir6.2 reduced both potency and efficacy of ATP in inhibiting glibenclamide binding; this was particularly marked for Kir6.2/SUR1. Glyburide 109-122 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 165-171 12145099-8 2002 5: Coexpression of SUR1 and SUR2B(Y1206S) with Kir6.2 reduced both potency and efficacy of ATP in inhibiting glibenclamide binding; this was particularly marked for Kir6.2/SUR1. Glyburide 109-122 ATP binding cassette subfamily C member 8 Homo sapiens 172-176 11927600-0 2002 Intrinsic sensitivity of Kir1.1 (ROMK) to glibenclamide in the absence of SUR2B. Glyburide 42-55 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 25-31 12392107-5 2002 Glibenclamide, a blocker of the cystic fibrosis transmembrane conductance regulator (CFTR), reduced the MTX-stimulated increase of Isc by 59 +/- 6%. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 32-83 12392107-5 2002 Glibenclamide, a blocker of the cystic fibrosis transmembrane conductance regulator (CFTR), reduced the MTX-stimulated increase of Isc by 59 +/- 6%. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 85-89 12091489-9 2002 Glyburide, an inhibitor of ABCA1 activity, attenuated the increase in basolateral cholesterol efflux induced by T0901317. Glyburide 0-9 ATP binding cassette subfamily A member 1 Homo sapiens 27-32 11927600-0 2002 Intrinsic sensitivity of Kir1.1 (ROMK) to glibenclamide in the absence of SUR2B. Glyburide 42-55 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 33-37 11927600-4 2002 The native channel is sensitive to inhibition by the sulfonylurea glibenclamide, and it has been proposed that an accessory protein is required to confer glibenclamide sensitivity to Kir1.1. Glyburide 66-79 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 183-189 11927600-4 2002 The native channel is sensitive to inhibition by the sulfonylurea glibenclamide, and it has been proposed that an accessory protein is required to confer glibenclamide sensitivity to Kir1.1. Glyburide 154-167 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 183-189 12173728-0 2002 The effect of combination treatment with acarbose and glibenclamide on postprandial glucose and insulin profiles: additive blood glucose lowering effect and decreased hypoglycaemia. Glyburide 54-67 insulin Homo sapiens 96-103 12044871-3 2002 Bpt1p, which is inhibited by vanadate and glibenclamide, accounts for one third of the total vacuolar transport of glutathione conjugates. Glyburide 42-55 ATP-binding cassette bilirubin transporter BPT1 Saccharomyces cerevisiae S288C 0-5 12060057-6 2002 We exemplify the method using HbA1c levels from data from patients on chlorpropamide (n = 64) or glibenclamide (n = 65) monotherapy in the Oxford cohort of the UKPDS. Glyburide 97-110 hemoglobin subunit alpha 1 Homo sapiens 30-34 12031979-10 2002 [(3)H]glibenclamide binding to membranes from HEK293 cells transfected with SUR1 was displaced by NNC 55-9216 (IC(50) = 105 micromol/l), and this effect was impaired when NBD2 of SUR1 was replaced by that of SUR2A. Glyburide 6-19 ATP binding cassette subfamily C member 8 Homo sapiens 76-80 12031979-10 2002 [(3)H]glibenclamide binding to membranes from HEK293 cells transfected with SUR1 was displaced by NNC 55-9216 (IC(50) = 105 micromol/l), and this effect was impaired when NBD2 of SUR1 was replaced by that of SUR2A. Glyburide 6-19 ATP binding cassette subfamily C member 8 Homo sapiens 179-183 11907163-12 2002 Glibenclamide also suppressed IFN-gamma-induced up-regulation of major histocompatibility complex II. Glyburide 0-13 interferon gamma Homo sapiens 30-39 11950482-8 2002 Efficacy of ANG II could be restored, when hCG was followed by glybenclamide. Glyburide 63-76 angiotensinogen Homo sapiens 12-18 12186116-12 2002 In subjects controlled on a single dose of insulin with glibenclamide it is preferable to give an evening dose rather than a morning dose. Glyburide 56-69 insulin Homo sapiens 43-50 11935401-11 2002 Inhibition of annexin 1 externalisation by glyburide suggests involvement of an ABC (ATP-binding cassette) transporter in externalisation. Glyburide 43-52 annexin A1 Homo sapiens 14-23 11935401-11 2002 Inhibition of annexin 1 externalisation by glyburide suggests involvement of an ABC (ATP-binding cassette) transporter in externalisation. Glyburide 43-52 ATP binding cassette subfamily A member 4 Homo sapiens 85-118 12023873-7 2002 We suggest that binding of glibenclamide leads to conformational changes in CL3 and CL8 leading to rearrangement of transmembrane helices. Glyburide 27-40 adhesion G protein-coupled receptor L3 Homo sapiens 76-79 11956508-9 2002 Results of in vitro experiments showed that glyburide is metabolized by cytochrome P450 (CYP) 2C9, 2C19, and 3A4. Glyburide 44-53 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 72-97 11956512-0 2002 Impact of CYP2C9 amino acid polymorphisms on glyburide kinetics and on the insulin and glucose response in healthy volunteers. Glyburide 45-54 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 10-16 11956512-2 2002 We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3). Glyburide 21-30 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 53-72 11956512-2 2002 We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3). Glyburide 21-30 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 74-80 11956512-2 2002 We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3). Glyburide 21-30 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 150-156 11956512-2 2002 We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3). Glyburide 21-30 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 150-156 11956512-8 2002 RESULTS: Pharmacokinetics of glyburide depended significantly on CYP2C9 genotypes. Glyburide 29-38 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 65-71 11956512-10 2002 Correspondingly, insulin secretion measured within 12 hours after glyburide ingestion was higher in carriers of the genotype *3/*3 compared with the other genotypes (P =.028), whereas the differences in glucose concentrations were not significant. Glyburide 66-75 insulin Homo sapiens 17-24 11956512-11 2002 CONCLUSIONS: Carriers of the CYP2C9 variant *3 had decreased oral clearances of glyburide. Glyburide 80-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 29-35 11956512-12 2002 This confirms that glyburide is metabolized by CYP2C9. Glyburide 19-28 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 47-53 11907163-4 2002 The general ABC transporter inhibitor glibenclamide suppressed both IL-12 p40 and nitric oxide production. Glyburide 38-51 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 12-15 11907163-4 2002 The general ABC transporter inhibitor glibenclamide suppressed both IL-12 p40 and nitric oxide production. Glyburide 38-51 interleukin 9 Homo sapiens 74-77 11907163-6 2002 The selective ABC1 inhibitors 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid and sulfobromophthalein mimicked the suppressive effect of glibenclamide on IL-12 p40 production. Glyburide 138-151 ATP binding cassette subfamily A member 1 Homo sapiens 14-18 11907163-6 2002 The selective ABC1 inhibitors 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid and sulfobromophthalein mimicked the suppressive effect of glibenclamide on IL-12 p40 production. Glyburide 138-151 interleukin 9 Homo sapiens 161-164 11907163-10 2002 Intracellular levels of IL-12 p40 were decreased by glibenclamide, suggesting that glibenclamide does not affect IL-12 p40 secretion. Glyburide 52-65 interleukin 9 Homo sapiens 30-33 12047399-1 2002 OBJECTIVE: To evaluate whether simultaneous initial treatment of both insulin resistance and impaired beta-cell insulin secretion with glyburide/metformin tablets is superior to monotherapy with each component agent. Glyburide 135-144 insulin Homo sapiens 112-119 11979388-10 2002 Insulin release by glibenclamide increased gradually reaching 10-fold basal (449 +/- 166 pmol/L, n = 6) at 60 minutes. Glyburide 19-32 insulin Canis lupus familiaris 0-7 11979388-15 2002 Glibenclamide, but not nateglinide, evoked prompt and sustained insulin release in the continuing presence of the other. Glyburide 0-13 insulin Canis lupus familiaris 64-71 11979388-18 2002 We conclude, therefore, that not only the different kinetics of gastrointestinal (GI) absorption, but also the inherent difference in the interaction with beta cells is attributed to the different insulin release characteristics between nateglinide and glibenclamide in vivo. Glyburide 253-266 insulin Canis lupus familiaris 197-204 11882918-5 2002 In HEK cells transfected with the recombinant vascular K(ATP) channel (Kir6.1 + SUR2B), the compound elicited a concentration-dependent outward current (pEC50 6.8) and in preloaded rat aortic rings it induced a concentration-dependent glibenclamide-sensitive 86Rb+ efflux (pEC50 7.51). Glyburide 235-248 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 71-77 11850098-0 2002 Different effects of acarbose and glibenclamide on proinsulin and insulin profiles in people with Type 2 diabetes. Glyburide 34-47 insulin Homo sapiens 51-61 11850098-0 2002 Different effects of acarbose and glibenclamide on proinsulin and insulin profiles in people with Type 2 diabetes. Glyburide 34-47 insulin Homo sapiens 54-61 11850098-5 2002 The breakfast increment of proinsulin was lower with acarbose than glibenclamide (6.8 vs. 19.3 pmol/l, P<0.05) as was the level at that time (37.3 +/- 5.3 vs. 56.4 +/- 7.5 pmol/l, P<0.05). Glyburide 67-80 insulin Homo sapiens 27-37 11850098-6 2002 A lower AUC of insulin after treatment was also observed with acarbose than glibenclamide (7.9 +/- 0.9 vs. 14.8 +/- 4.5 nmol/l per h, P<0.05), as also for 1-h increment (81 +/- 26, vs. 380 +/- 120 pmol/l, P<0.01) and 1-h level (325 +/- 30 vs. 621 +/- 132 pmol/l, P<0.01). Glyburide 76-89 insulin Homo sapiens 15-22 11850098-8 2002 CONCLUSIONS: Measurement of circadian excursions of proinsulin and insulin reveals distinct differences in meal-time proinsulin and insulin increment and level between acarbose and glibenclamide whereas fasting levels of these insulin fractions remained unaffected. Glyburide 181-194 insulin Homo sapiens 52-62 11850098-8 2002 CONCLUSIONS: Measurement of circadian excursions of proinsulin and insulin reveals distinct differences in meal-time proinsulin and insulin increment and level between acarbose and glibenclamide whereas fasting levels of these insulin fractions remained unaffected. Glyburide 181-194 insulin Homo sapiens 55-62 11850098-8 2002 CONCLUSIONS: Measurement of circadian excursions of proinsulin and insulin reveals distinct differences in meal-time proinsulin and insulin increment and level between acarbose and glibenclamide whereas fasting levels of these insulin fractions remained unaffected. Glyburide 181-194 insulin Homo sapiens 117-127 11850098-8 2002 CONCLUSIONS: Measurement of circadian excursions of proinsulin and insulin reveals distinct differences in meal-time proinsulin and insulin increment and level between acarbose and glibenclamide whereas fasting levels of these insulin fractions remained unaffected. Glyburide 181-194 insulin Homo sapiens 67-74 11815669-5 2002 In response to cAMP stimulation by isoproterenol, clearance was inhibited by the CFTR inhibitor glibenclamide in both wild-type mice and the normal human lung. Glyburide 96-109 cystic fibrosis transmembrane conductance regulator Mus musculus 81-85 11889571-0 2002 Point mutations in the pore region directly or indirectly affect glibenclamide block of the CFTR chloride channel. Glyburide 65-78 CF transmembrane conductance regulator Homo sapiens 92-96 11889571-3 2002 However, nothing is known about the physical nature of the glibenclamide-binding site on CFTR. Glyburide 59-72 CF transmembrane conductance regulator Homo sapiens 89-93 11889571-4 2002 Here we show that mutations in the pore-forming 6th and 12th transmembrane regions of CFTR affect block by intracellular glibenclamide, confirming previous suggestions that glibenclamide enters the pore in order to block the channel. Glyburide 121-134 CF transmembrane conductance regulator Homo sapiens 86-90 11889571-4 2002 Here we show that mutations in the pore-forming 6th and 12th transmembrane regions of CFTR affect block by intracellular glibenclamide, confirming previous suggestions that glibenclamide enters the pore in order to block the channel. Glyburide 173-186 CF transmembrane conductance regulator Homo sapiens 86-90 11889571-7 2002 These two mutations also abolished the dependence of block on the extracellular Cl(-) concentration, which in wild-type CFTR suggests an interaction between Cl(-) and glibenclamide within the channel pore that limits block. Glyburide 167-180 CF transmembrane conductance regulator Homo sapiens 120-124 11889571-9 2002 This work demonstrates that glibenclamide binds within the CFTR channel pore and begins to define its intrapore binding site. Glyburide 28-41 CF transmembrane conductance regulator Homo sapiens 59-63 11815472-2 2002 Insulin secretion was then assessed in response to glucose (16.7 mmol/l), arginine (20 mmol/l), and glyburide (200 micromol/l) during static incubation or by perifusion. Glyburide 100-109 insulin Homo sapiens 0-7 11891572-11 2002 The effect of PDE inhibitors on Isc were significantly blocked by apical treatment with glibenclamide (an inhibitor of the CFTR Cl channel) and by basolateral bumetanide, an inhibitor of Na-K-2Cl cotransport activity. Glyburide 88-101 CF transmembrane conductance regulator Homo sapiens 123-127 12047811-7 2002 The BFP-induced I(SC) was insensitive to the Na(+) channel blocker, amiloride, but partially inhibited by the Cl(-) channel blocker, DIDS (100 microM), and completely blocked by DPC (2 mM) or glibenclamide (1 mM) with a significant reduction in the apical conductance. Glyburide 192-205 ring finger protein 112 Homo sapiens 4-7 11325810-10 2001 The potency of glimepiride at the high-affinity site is close to that observed for glibenclamide (4 nM for SUR1, 27 nM for SUR2A), which has a similar structure. Glyburide 83-96 ATP-binding cassette sub-family C member 8 Xenopus laevis 107-111 11772910-9 2002 From PG = 3.8 onward, plasma growth hormone (GH) levels with placebo were nearly two times (1.9 [95% CI 1.2-2.9]) as high as with glyburide (P = 0.011). Glyburide 130-139 growth hormone 1 Homo sapiens 45-47 11772910-10 2002 AUC(60-180) for GH was lower after glyburide than after placebo (geometric mean [range] 665 [356-1,275] and 1,058 [392-1,818] mU. Glyburide 35-44 growth hormone 1 Homo sapiens 16-18 11751665-6 2002 RESULTS: One hour after glibenclamide, serum insulin increased from (mean (SD)) 7.4 (2.0) to 44.8 (25.5) mU/l (p < 0.005), and C peptide from 1.4 (0.4) to 3.4 (1.2) ng/l (p = 0.005). Glyburide 24-37 insulin Homo sapiens 45-52 11751665-11 2002 CONCLUSIONS: Glibenclamide, 0.05 mg/kg intravenously, is effective in increasing serum insulin, suggesting a K(ATP) channel blocking effect in pancreatic beta cells. Glyburide 13-26 insulin Homo sapiens 87-94 11903411-9 2001 RESULTS: There were significant correlations between daily Gb dose, on the one hand, and, on the other, HbAlc (r = 0.55), Delta-insulin (r = - 0.59) and Delta-proinsulin (r = - 0.52) levels. Glyburide 59-61 insulin Homo sapiens 159-169 11903411-10 2001 Significant correlations between Gb therapy duration and insulin (r = - 0.40) and proinsulin (r = - 0.34) secretion and between Gb dose and ratio proinsulin/insulin (RPI) at both time points (r = 0.32 and 0.30) were also found. Glyburide 33-35 insulin Homo sapiens 57-64 11903411-14 2001 CONCLUSIONS: Our results indicate that, in patients on chronic medication, Gb is capable of stimulating both insulin and proinsulin secretion; the effect on insulin release is relatively greater. Glyburide 75-77 insulin Homo sapiens 109-116 11903411-14 2001 CONCLUSIONS: Our results indicate that, in patients on chronic medication, Gb is capable of stimulating both insulin and proinsulin secretion; the effect on insulin release is relatively greater. Glyburide 75-77 insulin Homo sapiens 121-131 11903411-14 2001 CONCLUSIONS: Our results indicate that, in patients on chronic medication, Gb is capable of stimulating both insulin and proinsulin secretion; the effect on insulin release is relatively greater. Glyburide 75-77 insulin Homo sapiens 124-131 11714894-3 2001 HMR 1883 and glibenclamide inhibited [(3)H]glibenclamide binding to SUR1 with K(i) values of 63 microM and 1.5 nM, and [(3)H]opener binding to SUR2A/2B with K(i) values of 14/44 microM and 0.5/2.8 microM, respectively (values at 1 mM MgATP). Glyburide 13-26 ATP binding cassette subfamily C member 8 Homo sapiens 68-72 11714894-3 2001 HMR 1883 and glibenclamide inhibited [(3)H]glibenclamide binding to SUR1 with K(i) values of 63 microM and 1.5 nM, and [(3)H]opener binding to SUR2A/2B with K(i) values of 14/44 microM and 0.5/2.8 microM, respectively (values at 1 mM MgATP). Glyburide 43-56 ATP binding cassette subfamily C member 8 Homo sapiens 68-72 11714894-4 2001 The interaction of HMR 1883 with the SUR2 subtypes was more sensitive to inhibition by MgATP and MgADP than that of glibenclamide. Glyburide 116-129 ATP binding cassette subfamily C member 9 Homo sapiens 37-41 11714894-6 2001 In whole cells, the recombinant vascular K(ATP) channel, Kir6.1/SUR2B, was inhibited by HMR 1883 and glibenclamide with IC(50) values of 5.3 and 0.043 microM, respectively. Glyburide 101-114 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 57-63 11714894-7 2001 The data show that the sulfonylthiourea exhibits a selectivity profile quite different from that of glibenclamide with a major loss of affinity toward SUR1 and slight preference for SUR2A. Glyburide 100-113 ATP binding cassette subfamily C member 8 Homo sapiens 151-155 11567030-1 2001 ATP-regulated (K(ATP)) channels are formed by an inward rectifier pore-forming subunit (Kir) and a sulfonylurea (glibenclamide)-binding protein, a member of the ATP binding cassette family (sulfonylurea receptor (SUR) or cystic fibrosis transmembrane conductance regulator). Glyburide 113-126 CF transmembrane conductance regulator Rattus norvegicus 221-272 11567030-10 2001 These studies identified an amino acid triplet "IRA" within the conserved segment in the NH(2) terminus of ROMK1 and ROMK3 that blocks the ability of SUR2B to confer glibenclamide sensitivity to the expressed K(+) currents. Glyburide 166-179 potassium inwardly-rectifying channel, subfamily J, member 1 Rattus norvegicus 107-112 11602509-7 2001 In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide. Glyburide 212-221 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 52-58 11602509-7 2001 In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide. Glyburide 212-221 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 167-173 11675429-1 2001 In vitro studies have shown that glibenclamide sensitivity is conferred upon Kir 1.1 K(+) channels when they are co-expressed with the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 33-46 potassium inwardly-rectifying channel, subfamily J, member 1 Mus musculus 77-84 11675429-1 2001 In vitro studies have shown that glibenclamide sensitivity is conferred upon Kir 1.1 K(+) channels when they are co-expressed with the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 33-46 cystic fibrosis transmembrane conductance regulator Mus musculus 135-186 11675429-1 2001 In vitro studies have shown that glibenclamide sensitivity is conferred upon Kir 1.1 K(+) channels when they are co-expressed with the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 33-46 cystic fibrosis transmembrane conductance regulator Mus musculus 188-192 11675429-2 2001 In rats, glibenclamide acts as a K(+)-sparing diuretic by a mechanism that involves blockade of Kir 1.1 channels in the distal nephron. Glyburide 9-22 potassium inwardly-rectifying channel, subfamily J, member 1 Rattus norvegicus 96-103 11504722-8 2001 Moreover, endocytosis is similarly enhanced in normal fibroblasts when ABCA1 function is inhibited by glyburide, whereas glyburide has no effect on endocytosis in Tangier cells. Glyburide 102-111 ATP binding cassette subfamily A member 1 Homo sapiens 71-76 11585851-2 2001 To gain insight into these interactions, we investigated the effects of mutating positively charged residues in Kir6.2, previously implicated in the response to PIP2, on channel regulation by adenine nucleotides and the sulfonylurea glyburide. Glyburide 233-242 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 112-118 11676825-7 2001 We used the ATP-binding cassette 1 transporter inhibitor glybenclamide, which has been previously shown to block interleukin-1beta secretion in human monocytes. Glyburide 57-70 interleukin 1 beta Homo sapiens 113-130 11676825-8 2001 Using enzyme-linked immunosorbent assay, we assessed the effect of glybenclamide on interleukin-8 production in human dermal fibroblasts. Glyburide 67-80 C-X-C motif chemokine ligand 8 Homo sapiens 84-97 11676825-10 2001 Glybenclamide disabled this activation loop and significantly reduced interleukin-8. Glyburide 0-13 C-X-C motif chemokine ligand 8 Homo sapiens 70-83 11676825-11 2001 In human dermal fibroblasts that were stimulated with tumor necrosis factor alpha to reach high interleukin-1 expression levels, glybenclamide similarly suppressed interleukin-8. Glyburide 129-142 tumor necrosis factor Homo sapiens 54-81 11676825-11 2001 In human dermal fibroblasts that were stimulated with tumor necrosis factor alpha to reach high interleukin-1 expression levels, glybenclamide similarly suppressed interleukin-8. Glyburide 129-142 interleukin 1 alpha Homo sapiens 96-109 11676825-11 2001 In human dermal fibroblasts that were stimulated with tumor necrosis factor alpha to reach high interleukin-1 expression levels, glybenclamide similarly suppressed interleukin-8. Glyburide 129-142 C-X-C motif chemokine ligand 8 Homo sapiens 164-177 11676825-15 2001 These results are consistent with glybenclamide preventing externalization of interleukin-1 and subsequent autocrine induction of interleukin-8 in human dermal fibroblasts. Glyburide 34-47 interleukin 1 alpha Homo sapiens 78-91 11676825-15 2001 These results are consistent with glybenclamide preventing externalization of interleukin-1 and subsequent autocrine induction of interleukin-8 in human dermal fibroblasts. Glyburide 34-47 C-X-C motif chemokine ligand 8 Homo sapiens 130-143 12030807-6 2001 Likewise, glibenclamide suppressed the stimulation of ANP secretion by bremazocine. Glyburide 10-23 natriuretic peptides A Oryctolagus cuniculus 54-57 11502593-4 2001 Apical addition of 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) or glibenclamide partially inhibited the rise in I(sc) induced by dDAVP and ISO in BAm-treated CFTR(+/+) CCDs, whereas dDAVP, ISO, and NPPB did not alter I(sc) in BAm-treated CFTR(-/-) CCDs. Glyburide 70-83 cystic fibrosis transmembrane conductance regulator Mus musculus 162-166 11502593-4 2001 Apical addition of 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) or glibenclamide partially inhibited the rise in I(sc) induced by dDAVP and ISO in BAm-treated CFTR(+/+) CCDs, whereas dDAVP, ISO, and NPPB did not alter I(sc) in BAm-treated CFTR(-/-) CCDs. Glyburide 70-83 cystic fibrosis transmembrane conductance regulator Mus musculus 242-246 11588016-8 2001 In addition, pretreatment with glybenclamide, an inhibitor of cystic fibrosis transmembrane conductance regulator, reduced the second peak of Isc induced by ATP but was without effect on that induced by UTP. Glyburide 31-44 CF transmembrane conductance regulator Bos taurus 62-113 11527951-7 2001 Furthermore, this conductance exhibited voltage-dependent inhibition in the presence of the CFTR chloride channel blocker glibenclamide (250 microM), but was DIDS insensitive (500 microM). Glyburide 122-135 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 92-96 11454910-9 2001 However, diazoxide induced a glibenclamide-sensitive outward current in hippocampal CA1 neurons. Glyburide 29-42 carbonic anhydrase 1 Rattus norvegicus 84-87 11406498-6 2001 After FPI, CGRP-induced vasodilation restored by genistein (10 micromol/l) was strongly antagonized by iberiotoxin but not by glibenclamide, whereas LMK-induced vasodilation was, in contrast, inhibited by glibenclamide but not by iberiotoxin. Glyburide 205-218 calcitonin-related polypeptide alpha Rattus norvegicus 11-15 11427487-4 2001 The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM. Glyburide 29-38 ATP binding cassette subfamily A member 1 Homo sapiens 13-18 11427487-4 2001 The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM. Glyburide 29-38 ATP binding cassette subfamily A member 1 Homo sapiens 87-92 11427487-4 2001 The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM. Glyburide 29-38 apolipoprotein E Homo sapiens 120-124 11427487-4 2001 The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM. Glyburide 29-38 GLI family zinc finger 2 Homo sapiens 140-144 11408614-2 2001 SUR1, expressed in pancreatic beta-cells, has a higher affinity for sulfonylureas, such as glibenclamide, than SUR2B, expressed in smooth muscle. Glyburide 91-104 ATP binding cassette subfamily C member 8 Homo sapiens 0-4 11408614-5 2001 In whole-cell patch-clamp experiments, glibenclamide inhibited the channel formed by coexpression of mutant SUR2B with Kir6.1 or 6.2 in human embryonic kidney cells with IC(50) values of 2.7 and 13 nM, respectively (wild-type, 43 and 167 nM). Glyburide 39-52 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 119-125 11408614-6 2001 In intact cells, [(3)H]glibenclamide bound to mutant SUR2B with a K(D) value of 4.7 nM (wild-type, 32 nM); coexpression with Kir6.1 or 6.2 increased affinity by 4- and 8-fold, respectively. Glyburide 23-36 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 125-131 11309399-4 2001 Inhibition of lipid efflux by glybenclamide treatment or by mutation of the ATP-binding cassette of ABCA1 showed a close correlation between lipid efflux, the binding of apoA-I to cells, and cross-linking of apoA-I to ABCA1. Glyburide 30-43 apolipoprotein A1 Homo sapiens 170-176 11309399-4 2001 Inhibition of lipid efflux by glybenclamide treatment or by mutation of the ATP-binding cassette of ABCA1 showed a close correlation between lipid efflux, the binding of apoA-I to cells, and cross-linking of apoA-I to ABCA1. Glyburide 30-43 apolipoprotein A1 Homo sapiens 208-214 11309399-4 2001 Inhibition of lipid efflux by glybenclamide treatment or by mutation of the ATP-binding cassette of ABCA1 showed a close correlation between lipid efflux, the binding of apoA-I to cells, and cross-linking of apoA-I to ABCA1. Glyburide 30-43 ATP binding cassette subfamily A member 1 Homo sapiens 218-223 11418131-5 2001 By using N-terminally truncated recombinant proteins we have shown that CL3 - the cytosolic loop between TM5 and TM6 - plays a key role in formation of the N-terminal component of the glibenclamide binding site. Glyburide 184-197 adhesion G protein-coupled receptor L3 Homo sapiens 72-75 11418131-5 2001 By using N-terminally truncated recombinant proteins we have shown that CL3 - the cytosolic loop between TM5 and TM6 - plays a key role in formation of the N-terminal component of the glibenclamide binding site. Glyburide 184-197 tropomyosin 3 Homo sapiens 105-108 11418131-6 2001 Analysis of deletion variants of the C-terminal part of SUR1 showed that CL8 - the cytosolic loop between TM15 and TM16 - is the only determinant for the C-terminal component of the glibenclamide binding site. Glyburide 182-195 ATP binding cassette subfamily C member 8 Homo sapiens 56-60 11418131-7 2001 We suggest that in SUR1 in the native K(ATP) channel close proximity of CL3 and CL8 leads to formation of the glibenclamide binding site. Glyburide 110-123 ATP binding cassette subfamily C member 8 Homo sapiens 19-23 11418131-7 2001 We suggest that in SUR1 in the native K(ATP) channel close proximity of CL3 and CL8 leads to formation of the glibenclamide binding site. Glyburide 110-123 adhesion G protein-coupled receptor L3 Homo sapiens 72-75 11356916-1 2001 Insulin secretion from MIN6 cells (a pancreatic beta-cell line) induced by high glucose (greater than 16.8 mM) was potentiated by a novel hypoglycemic agent [trans-4-(4-methylcyclohexyl)-4-oxobutyric acid (JTT-608)] (but not glibenclamide, a sulfonylurea). Glyburide 225-238 insulin Homo sapiens 0-7 12564657-7 2002 The vasorelaxant effect of CGRP was not significantly influenced by the inhibitor of voltage-gated potassium (KV) channels (4-aminopyridin), but was significantly attenuated by an inhibitor of calcium-regulated potassium (KCa) channels (tetraethylammonium) and by an inhibitor of adenosine triphosphate-sensitive potassium (KATP) channels (glibenclamide). Glyburide 340-353 calcitonin-related polypeptide alpha Rattus norvegicus 27-31 12390047-9 2002 However, OAHAs, especially glibenclamide (glyburide), may be beneficial in a situation where the proper use of insulin is problematic. Glyburide 27-40 insulin Homo sapiens 111-118 12390047-9 2002 However, OAHAs, especially glibenclamide (glyburide), may be beneficial in a situation where the proper use of insulin is problematic. Glyburide 42-51 insulin Homo sapiens 111-118 11739446-6 2001 Both nateglinide and glyburide enhanced glucose-induced insulin release, compared with placebo (area under the curve -15-300 min: nateglinide 23,595 +/- 11,212 pM/min, glyburide 54,556 +/- 15,253 pM/min, placebo 10,242 +/- 2,414 pM/min). Glyburide 21-30 insulin Homo sapiens 56-63 11739446-9 2001 The enhancement of insulin release by glyburide resulted in a lower minimal glucose concentration with glyburide (3.8 +/- 0.2 mM), compared with nateglinide (5.0 +/- 0.2 mM) and placebo (5.9 +/- 0.2 mM). Glyburide 38-47 insulin Homo sapiens 19-26 11739446-9 2001 The enhancement of insulin release by glyburide resulted in a lower minimal glucose concentration with glyburide (3.8 +/- 0.2 mM), compared with nateglinide (5.0 +/- 0.2 mM) and placebo (5.9 +/- 0.2 mM). Glyburide 103-112 insulin Homo sapiens 19-26 11739446-11 2001 Further, the differences in the kinetics of nateglinide and glyburide action results in continued insulin release with glyburide despite the fact that glucose levels have returned to basal, thus resulting in a further reduction in glucose levels and a lower nadir. Glyburide 60-69 insulin Homo sapiens 98-105 11739446-11 2001 Further, the differences in the kinetics of nateglinide and glyburide action results in continued insulin release with glyburide despite the fact that glucose levels have returned to basal, thus resulting in a further reduction in glucose levels and a lower nadir. Glyburide 119-128 insulin Homo sapiens 98-105 11789865-3 2001 This effect could be reversed with glibenclamide, indicating that GBP-L acts as an opener of ATP-sensitive potassium channels. Glyburide 35-48 transmembrane protein 132A Rattus norvegicus 66-69 11504818-4 2001 Ketoprofen, indocyanine green and glibenclamide are potent inhibitors of the uptake of [(14)C]salicylate via rOat2 (K(i) of approximately 12 microM), while diclofenac, benzoate, verapamil, ibuprofen, and tolbutamide are moderate inhibitors (K(i) of approximately 150 microM). Glyburide 34-47 solute carrier family 22 (organic anion transporter), member 7, pseudogene 1 Rattus norvegicus 109-114 11680619-8 2001 The observation that subconductance states can be induced by low concentrations of glybenclamide may have implications for models of how the binding of glybenclamide is translated into closure of the Kir6.2 pore. Glyburide 83-96 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 200-206 11680619-8 2001 The observation that subconductance states can be induced by low concentrations of glybenclamide may have implications for models of how the binding of glybenclamide is translated into closure of the Kir6.2 pore. Glyburide 152-165 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 200-206 11476748-7 2001 In presence of glibenclamide, CNP reduced perfusion pressure to 92 +/- 2 mmHg (-32%), in presence of iberiotoxin to 93 +/- 1 mmHg (-30% and in their combined presence to 102+/-2 mmHg (-23%) (P<0.05 vs. corresponding control). Glyburide 15-28 natriuretic peptide C Rattus norvegicus 30-33 11487526-2 2001 In the presence of 300 microM L-nitroarginine and 10 microM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 microM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected. Glyburide 148-161 kininogen 1 Homo sapiens 202-212 11406469-6 2001 Glibenclamide (1 x 10(-6) M) significantly suppressed the inhibitory responses of the lymphatic pump activity induced by PTHrP-(1-34) and S-nitroso-N-acetyl-penicillamine. Glyburide 0-13 parathyroid hormone-like peptide Mus musculus 121-126 11418131-4 2001 Co-expression in a baculovirus expression system of two parts of SUR1 between NBD1 and TM12 leads to restoration of glibenclamide binding activity, whereas expression of either individual N- or C-terminal part alone gave no glibenclamide binding activity, confirming a bivalent structure of the glibenclamide binding site. Glyburide 116-129 ATP binding cassette subfamily C member 8 Homo sapiens 65-69 11418131-4 2001 Co-expression in a baculovirus expression system of two parts of SUR1 between NBD1 and TM12 leads to restoration of glibenclamide binding activity, whereas expression of either individual N- or C-terminal part alone gave no glibenclamide binding activity, confirming a bivalent structure of the glibenclamide binding site. Glyburide 224-237 ATP binding cassette subfamily C member 8 Homo sapiens 65-69 11418131-4 2001 Co-expression in a baculovirus expression system of two parts of SUR1 between NBD1 and TM12 leads to restoration of glibenclamide binding activity, whereas expression of either individual N- or C-terminal part alone gave no glibenclamide binding activity, confirming a bivalent structure of the glibenclamide binding site. Glyburide 224-237 ATP binding cassette subfamily C member 8 Homo sapiens 65-69 11406737-12 2001 The mechanism underlying the interaction between rifampin and glyburide is probably induction of either CYP2C9 or P-glycoprotein or both. Glyburide 62-71 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 104-110 11406737-12 2001 The mechanism underlying the interaction between rifampin and glyburide is probably induction of either CYP2C9 or P-glycoprotein or both. Glyburide 62-71 ATP binding cassette subfamily B member 1 Homo sapiens 114-128 11375357-10 2001 h/l, P < 0.01), and only glyburide increased fasting insulin levels. Glyburide 28-37 insulin Homo sapiens 56-63 11523909-5 2001 PCO-400 and nicorandil dose-dependently inhibited insulin-stimulated glucose uptake, and their inhibitory effects were reversed by glibenclamide or gliclazide. Glyburide 131-144 insulin Homo sapiens 50-57 11344200-0 2001 Glucose-dependent insulinotropic hormone potentiates the hypoglycemic effect of glibenclamide in healthy volunteers: evidence for an effect on insulin extraction. Glyburide 80-93 gastric inhibitory polypeptide Homo sapiens 0-40 11343252-7 2001 Cyclosporin A, glibenclamide and rifamycin SV, all competitive inhibitors of Bsep transport, also reduced the bile salt-stimulated ATPase activity. Glyburide 15-28 ATP-binding cassette, sub-family B (MDR/TAP), member 11 Mus musculus 77-81 11343252-7 2001 Cyclosporin A, glibenclamide and rifamycin SV, all competitive inhibitors of Bsep transport, also reduced the bile salt-stimulated ATPase activity. Glyburide 15-28 dynein, axonemal, heavy chain 8 Mus musculus 131-137 11344200-0 2001 Glucose-dependent insulinotropic hormone potentiates the hypoglycemic effect of glibenclamide in healthy volunteers: evidence for an effect on insulin extraction. Glyburide 80-93 insulin Homo sapiens 18-25 11344200-4 2001 We now show that an infusion of GIP in healthy volunteers in whom blood glucose levels were maintained at 5 mmol/L, increased glibenclamide-stimulated levels of plasma insulin without significantly changing the C peptide profile. Glyburide 126-139 gastric inhibitory polypeptide Homo sapiens 32-35 11344200-4 2001 We now show that an infusion of GIP in healthy volunteers in whom blood glucose levels were maintained at 5 mmol/L, increased glibenclamide-stimulated levels of plasma insulin without significantly changing the C peptide profile. Glyburide 126-139 insulin Homo sapiens 168-175 11306691-4 2001 Application of the phosphatidylinositol phosphates (PIPs) phosphatidylinositiol-4-phosphate, PIP(2), and phosphatidylinositol-3,4,5-trisphosphate reduced sensitivity to ATP and glibenclamide closely resembling the native variability. Glyburide 177-190 prolactin induced protein Homo sapiens 52-55 11306691-10 2001 Second, PIP(2) had clearly distinct effects on the concentration-response curves for ATP and glibenclamide. Glyburide 93-106 prolactin induced protein Homo sapiens 8-11 11306691-11 2001 However, PIPs seemed to mediate the different effects via the Kir6.2 subunits because a mutation in Kir6.2 (R176A) attenuated simultaneously the effects of PIP(2) on ATP and glibenclamide inhibition. Glyburide 174-187 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 62-68 11306691-11 2001 However, PIPs seemed to mediate the different effects via the Kir6.2 subunits because a mutation in Kir6.2 (R176A) attenuated simultaneously the effects of PIP(2) on ATP and glibenclamide inhibition. Glyburide 174-187 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 100-106 11306691-11 2001 However, PIPs seemed to mediate the different effects via the Kir6.2 subunits because a mutation in Kir6.2 (R176A) attenuated simultaneously the effects of PIP(2) on ATP and glibenclamide inhibition. Glyburide 174-187 prolactin induced protein Homo sapiens 9-12 21171413-4 2001 But glibenclamide (10(-6) mol/L) and propranolol (10(-6) mol/L) could decrease the vasodilation of CNP obviously, in addition, CNP couldn"t inhibit the vasoconstriction of NE. Glyburide 4-17 2',3'-cyclic-nucleotide 3'-phosphodiesterase Oryctolagus cuniculus 99-102 11284200-3 2001 The forskolin-induced anion current was sustained and significantly (54%) suppressed by glibenclamide (200 microM), a blocker of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. Glyburide 88-101 CF transmembrane conductance regulator Rattus norvegicus 133-184 11381676-5 2001 The involvement of NO and adenosine triphosphate-sensitive potassium (KATP) channels in bFGF-induced vasodilation and membrane hyperpolarization was evaluated using specific inhibitors, NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) and glibenclamide (GB, 10(-5) M), respectively. Glyburide 234-247 fibroblast growth factor 2 Rattus norvegicus 88-92 11381676-5 2001 The involvement of NO and adenosine triphosphate-sensitive potassium (KATP) channels in bFGF-induced vasodilation and membrane hyperpolarization was evaluated using specific inhibitors, NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) and glibenclamide (GB, 10(-5) M), respectively. Glyburide 249-251 fibroblast growth factor 2 Rattus norvegicus 88-92 11381676-9 2001 In the presence of GB, the membrane potential was significantly depolarized but the vessel diameter was only marginally reduced, so bFGF-induced membrane hyperpolarization was inhibited while arteriolar dilation was attenuated. Glyburide 19-21 fibroblast growth factor 2 Rattus norvegicus 132-136 11344200-7 2001 Hence, our results show that at a blood glucose concentration of 5 mmol/L, GIP augments the increase in plasma insulin levels stimulated by glibenclamide, possibly acting through a mechanism involving decreased insulin extraction in the liver or peripheral tissues, thus increasing insulin availability. Glyburide 140-153 gastric inhibitory polypeptide Homo sapiens 75-78 11344200-7 2001 Hence, our results show that at a blood glucose concentration of 5 mmol/L, GIP augments the increase in plasma insulin levels stimulated by glibenclamide, possibly acting through a mechanism involving decreased insulin extraction in the liver or peripheral tissues, thus increasing insulin availability. Glyburide 140-153 insulin Homo sapiens 111-118 11250874-12 2001 In resting coronary arteries, only pretreatment with the combination of 1 microM glibenclamide and 100 nM charybdotoxin attenuated the CGRP-induced decrease in the [Ca(2+)](i) and tension, suggesting a different mechanism of action for CGRP in resting coronary arteries. Glyburide 81-94 calcitonin-related polypeptide alpha Rattus norvegicus 135-139 11250874-12 2001 In resting coronary arteries, only pretreatment with the combination of 1 microM glibenclamide and 100 nM charybdotoxin attenuated the CGRP-induced decrease in the [Ca(2+)](i) and tension, suggesting a different mechanism of action for CGRP in resting coronary arteries. Glyburide 81-94 calcitonin-related polypeptide alpha Rattus norvegicus 236-240 11284200-3 2001 The forskolin-induced anion current was sustained and significantly (54%) suppressed by glibenclamide (200 microM), a blocker of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel. Glyburide 88-101 CF transmembrane conductance regulator Rattus norvegicus 186-190 11230779-9 2001 Glibenclamide treatment was associated with a reduction in alpha-1-antitrypsin (P <.05), ceruloplasmin (P <.01), and complement C3 protein (C3) (P <.05). Glyburide 0-13 serpin family A member 1 Homo sapiens 59-78 11230779-9 2001 Glibenclamide treatment was associated with a reduction in alpha-1-antitrypsin (P <.05), ceruloplasmin (P <.01), and complement C3 protein (C3) (P <.05). Glyburide 0-13 ceruloplasmin Homo sapiens 92-105 11305519-7 2001 RESULTS: Glibenclamide (i.e. glibenclamide plus glucose) significantly increased plasma insulin concentrations and glycemia while placebo (i.e. glucose alone) significantly increased glycemia but did not change plasma insulin levels. Glyburide 9-22 insulin Homo sapiens 88-95 11305519-7 2001 RESULTS: Glibenclamide (i.e. glibenclamide plus glucose) significantly increased plasma insulin concentrations and glycemia while placebo (i.e. glucose alone) significantly increased glycemia but did not change plasma insulin levels. Glyburide 29-42 insulin Homo sapiens 88-95 11165940-15 2001 Message for the sulphonylurea receptor SUR2, a subunit of glibenclamide-insensitive ATP-dependent K(+) channels (K(ATP)), was also detected, but the glibenclamide-sensitive SUR1 subunit was not. Glyburide 58-71 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 39-43 11181077-4 2001 Bumetanide and furosemide, NKCC inhibitors, significantly inhibited the Pin-induced increased [K(+)](i) and apoptosis, whereas K(ATP) inhibitors (glibenclamide and tolbutamide) had no effects. Glyburide 146-159 dynein light chain LC8-type 1 Homo sapiens 72-75 11159731-0 2001 The sulphonylurea glibenclamide inhibits multidrug resistance protein (MRP1) activity in human lung cancer cells. Glyburide 18-31 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 11159731-2 2001 Glibenclamide, a sulphonylurea widely used for the treatment of non-insulin-dependent diabetes mellitus, has been shown to inhibit the activities of various ATP-binding cassette (ABC) transporters. Glyburide 0-13 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 157-177 11159731-2 2001 Glibenclamide, a sulphonylurea widely used for the treatment of non-insulin-dependent diabetes mellitus, has been shown to inhibit the activities of various ATP-binding cassette (ABC) transporters. Glyburide 0-13 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 179-182 11159731-5 2001 Intracellular accumulation of calcein, an anionic dye substrate for MRP1, was strongly increased by glibenclamide in a dose-dependent manner in MRP1-overexpressing lung tumour GLC4/Sb30 cells through inhibition of MRP1-related calcein efflux. Glyburide 100-113 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 11159731-5 2001 Intracellular accumulation of calcein, an anionic dye substrate for MRP1, was strongly increased by glibenclamide in a dose-dependent manner in MRP1-overexpressing lung tumour GLC4/Sb30 cells through inhibition of MRP1-related calcein efflux. Glyburide 100-113 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 11159731-5 2001 Intracellular accumulation of calcein, an anionic dye substrate for MRP1, was strongly increased by glibenclamide in a dose-dependent manner in MRP1-overexpressing lung tumour GLC4/Sb30 cells through inhibition of MRP1-related calcein efflux. Glyburide 100-113 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 11159731-9 2001 Glibenclamide used at 12.5 microM was, moreover, found to strongly enhance the sensitivity of GLC4/Sb30 cells towards vincristine, an anticancer drug handled by MRP1. Glyburide 0-13 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 11159731-11 2001 Efflux of carboxy-2",7"-dichlorofluorescein, an anionic dye handled by the ABC transporter MRP2 sharing numerous substrates with MRP1 and expressed at high levels in liver, was also strongly inhibited by glibenclamide in isolated rat hepatocytes. Glyburide 204-217 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 75-78 11159731-11 2001 Efflux of carboxy-2",7"-dichlorofluorescein, an anionic dye handled by the ABC transporter MRP2 sharing numerous substrates with MRP1 and expressed at high levels in liver, was also strongly inhibited by glibenclamide in isolated rat hepatocytes. Glyburide 204-217 ATP binding cassette subfamily C member 2 Rattus norvegicus 91-95 11159731-11 2001 Efflux of carboxy-2",7"-dichlorofluorescein, an anionic dye handled by the ABC transporter MRP2 sharing numerous substrates with MRP1 and expressed at high levels in liver, was also strongly inhibited by glibenclamide in isolated rat hepatocytes. Glyburide 204-217 ATP binding cassette subfamily C member 1 Rattus norvegicus 129-133 11159731-13 2001 In summary, glibenclamide reversed MRP1-mediated drug resistance likely through inhibiting MRP1 activity and blocked organic anion efflux from MRP2-expressing hepatocytes. Glyburide 12-25 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 11159731-13 2001 In summary, glibenclamide reversed MRP1-mediated drug resistance likely through inhibiting MRP1 activity and blocked organic anion efflux from MRP2-expressing hepatocytes. Glyburide 12-25 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 11159731-13 2001 In summary, glibenclamide reversed MRP1-mediated drug resistance likely through inhibiting MRP1 activity and blocked organic anion efflux from MRP2-expressing hepatocytes. Glyburide 12-25 ATP binding cassette subfamily C member 2 Homo sapiens 143-147 11159731-14 2001 Such effects associated with the known inhibitory properties of glibenclamide towards various others ABC proteins suggest that this sulphonylurea is a general inhibitor of ABC transporters. Glyburide 64-77 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 101-104 11159731-14 2001 Such effects associated with the known inhibitory properties of glibenclamide towards various others ABC proteins suggest that this sulphonylurea is a general inhibitor of ABC transporters. Glyburide 64-77 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 172-175 11158395-7 2001 The dDAVP-dependent I(sc) measured under apical Na(+)-free condition was reduced by Cl(-) channel blockers with a profile (NPPB>glibenclamide>DIDS), similar to that for rat CFTR. Glyburide 131-144 natriuretic peptide B Rattus norvegicus 123-127 11218064-4 2001 When ATPi was omitted from the pipette solution I(K)(ATP) activated with a time lag of 4.92+/-0.92 min (n=6) and was completely inhibited by glibenclamide. Glyburide 141-154 ATP synthase inhibitory factor subunit 1 Homo sapiens 5-9 11218730-1 2001 Glibenclamide(GLI) is widely used as an oral hypoglycemic drug in the treatment of non-insulin dependent diabetes mellitus (NIDDM). Glyburide 0-13 GLI family zinc finger 1 Homo sapiens 14-17 11356184-3 2001 Application of a phosphorylating cocktail activated a Cl- current with characteristics similar to those of CFTR mediated currents in other cells types (slow activation by cAMP, absence of rectification, block by glibenclamide). Glyburide 212-225 cystic fibrosis transmembrane conductance regulator Mus musculus 107-111 11165940-15 2001 Message for the sulphonylurea receptor SUR2, a subunit of glibenclamide-insensitive ATP-dependent K(+) channels (K(ATP)), was also detected, but the glibenclamide-sensitive SUR1 subunit was not. Glyburide 149-162 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 173-177 10965903-3 2000 A representative SU glibenclamide inhibited the basal POMC 5"-promoter activity. Glyburide 20-33 pro-opiomelanocortin-alpha Mus musculus 54-58 11368292-15 2001 The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin. Glyburide 70-83 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 27-33 11368292-15 2001 The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin. Glyburide 85-94 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 27-33 12622887-6 2001 The association biguanides and S, in particular glibenclamide plus metformin, is now widely used by diabetologists in SF since glibenclamide improves insulin secretion while metformin exerts its antidiabetic. Glyburide 48-61 insulin Homo sapiens 150-157 12622887-6 2001 The association biguanides and S, in particular glibenclamide plus metformin, is now widely used by diabetologists in SF since glibenclamide improves insulin secretion while metformin exerts its antidiabetic. Glyburide 127-140 insulin Homo sapiens 150-157 11180400-1 2001 Previously, we have reported that inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels by glibenclamide induced intracellular Ca2+ release from IP(3)-sensitive stores and apoptosis in HepG2 human hepatoblastoma cells (Kim JA, Kang YS, Lee SH, Lee EH, Yoo BH, Lee YS. Glyburide 123-136 CF transmembrane conductance regulator Homo sapiens 48-99 11180400-1 2001 Previously, we have reported that inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels by glibenclamide induced intracellular Ca2+ release from IP(3)-sensitive stores and apoptosis in HepG2 human hepatoblastoma cells (Kim JA, Kang YS, Lee SH, Lee EH, Yoo BH, Lee YS. Glyburide 123-136 CF transmembrane conductance regulator Homo sapiens 101-105 11180400-6 2001 The glibenclamide-induced formation of IP(3) was significantly inhibited by CFTR activators (levamisole and bromotetramisole). Glyburide 4-17 CF transmembrane conductance regulator Homo sapiens 76-80 11078708-7 2000 With the use of short-circuit recordings, X-33 and IBMX were able to stimulate a large concentration-dependent CFTR transport that was blocked by glibenclamide but not by DIDS. Glyburide 146-159 CF transmembrane conductance regulator Homo sapiens 111-115 11090651-2 2000 In acute 20-min incubations, 200 microM of tolbutamide or glibenclamide stimulated insulin release from non-depolarized and depolarized cells, which was dramatically reduced following 18-h culture with 100 microM glibenclamide. Glyburide 58-71 insulin Homo sapiens 83-90 11090651-2 2000 In acute 20-min incubations, 200 microM of tolbutamide or glibenclamide stimulated insulin release from non-depolarized and depolarized cells, which was dramatically reduced following 18-h culture with 100 microM glibenclamide. Glyburide 213-226 insulin Homo sapiens 83-90 11090651-4 2000 However, desensitization of insulinotropic effects of sulphonylureas in depolarized cells following glibenclamide culture and associated decline in cellular insulin content was not fully reversible. Glyburide 100-113 insulin Homo sapiens 28-35 11087359-3 2000 Smooth muscle cells (SMC) expressed high levels of ABC-1 transporter mRNA, and glyburide-dependent PL and FC efflux to apolipoprotein A-1 (apo A-1), the major protein of high-density lipoprotein. Glyburide 79-88 apolipoprotein A1 Homo sapiens 119-137 11087359-3 2000 Smooth muscle cells (SMC) expressed high levels of ABC-1 transporter mRNA, and glyburide-dependent PL and FC efflux to apolipoprotein A-1 (apo A-1), the major protein of high-density lipoprotein. Glyburide 79-88 apolipoprotein A1 Homo sapiens 139-146 11068185-3 2000 We used a freshly isolated rat adipose tissue culture model to examine the effect of insulin, metformin and glibenclamide on basal and steroid-stimulated leptin secretion. Glyburide 108-121 leptin Rattus norvegicus 154-160 11257323-11 2000 Insulin resistance measured by the homeostasis model decreased more in the metformin group than in the glibenclamide group. Glyburide 103-116 insulin Homo sapiens 0-7 11032738-0 2000 Glibenclamide acts as an inhibitor of acyl-CoA:cholesterol acyltransferase enzyme. Glyburide 0-13 sterol O-acyltransferase 2 Mus musculus 38-74 11032738-4 2000 GB inhibited intracellular accumulation of CE induced by acetylated LDL or oxidized LDL in J774 cells, but no such effect on total cholesterol, suggesting that the target of GB was acyl-CoA:cholesterol acyltransferase (ACAT). Glyburide 0-2 sterol O-acyltransferase 2 Mus musculus 181-217 11032738-4 2000 GB inhibited intracellular accumulation of CE induced by acetylated LDL or oxidized LDL in J774 cells, but no such effect on total cholesterol, suggesting that the target of GB was acyl-CoA:cholesterol acyltransferase (ACAT). Glyburide 0-2 sterol O-acyltransferase 2 Mus musculus 219-223 11032738-4 2000 GB inhibited intracellular accumulation of CE induced by acetylated LDL or oxidized LDL in J774 cells, but no such effect on total cholesterol, suggesting that the target of GB was acyl-CoA:cholesterol acyltransferase (ACAT). Glyburide 174-176 sterol O-acyltransferase 2 Mus musculus 181-217 11032738-5 2000 In the cell-free reconstitution ACAT assay, GB inhibited the ACAT activity with an IC(50) value of 20 microM. Glyburide 44-46 sterol O-acyltransferase 1 Homo sapiens 32-36 11032738-5 2000 In the cell-free reconstitution ACAT assay, GB inhibited the ACAT activity with an IC(50) value of 20 microM. Glyburide 44-46 sterol O-acyltransferase 1 Homo sapiens 61-65 11032738-6 2000 Furthermore, GB effectively inhibited the ACAT activity of PMA-stimulated THP-1 cells to the undifferentiated level of THP-1. Glyburide 13-15 sterol O-acyltransferase 1 Homo sapiens 42-46 11032738-6 2000 Furthermore, GB effectively inhibited the ACAT activity of PMA-stimulated THP-1 cells to the undifferentiated level of THP-1. Glyburide 13-15 GLI family zinc finger 2 Homo sapiens 74-79 11032738-6 2000 Furthermore, GB effectively inhibited the ACAT activity of PMA-stimulated THP-1 cells to the undifferentiated level of THP-1. Glyburide 13-15 GLI family zinc finger 2 Homo sapiens 119-124 11032738-7 2000 In the whole-cell ACAT assay using CHO cells overexpressed with ACAT-1 or ACAT-2, GB inhibited the activity of both isozymes with similar potency. Glyburide 82-84 sterol O-acyltransferase 1 Cricetulus griseus 18-22 11032738-7 2000 In the whole-cell ACAT assay using CHO cells overexpressed with ACAT-1 or ACAT-2, GB inhibited the activity of both isozymes with similar potency. Glyburide 82-84 acetyl-CoA acetyltransferase, mitochondrial Cricetulus griseus 64-70 11032738-7 2000 In the whole-cell ACAT assay using CHO cells overexpressed with ACAT-1 or ACAT-2, GB inhibited the activity of both isozymes with similar potency. Glyburide 82-84 acetyl-CoA acetyltransferase, cytosolic Cricetulus griseus 74-80 11036118-9 2000 Eight women in the glyburide group (4 percent) required insulin therapy. Glyburide 19-28 insulin Homo sapiens 56-63 11054556-6 2000 Each of the SUR2 splice variants transiently expressed with the inward rectifier Kir 6.2 formed functional K(ATP) channels in HEK 293 cells as assessed either by changes in DiBAC(4)(3) fluorescence responses or glyburide-sensitive whole cell currents. Glyburide 211-220 ATP binding cassette subfamily C member 9 Homo sapiens 12-16 11054556-6 2000 Each of the SUR2 splice variants transiently expressed with the inward rectifier Kir 6.2 formed functional K(ATP) channels in HEK 293 cells as assessed either by changes in DiBAC(4)(3) fluorescence responses or glyburide-sensitive whole cell currents. Glyburide 211-220 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 81-88 11018117-3 2000 Glibenclamide, added to the basolateral medium, significantly enhanced the osmotic flow induced by low doses of antidiuretic hormone (ADH) or forskolin (FK), while it inhibited the effect of exogenous cyclic adenosine monophosphate (cAMP) or its non-hydrolysable bromo derivative, 8-Br-cAMP, added to the basolateral medium. Glyburide 0-13 cathelicidin antimicrobial peptide Homo sapiens 233-237 11018117-3 2000 Glibenclamide, added to the basolateral medium, significantly enhanced the osmotic flow induced by low doses of antidiuretic hormone (ADH) or forskolin (FK), while it inhibited the effect of exogenous cyclic adenosine monophosphate (cAMP) or its non-hydrolysable bromo derivative, 8-Br-cAMP, added to the basolateral medium. Glyburide 0-13 cathelicidin antimicrobial peptide Homo sapiens 281-290 11018117-4 2000 These opposite effects of glibenclamide on the transepithelial osmotic flow can be explained by a reduction of cAMP permeability across the basolateral membrane of the epithelium. Glyburide 26-39 cathelicidin antimicrobial peptide Homo sapiens 111-115 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 16-20 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 192-205 cathelicidin antimicrobial peptide Homo sapiens 303-312 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 347-360 cathelicidin antimicrobial peptide Homo sapiens 16-20 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 347-360 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 347-360 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 347-360 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-5 2000 The decrease in cAMP permeability leads, according to the direction of the cAMP gradient, to firstly an enhanced osmotic flow when cAMP is generated intracellularly by addition of ADH and FK, glibenclamide reducing cAMP exit from the cell, and secondly a decreased osmotic flow in response to cAMP (and 8-Br-cAMP) added to the basolateral medium, glibenclamide inhibiting, in this case, their entry into the cell. Glyburide 347-360 cathelicidin antimicrobial peptide Homo sapiens 75-79 11018117-7 2000 The demonstration that glibenclamide actually inhibits the basolateral cAMP permeability rests on the fact that firstly it decreases the release of cAMP into the basolateral medium by about 40 %, at each concentration of ADH or forskolin tested, secondly it increases the cAMP content of paired hemibladders incubated in the presence of ADH or FK, when intracellular degradation was prevented by phosphodiesterase inhibition, and thirdly it decreases also the uptake of basolateral 8-Br-[3H]cAMP into paired toad hemibladders. Glyburide 23-36 cathelicidin antimicrobial peptide Homo sapiens 71-75 11018117-7 2000 The demonstration that glibenclamide actually inhibits the basolateral cAMP permeability rests on the fact that firstly it decreases the release of cAMP into the basolateral medium by about 40 %, at each concentration of ADH or forskolin tested, secondly it increases the cAMP content of paired hemibladders incubated in the presence of ADH or FK, when intracellular degradation was prevented by phosphodiesterase inhibition, and thirdly it decreases also the uptake of basolateral 8-Br-[3H]cAMP into paired toad hemibladders. Glyburide 23-36 cathelicidin antimicrobial peptide Homo sapiens 148-152 11018117-7 2000 The demonstration that glibenclamide actually inhibits the basolateral cAMP permeability rests on the fact that firstly it decreases the release of cAMP into the basolateral medium by about 40 %, at each concentration of ADH or forskolin tested, secondly it increases the cAMP content of paired hemibladders incubated in the presence of ADH or FK, when intracellular degradation was prevented by phosphodiesterase inhibition, and thirdly it decreases also the uptake of basolateral 8-Br-[3H]cAMP into paired toad hemibladders. Glyburide 23-36 cathelicidin antimicrobial peptide Homo sapiens 148-152 11018117-7 2000 The demonstration that glibenclamide actually inhibits the basolateral cAMP permeability rests on the fact that firstly it decreases the release of cAMP into the basolateral medium by about 40 %, at each concentration of ADH or forskolin tested, secondly it increases the cAMP content of paired hemibladders incubated in the presence of ADH or FK, when intracellular degradation was prevented by phosphodiesterase inhibition, and thirdly it decreases also the uptake of basolateral 8-Br-[3H]cAMP into paired toad hemibladders. Glyburide 23-36 cathelicidin antimicrobial peptide Homo sapiens 148-152 11018117-9 2000 Taken together, the present data demonstrate that glibenclamide inhibits the toad urinary bladder basolateral membrane permeability to cAMP, most probably by a direct interaction with a membrane protein not yet indentified but distinct from the sulphonylurea receptor. Glyburide 50-63 cathelicidin antimicrobial peptide Homo sapiens 135-139 11018523-4 2000 Previously we showed that co-expression in a baculovirus expression system of two parts of SUR1 divided at Pro1042 between TM12 and 13 leads to restoration of glibenclamide binding activity, whereas expression of either individual N- or C-terminal domain alone gave no glibenclamide binding activity [M.V. Glyburide 159-172 ATP binding cassette subfamily C member 8 Homo sapiens 91-95 11018523-4 2000 Previously we showed that co-expression in a baculovirus expression system of two parts of SUR1 divided at Pro1042 between TM12 and 13 leads to restoration of glibenclamide binding activity, whereas expression of either individual N- or C-terminal domain alone gave no glibenclamide binding activity [M.V. Glyburide 269-282 ATP binding cassette subfamily C member 8 Homo sapiens 91-95 11018523-9 2000 Here we show that the two half-molecules formed by division of SUR1 between NBD1 and TM12 or between TM13 and 14 also self-assemble to give glibenclamide binding activity. Glyburide 140-153 ATP binding cassette subfamily C member 8 Homo sapiens 63-67 11018523-12 2000 Simultaneous expression of Kir6.2 resulted in enhanced glibenclamide binding activity only when the N-half of SUR1 included TM12. Glyburide 55-68 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 27-33 11018523-12 2000 Simultaneous expression of Kir6.2 resulted in enhanced glibenclamide binding activity only when the N-half of SUR1 included TM12. Glyburide 55-68 ATP binding cassette subfamily C member 8 Homo sapiens 110-114 10965903-4 2000 In contrast, glibenclamide enhanced forskolin- or CRH-induced POMC expression in a dose-dependent manner. Glyburide 13-26 corticotropin releasing hormone Mus musculus 50-53 10965903-4 2000 In contrast, glibenclamide enhanced forskolin- or CRH-induced POMC expression in a dose-dependent manner. Glyburide 13-26 pro-opiomelanocortin-alpha Mus musculus 62-66 11225657-0 2000 Erythrocyte insulin receptor tyrosine kinase activity is increased in glyburide-treated patients with type 2 diabetes in good glycaemic control. Glyburide 70-79 insulin Homo sapiens 12-19 11854558-6 2000 On the contrary, glibenclamide (100 nmol/L) specifically blocked ATP-sensitive K(+) channels, and increased both [Ca(2+)]i and insulin secretion, but staurosporine had no effect on them. Glyburide 17-30 insulin Mesocricetus auratus 127-134 11225657-1 2000 AIM: The goal of this study was to test the hypothesis that insulin receptor tyrosine kinase activity of isolated erythrocytes would be greater in glyburide-treated patients with type 2 diabetes in good glycaemic control (n = 13) than in untreated patients (n = 12) with significant fasting hyperglycaemia. Glyburide 147-156 insulin Homo sapiens 60-67 11225657-5 2000 In addition, insulin-stimulated tyrosine kinase activity was increased in erythrocytes from glyburide -treated patients (p < 0.01). Glyburide 92-101 insulin Homo sapiens 13-20 11225657-6 2000 RESULTS: Although insulin receptor number was similar in solubilized erythrocytes from the two groups, tyrosine kinase activity per insulin receptor was significantly (p < 0.02) greater in erythrocytes from glyburide-treated patients with type 2 diabetes. Glyburide 210-219 insulin receptor Homo sapiens 132-148 10810315-0 2000 Glibenclamide but not other sulphonylureas stimulates release of neuropeptide Y from perifused rat islets and hamster insulinoma cells. Glyburide 0-13 neuropeptide Y Rattus norvegicus 65-79 10903923-3 2000 The Na(+)-K(+)-pump activity was diminished by a selective CFTR blocker (glybenclamide) or nonspecific Cl(-) channel inhibitors (NPPB and DPC) but not by outwardly rectifying Cl(-) channel blockers (DNDS, DIDS). Glyburide 73-86 CF transmembrane conductance regulator Homo sapiens 59-63 10873674-10 2000 Leptin normally relaxed arterial rings during superfusion of K channel blockers, including 3 x 10(-5) mol/l of glibenclamide, 1 x 10(-6) of mol/l apamin, and 5 x 10(-7) mol/l of charybdotoxin. Glyburide 111-124 leptin Homo sapiens 0-6 10892667-11 2000 Glibenclamide promoted the HDL-independent cholesterol efflux by decreasing esterified cholesterol and increasing the release of free cholesterol and secretion of apolipoprotein E into the medium. Glyburide 0-13 apolipoprotein E Homo sapiens 163-179 10892667-13 2000 These results suggest that glibenclamide inhibits the accumulation of cholesteryl ester in macrophages by enhancing the hydrolysis of cholesteryl ester as well as by increasing cholesterol efflux, and possibly, by increasing the secretion of apolipoprotein E. Glyburide 27-40 apolipoprotein E Homo sapiens 242-258 10828238-9 2000 Inclusion of the K(+)ATP channel blocker, glibenclamide, selectively abolished the arterial flow-induced changes in ICAM-1 and VCAM-1. Glyburide 42-55 intercellular adhesion molecule 1 Homo sapiens 116-122 10828238-9 2000 Inclusion of the K(+)ATP channel blocker, glibenclamide, selectively abolished the arterial flow-induced changes in ICAM-1 and VCAM-1. Glyburide 42-55 vascular cell adhesion molecule 1 Homo sapiens 127-133 11798815-12 2000 Study two: Glibenclamide-treated non-diabetic rats had higher mRNA expression levels of SUR1 and SUR2 in heart than normal control. Glyburide 11-24 ATP binding cassette subfamily C member 8 Rattus norvegicus 88-92 11798815-12 2000 Study two: Glibenclamide-treated non-diabetic rats had higher mRNA expression levels of SUR1 and SUR2 in heart than normal control. Glyburide 11-24 ATP binding cassette subfamily C member 9 Rattus norvegicus 97-101 10854830-2 2000 Uptake of p-aminohippurate via rOAT1 was markedly inhibited by glibenclamide and nateglinide, and moderately by chlorpropamide and tolbutamide. Glyburide 63-76 solute carrier family 22 member 6 Rattus norvegicus 31-36 10844111-2 2000 Spontaneous detrusor muscle contractions were unaffected by glibenclamide (K(ATP) channel blocker) but were reduced when pinacidil (K(ATP) channel opener) concentrations exceeded 10(-5) M. Inhibition by beta(2)-adrenoceptor agonist clenbuterol [10(-6) M] of 1 Hz electrical field stimulated contractions was abolished by glibenclamide [10(-6) M]. Glyburide 321-334 adrenoceptor beta 2 Rattus norvegicus 203-223 10872292-6 2000 Among the stimulators of insulin secretion are the sulfonylureas (e.g. glibenclamide, glibonuride, glisoxepid, glimepiride), and the so-called prandial glucose regulators, such as repaglinide, which differ from the sulfonylureas both chemically and in their pharmacodynamic properties. Glyburide 71-84 insulin Homo sapiens 25-32 10810315-6 2000 However, only glibenclamide stimulated the release of NPY from the islets (control 3.4+/-0.8 vs GLIB 24.5+/-5 attomol/min per islet, P<0.01, n=6). Glyburide 14-27 neuropeptide Y Rattus norvegicus 54-57 10810315-8 2000 Glibenclamide treatment of HIT cells showed a prompt insulin release (10 min) while NPY secretion was slower (60 min), suggesting that internalization of the sulphonylurea is required to stimulate NPY release. Glyburide 0-13 neuropeptide Y Rattus norvegicus 197-200 10810315-9 2000 Glibenclamide, the most common oral therapeutic agent in type 2 diabetes mellitus, is associated with release of the autocrine insulin secretion inhibitor, NPY. Glyburide 0-13 neuropeptide Y Rattus norvegicus 156-159 10799348-5 2000 This cardioprotective effect of FGF-1 was blocked by glibenclamide. Glyburide 53-66 fibroblast growth factor 1 Rattus norvegicus 32-37 10751228-1 2000 Recent studies showed that coexpression of Kir6.1 or Kir6.2 with the sulfonylurea receptor (SUR1, SUR2A, or SUR2B) reconstituted an inwardly rectifying, ATP-sensitive K(+) channel that was inhibited by glibenclamide (2, 15-17). Glyburide 202-215 potassium inwardly-rectifying channel, subfamily J, member 8 Rattus norvegicus 43-49 10751228-1 2000 Recent studies showed that coexpression of Kir6.1 or Kir6.2 with the sulfonylurea receptor (SUR1, SUR2A, or SUR2B) reconstituted an inwardly rectifying, ATP-sensitive K(+) channel that was inhibited by glibenclamide (2, 15-17). Glyburide 202-215 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 53-59 10751228-1 2000 Recent studies showed that coexpression of Kir6.1 or Kir6.2 with the sulfonylurea receptor (SUR1, SUR2A, or SUR2B) reconstituted an inwardly rectifying, ATP-sensitive K(+) channel that was inhibited by glibenclamide (2, 15-17). Glyburide 202-215 ATP binding cassette subfamily C member 8 Rattus norvegicus 92-96 10751228-1 2000 Recent studies showed that coexpression of Kir6.1 or Kir6.2 with the sulfonylurea receptor (SUR1, SUR2A, or SUR2B) reconstituted an inwardly rectifying, ATP-sensitive K(+) channel that was inhibited by glibenclamide (2, 15-17). Glyburide 202-215 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 108-113 10789825-8 2000 The reasons for this are unclear, but the more abnormal pattern of insulin release produced by glibenclamide may be partly responsible and, indeed, may explain the increased risk of hypoglycaemia with this agent. Glyburide 95-108 insulin Homo sapiens 67-74 10742701-5 2000 METHODS: The effects of acute administration of glyburide (0.3 mg/kg), a prototype sulfonylurea, on ANP release and sodium excretion were measured in vivo in a canine model of pacing-induced acute heart failure characterized by acute atrial stretch. Glyburide 48-57 natriuretic peptide A Canis lupus familiaris 100-103 10742701-8 2000 Glyburide delayed the time required for peak plasma ANP secretion to 48+/-5 min. Glyburide 0-9 natriuretic peptide A Canis lupus familiaris 52-55 10742701-12 2000 CONCLUSIONS: Glyburide delays release of ANP in acute heart failure resulting in impaired natriuresis. Glyburide 13-22 natriuretic peptide A Canis lupus familiaris 41-44 10693958-1 2000 Using the scrape-loading technique in cultured astrocytes, we show that sulfonylureas such as tolbutamide and glybenzcyclamide, which inhibit the ATP-sensitive K+ channel, prevent the inhibition of gap junction permeability caused by several structurally unrelated uncouplers such as oleic acid, arachidonic acid, endothelin-1, octanol, and alpha-glycyrrhetinic acid. Glyburide 110-126 endothelin 1 Homo sapiens 314-326 10594485-10 1999 Glibenclamide had the expected effect on insulin and glucose levels independent of comedication. Glyburide 0-13 insulin Homo sapiens 41-48 10648470-6 2000 Cyclosporin A, rifamycin SV, rifampicin, and glibenclamide cis-inhibited Bsep-mediated bile salt transport to similar extents as ATP-dependent taurocholate transport in cLPM vesicles. Glyburide 45-58 ATP binding cassette subfamily B member 11 Homo sapiens 73-77 10663449-1 2000 OBJECTIVE: We analysed the kinetics and effects of glibenclamide (Gb) on glucose, insulin and proinsulin secretion in two ethnic groups (10 in each) of type-2 diabetic patients, one of Caucasian, the other of Chinese origin. Glyburide 66-68 insulin Homo sapiens 94-104 10663449-12 2000 When Gb was administered, the plasma glucose increases were reduced, and the increases of serum insulin and proinsulin levels were greater in both ethnic groups. Glyburide 5-7 insulin Homo sapiens 96-103 10663449-12 2000 When Gb was administered, the plasma glucose increases were reduced, and the increases of serum insulin and proinsulin levels were greater in both ethnic groups. Glyburide 5-7 insulin Homo sapiens 108-118 10663449-20 2000 Gb augmented glucose-induced release of both insulin and proinsulin in both ethnic groups; the effect on insulin secretion was more pronounced. Glyburide 0-2 insulin Homo sapiens 45-52 10663449-20 2000 Gb augmented glucose-induced release of both insulin and proinsulin in both ethnic groups; the effect on insulin secretion was more pronounced. Glyburide 0-2 insulin Homo sapiens 57-67 10674713-9 2000 Nevertheless, K(ATP) and K(NDP) channels are both activated by K+ channel openers, including pinacidil and nicorandil, and inhibited by sulfonylurea derivatives such as glibenclamide. Glyburide 169-182 ATPase phospholipid transporting 8A2 Homo sapiens 16-19 10601248-5 1999 Two inhibitors of anion transport, glyburide and ethacrynic acid, blocked maturation of both caspase-1 and pro-IL-1beta and prevented release of the propolypeptides. Glyburide 35-44 caspase 1 Homo sapiens 93-102 10601248-5 1999 Two inhibitors of anion transport, glyburide and ethacrynic acid, blocked maturation of both caspase-1 and pro-IL-1beta and prevented release of the propolypeptides. Glyburide 35-44 interleukin 1 beta Homo sapiens 107-119 10600858-6 1999 The K(ATP) channel blocker glyburide (10 microM) reversed the depression of C1q, C1r, C3, C8, and C9 mRNA expression observed in the pinacidil-treated hearts. Glyburide 27-36 complement C1r subcomponent Oryctolagus cuniculus 81-88 10556530-5 1999 This delayed effect of AVP was inhibited by basal addition of 10(-4) M bumetanide and apical addition of 10(-4) M glibenclamide, suggesting chloride entry at the basal membrane through a Na(+)/K(+)/2Cl(-) and apical secretion through a chloride conductance. Glyburide 114-127 arginine vasopressin Rattus norvegicus 23-26 10562333-13 1999 Glibenclamide (50 microM) significantly blocked ICl,ATP activated by ATPgammaS or by the CFTR channel activator, levamisole. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 89-93 10531400-0 1999 Coexpression with the inward rectifier K(+) channel Kir6.1 increases the affinity of the vascular sulfonylurea receptor SUR2B for glibenclamide. Glyburide 130-143 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 22-58 10578127-0 1999 Effects of glibenclamide on glycylsarcosine transport by the rat peptide transporters PEPT1 and PEPT2. Glyburide 11-24 solute carrier family 15 member 1 Rattus norvegicus 86-91 10578127-3 1999 In the present study, we examined the effects of glibenclamide on the function of the H+/peptide cotransporters PEPT1 and PEPT2 by using stable transfectants. Glyburide 49-62 solute carrier family 15 member 1 Rattus norvegicus 112-117 10578127-4 1999 2 Uptake of [14C]-glycylsarcosine, a typical substrate for peptide transporters, by PEPT1- or PEPT2-expressing transfectant was inhibited by glibenclamide as well as other sulphonylureas including tolbutamide. Glyburide 141-154 solute carrier family 15 member 1 Rattus norvegicus 84-89 10578127-9 1999 6 In summary, glibenclamide inhibited the [14C]-glycylsarcosine transport by PEPT1 and PEPT2 in a noncompetitive fashion, although glibenclamide per se was not transported through these transporters. Glyburide 14-27 solute carrier family 15 member 1 Rattus norvegicus 77-82 10531400-0 1999 Coexpression with the inward rectifier K(+) channel Kir6.1 increases the affinity of the vascular sulfonylurea receptor SUR2B for glibenclamide. Glyburide 130-143 ATP binding cassette subfamily C member 8 Homo sapiens 98-119 10516647-6 1999 K+ channel currents due to hKir6.1+SUR1 or mouse Kir6.2+SUR1 were strongly inhibited by 1 microM glibenclamide. Glyburide 97-110 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 27-34 10516209-8 1999 When bronchi were pretreated with glibenclamide or 5-nitro-2-(3-phenylpropylamino)benzoic acid (both inhibitors of CFTR), the rate of ACh-induced liquid secretion was significantly reduced by 39 and 91%, respectively, compared with controls. Glyburide 34-47 CF transmembrane conductance regulator Homo sapiens 115-119 10516647-6 1999 K+ channel currents due to hKir6.1+SUR1 or mouse Kir6.2+SUR1 were strongly inhibited by 1 microM glibenclamide. Glyburide 97-110 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 35-39 10516647-6 1999 K+ channel currents due to hKir6.1+SUR1 or mouse Kir6.2+SUR1 were strongly inhibited by 1 microM glibenclamide. Glyburide 97-110 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 49-55 10516647-6 1999 K+ channel currents due to hKir6.1+SUR1 or mouse Kir6.2+SUR1 were strongly inhibited by 1 microM glibenclamide. Glyburide 97-110 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 56-60 10497157-5 1999 High glibenclamide affinity of SUR1 is not reduced by transfer of KCO I plus II from SUR2B, demonstrating that high SU and KCO affinity can coexist in the same SUR molecule. Glyburide 5-18 ATP binding cassette subfamily C member 8 Homo sapiens 31-35 10526729-4 1999 Plasma insulin concentrations were always increased by glibenclamide, and they were lowered identically by exercise with and without glibenclamide. Glyburide 55-68 insulin Homo sapiens 7-14 10526729-5 1999 However, throughout exercise, absolute concentrations of insulin were lower on days without glibenclamide compared with days with glibenclamide (34.5 +/- 4.7 vs. 47.4 +/- 5.5 pmol/l; P < 0.05). Glyburide 92-105 insulin Homo sapiens 57-64 10526729-12 1999 The interaction reflects an increased inhibition by glibenclamide-enhanced insulin levels of hepatic glucose production when hepatic glucose production is accelerated by exercise. Glyburide 52-65 insulin Homo sapiens 75-82 10564350-4 1999 Neuropeptide Y phase advances in the suprachiasmatic nuclei brain slice preparation were blocked by a number of K+ channel blockers (tetraethylammonium chloride, dendrotoxin-I, glybenclamide). Glyburide 177-190 neuropeptide Y Homo sapiens 0-14 10506587-2 1999 Compounds acting on the pancreatic sulfonylurea receptor (SUR) to increase (e.g., glibenclamide) or decrease (e.g., diazoxide) [Ca2+]i cause corresponding increases and decreases in weight gain. Glyburide 82-95 ATP binding cassette subfamily C member 8 Homo sapiens 35-56 10506587-2 1999 Compounds acting on the pancreatic sulfonylurea receptor (SUR) to increase (e.g., glibenclamide) or decrease (e.g., diazoxide) [Ca2+]i cause corresponding increases and decreases in weight gain. Glyburide 82-95 ATP binding cassette subfamily C member 8 Homo sapiens 58-61 10497157-2 1999 Notably, the neuronal/pancreatic beta-cell receptor, SUR1, imparts high sensitivity to hypoglycemic sulfonylureas (SUs; e.g. glibenclamide) and low to potassium channel openers (KCOs; e.g. P1075), whereas the opposite drug sensitivities are conferred by cardiovascular receptors, SUR2A and SUR2B. Glyburide 125-138 ATP binding cassette subfamily C member 8 Homo sapiens 53-57 10497157-5 1999 High glibenclamide affinity of SUR1 is not reduced by transfer of KCO I plus II from SUR2B, demonstrating that high SU and KCO affinity can coexist in the same SUR molecule. Glyburide 5-18 ATP binding cassette subfamily C member 8 Homo sapiens 31-34 10484343-3 1999 A linear 7-pS Cl- conductance, which is stimulated by ATP and cAMP analogs and inhibited by glibenclamide, consistent with CFTR activity, has been identified in GT1-7 cells. Glyburide 92-105 cystic fibrosis transmembrane conductance regulator Mus musculus 123-127 10551285-5 1999 In comparison, glibenclamide inhibited I(CFTR) with an IC50 value of approximately 20 microM. Glyburide 15-28 CF transmembrane conductance regulator Homo sapiens 41-45 10629872-6 1999 The results suggest that GB acts on acyl-CoA: cholesterol acyltransferase (ACAT) and inhibits its activity. Glyburide 25-27 sterol O-acyltransferase 1 Homo sapiens 36-73 10629872-6 1999 The results suggest that GB acts on acyl-CoA: cholesterol acyltransferase (ACAT) and inhibits its activity. Glyburide 25-27 sterol O-acyltransferase 1 Homo sapiens 75-79 10629872-8 1999 GB inhibition was not so much effective as those by CI-976 and NTE-122, known ACAT inhibitors, but the inhibition was complete in the presence of 100 microM GB. Glyburide 157-159 sterol O-acyltransferase 1 Homo sapiens 78-82 10629872-9 1999 Using cell homogenates of PMA-stimulated THP-1 cells, GB also inhibited the ACAT activity to the level of undifferentiated THP-1 cells. Glyburide 54-56 sterol O-acyltransferase 1 Homo sapiens 76-80 10629872-10 1999 These results indicate that GB acts as ACAT inhibitor but the chemical structure is quite different from the conventional ACAT inhibitors, suggesting it can be a seed to generate potential ACAT inhibitors which do not exhibit toxicity in adrenal gland. Glyburide 28-30 sterol O-acyltransferase 1 Homo sapiens 39-43 10550520-7 1999 Human calcitonin gene related peptide (hCGRP) (100 nM applied for 2-5 min) induced a time-dependent decrease in the frequency amplitude and duration of the spontaneous action potentials, in a manner blocked by glibenclamide (1 microM). Glyburide 210-223 calcitonin related polypeptide alpha Homo sapiens 39-44 10488073-10 1999 The activation of CFTR by MPB compounds was glibenclamide-sensitive and 4, 4"-diisothiocyanostilbene-2,2"-disulfonic acid-insensitive. Glyburide 44-57 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 18-22 10488073-10 1999 The activation of CFTR by MPB compounds was glibenclamide-sensitive and 4, 4"-diisothiocyanostilbene-2,2"-disulfonic acid-insensitive. Glyburide 44-57 AFA1 Homo sapiens 26-29 10484343-3 1999 A linear 7-pS Cl- conductance, which is stimulated by ATP and cAMP analogs and inhibited by glibenclamide, consistent with CFTR activity, has been identified in GT1-7 cells. Glyburide 92-105 myosin, light polypeptide 4 Mus musculus 161-164 10498831-12 1999 Glibenclamide bound to the SUR2 isoforms with 300 - 500 fold lower affinity than to SUR1. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 27-31 10498831-12 1999 Glibenclamide bound to the SUR2 isoforms with 300 - 500 fold lower affinity than to SUR1. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 84-88 10498841-2 1999 Hypoglycaemia-inducing sulphonylureas, such as glibenclamide, inhibit cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels. Glyburide 47-60 CF transmembrane conductance regulator Homo sapiens 70-121 10498831-16 1999 Hypoglycaemic sulphonylureas (e.g. glibenclamide) owe selectivity for SUR1 to lipophilic substitution on their urea group. Glyburide 35-48 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 70-74 10498841-2 1999 Hypoglycaemia-inducing sulphonylureas, such as glibenclamide, inhibit cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels. Glyburide 47-60 CF transmembrane conductance regulator Homo sapiens 123-127 10233156-6 1999 Treatment of monocytes with the sulfonylurea glibenclamide inhibits both IL-1beta secretion and vesicular accumulation, suggesting that this drug prevents the translocation of proIL-1beta from the cytosol into the vesicles. Glyburide 45-58 interleukin 1 beta Homo sapiens 73-81 10498841-19 1999 Like glibenclamide, non-sulphonylurea hypoglycaemic agents may inhibit CFTR by occluding the channel pore and preventing Cl- permeation. Glyburide 5-18 CF transmembrane conductance regulator Homo sapiens 71-75 10566126-0 1999 The effect of octreotide on glucose and insulin levels in a patient with type 2 diabetes on glibenclamide. Glyburide 92-105 insulin Homo sapiens 40-47 10342826-9 1999 These results suggest that a site in the COOH-terminal set of TMs of the SUR1 subunit of the K(ATP) channel is involved in the binding of tolbutamide and glibenclamide. Glyburide 154-167 ATP-binding cassette sub-family C member 8 Xenopus laevis 73-77 10347249-6 1999 Consistent with these findings, reconstituted SUR2A/KIR6.2 and SUR2B/KIR6.2 channels revealed similar sensitivities for glibenclamide and tolbutamide. Glyburide 120-133 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 52-58 10347249-6 1999 Consistent with these findings, reconstituted SUR2A/KIR6.2 and SUR2B/KIR6.2 channels revealed similar sensitivities for glibenclamide and tolbutamide. Glyburide 120-133 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 69-75 10347249-8 1999 Potencies of glibenclamide, glipizide, tolbutamide, and meglitinide to inhibit activity of SUR1/KIR6.2 and SUR2B/KIR6.2 channels were 3- to 6-fold higher than binding affinities of these drugs with concentration-inhibition relations being significantly steeper (Hill coefficients 1.23-1.32) than binding curves (Hill coefficients 0.93-1.06). Glyburide 13-26 ATP binding cassette subfamily C member 8 Rattus norvegicus 91-95 10347249-8 1999 Potencies of glibenclamide, glipizide, tolbutamide, and meglitinide to inhibit activity of SUR1/KIR6.2 and SUR2B/KIR6.2 channels were 3- to 6-fold higher than binding affinities of these drugs with concentration-inhibition relations being significantly steeper (Hill coefficients 1.23-1.32) than binding curves (Hill coefficients 0.93-1.06). Glyburide 13-26 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 96-102 10347249-8 1999 Potencies of glibenclamide, glipizide, tolbutamide, and meglitinide to inhibit activity of SUR1/KIR6.2 and SUR2B/KIR6.2 channels were 3- to 6-fold higher than binding affinities of these drugs with concentration-inhibition relations being significantly steeper (Hill coefficients 1.23-1.32) than binding curves (Hill coefficients 0.93-1.06). Glyburide 13-26 potassium inwardly-rectifying channel, subfamily J, member 11 Rattus norvegicus 113-119 10368184-1 1999 These two ABC proteins possess an ion channel activity and bind specific sulfonylureas, such as glibenclamide, but homologs have not been identified in plant cells. Glyburide 97-110 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 11-14 10368184-3 1999 Because the CFTR, a chloride channel, is sensitive to glibenclamide and able to interact with K+ channels, we investigated its presence in guard cells. Glyburide 55-68 CF transmembrane conductance regulator Homo sapiens 13-17 10368184-4 1999 Potent CFTR inhibitors, such as glibenclamide and diphenylamine-2-carboxylic acid, triggered stomatal opening in darkness. Glyburide 33-46 CF transmembrane conductance regulator Homo sapiens 8-12 10368184-7 1999 Moreover, in epidermal strip bioassays, the stomatal closure triggered by Ca2+ or abscisic acid was reversed by glibenclamide. These results suggest that the slow anion channel is an ABC protein or is tightly controlled by such a protein that interacts with the abscisic acid signal transduction pathway in guard cells. Glyburide 113-126 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 184-187 10370080-1 1999 The sulphonylurea receptor (SUR) is the site of action for sulphonylurea derivatives such as glibenclamide, which are widely used as oral hypoglycaemic agents. Glyburide 93-106 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 4-26 10370080-1 1999 The sulphonylurea receptor (SUR) is the site of action for sulphonylurea derivatives such as glibenclamide, which are widely used as oral hypoglycaemic agents. Glyburide 93-106 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 28-31 10487677-0 1999 Oral glibenclamide suppresses glucagon secretion during insulin-induced hypoglycemia in patients with type 2 diabetes. Glyburide 5-18 insulin Homo sapiens 56-63 10543431-7 1999 Glibenclamide, which was antifibrillatory at 0.3 mg/kg and 1 mg/kg, increased plasma insulin and lowered blood glucose already at a dose as low as 0.01 mg/kg. Glyburide 0-13 insulin Homo sapiens 85-92 10522750-3 1999 The inhibitory effect of endothelin-1 on the contraction induced by 5-HT is abolished by deendothelialization, by the endothelin ET(B) receptor antagonist RES 701-1, by indomethacin, or by glibenclamide. Glyburide 189-202 endothelin 1 Rattus norvegicus 25-37 10471448-22 1999 Glibenclamide treatment of hypoxic animals significantly reduced CBF in all brain areas (P<0.05). Glyburide 0-13 CCAAT/enhancer binding protein zeta Rattus norvegicus 65-68 10471448-24 1999 Glibenclamide treatment significantly attenuated the CBF increase during hypoxia but not after hemodilution. Glyburide 0-13 CCAAT/enhancer binding protein zeta Rattus norvegicus 53-56 10441486-0 1999 Glibenclamide induces apoptosis through inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels and intracellular Ca(2+) release in HepG2 human hepatoblastoma cells. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 54-105 10441486-0 1999 Glibenclamide induces apoptosis through inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels and intracellular Ca(2+) release in HepG2 human hepatoblastoma cells. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 107-111 10441486-1 1999 Glibenclamide, an inhibitor of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels, induced apoptosis in a dose- and time-dependent manner in HepG2 human hepatoblastoma cells. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 31-82 10441486-1 1999 Glibenclamide, an inhibitor of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels, induced apoptosis in a dose- and time-dependent manner in HepG2 human hepatoblastoma cells. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 84-88 10441486-7 1999 These results suggest that glibenclamide induced apoptosis through inhibition of CFTR Cl(-) channels and intracellular Ca(2+) release and that this protein may be a good target for treatment of human hepatomas. Glyburide 27-40 CF transmembrane conductance regulator Homo sapiens 81-85 10482912-6 1999 Glibenclamide, an antagonist of CFTR, and anthracene-9-carboxylate (9-AC) inhibited current less than 25% at 100 microM. Glyburide 0-13 CF transmembrane conductance regulator Canis lupus familiaris 32-36 10466081-1 1999 The effects of simultaneous administrations of Cyclosporin A (CsA) and Glyburide on the immune system of rats has been evaluated in terms of Interleukin-2 (IL-2) production by Concanavalin A (ConA) stimulated splenocytes and exogenous IL-2 binding capacity. Glyburide 71-80 interleukin 2 Rattus norvegicus 141-154 10466081-1 1999 The effects of simultaneous administrations of Cyclosporin A (CsA) and Glyburide on the immune system of rats has been evaluated in terms of Interleukin-2 (IL-2) production by Concanavalin A (ConA) stimulated splenocytes and exogenous IL-2 binding capacity. Glyburide 71-80 interleukin 2 Rattus norvegicus 235-239 10466081-3 1999 Spleen cells from rats receiving CsA had reduced levels of IL-2 when compared to untreated controls or rats receiving Glyburide only. Glyburide 118-127 interleukin 2 Rattus norvegicus 59-63 10466081-5 1999 These findings let us hypothesize that when there are lower concentrations of CsA in lymphocytes there is an increase of cellular metabolism induced by Glyburide that leads to an increase in IL-2 secretion and in IL-2 receptor expression on cellular surface restoring these levels to normal or slightly above normal levels. Glyburide 152-161 interleukin 2 Rattus norvegicus 191-195 10466081-5 1999 These findings let us hypothesize that when there are lower concentrations of CsA in lymphocytes there is an increase of cellular metabolism induced by Glyburide that leads to an increase in IL-2 secretion and in IL-2 receptor expression on cellular surface restoring these levels to normal or slightly above normal levels. Glyburide 152-161 interleukin 2 Rattus norvegicus 213-217 10614063-8 1999 CONCLUSIONS: The postprandial levels of glucose, triglycerides, fibrinogen, F1.2, TAT and d-dimers were lower after glibenclamide administration as compared to placebo, while the concentrations of insulin and c-peptide were higher. Glyburide 116-129 fibrinogen beta chain Homo sapiens 64-74 10614063-8 1999 CONCLUSIONS: The postprandial levels of glucose, triglycerides, fibrinogen, F1.2, TAT and d-dimers were lower after glibenclamide administration as compared to placebo, while the concentrations of insulin and c-peptide were higher. Glyburide 116-129 coagulation factor XII Homo sapiens 76-80 10614063-8 1999 CONCLUSIONS: The postprandial levels of glucose, triglycerides, fibrinogen, F1.2, TAT and d-dimers were lower after glibenclamide administration as compared to placebo, while the concentrations of insulin and c-peptide were higher. Glyburide 116-129 tyrosine aminotransferase Homo sapiens 82-85 10614063-8 1999 CONCLUSIONS: The postprandial levels of glucose, triglycerides, fibrinogen, F1.2, TAT and d-dimers were lower after glibenclamide administration as compared to placebo, while the concentrations of insulin and c-peptide were higher. Glyburide 116-129 insulin Homo sapiens 197-204 10614063-8 1999 CONCLUSIONS: The postprandial levels of glucose, triglycerides, fibrinogen, F1.2, TAT and d-dimers were lower after glibenclamide administration as compared to placebo, while the concentrations of insulin and c-peptide were higher. Glyburide 116-129 insulin Homo sapiens 209-218 10381797-4 1999 Glibenclamide, a known inhibitor of sulfonylurea receptor and cystic fibrosis conductance regulator, induced a dose-dependent and reversible stimulation (of the order of 40-50%) of the amiloride-sensitive current in oocytes expressing Xenopus ENaC, with a K1/2 of 45 +/- 5 microM. Glyburide 0-13 sodium channel epithelial 1 subunit gamma Rattus norvegicus 243-247 10422791-8 1999 Glibenclamide abolished their effects on myeloperoxidase activity and, alone, increased this parameter. Glyburide 0-13 myeloperoxidase Rattus norvegicus 41-56 10358118-3 1999 Here we report the effects of levcromakalim (LCRK, a channel opener) and glibenclamide (GBC, a blocker) on membrane potential, whole-cell current and the cytoplasmic Ca2+ concentration of renin-secreting cells (RSC). Glyburide 73-86 renin Rattus norvegicus 188-193 10233156-6 1999 Treatment of monocytes with the sulfonylurea glibenclamide inhibits both IL-1beta secretion and vesicular accumulation, suggesting that this drug prevents the translocation of proIL-1beta from the cytosol into the vesicles. Glyburide 45-58 interleukin 1 beta Homo sapiens 176-187 10208857-0 1999 Characterization of low-affinity binding sites for glibenclamide on the Kir6.2 subunit of the beta-cell KATP channel. Glyburide 51-64 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 72-78 10208857-5 1999 Binding studies and Scatchard analysis revealed the presence of a single class of low affinity binding sites for glibenclamide on the COS/Kir6.2 cells with characteristics similar to that observed for the low affinity site of the MIN6 beta cells. Glyburide 113-126 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 138-144 10337452-4 1999 In 10 patients with NIDDM receiving glibenclamide (CAS 10238-21-8) the fasting plasma amylin level was twofold higher than in healthy control (2.72 +/- 0.38 pmol/l; p < 0.025) but following glucagon administration it increased only twofold. Glyburide 36-49 islet amyloid polypeptide Homo sapiens 86-92 10337452-5 1999 In 15 patients treated with metformin (CAS 657-24-9) the fasting plasma amylin level was similar to that in healthy individuals (1.64 +/- 0.25 pmol/l), but after glucagon stimulation the increment of plasma amylin was minimal and the relevant mean value was significantly lower when compared with those in healthy individuals and with NIDDM patients treated with glibenclamide. Glyburide 363-376 islet amyloid polypeptide Homo sapiens 72-78 10337452-6 1999 In 10 untreated obese patients with newly diagnosed NIDDM the administration of glibenclamide (14 days) resulted in the increase of basal (2.47 +/- 0.23 and 3.16 +/- 0.29 pmol/l; p < 0.1), and glucagon stimulated (3.34 +/- 0.39 and 4.56 +/- 0.38; p < 0.05) plasma amylin concentrations, whereas other 10 patients receiving metformin showed a decrease in fasting plasma level of this peptide before (2.64 +/- 0.59 and 1.28 +/- 0.38 pmol/l; p < 0.1), and after glucagon injection (5.02 +/- 0.55 and 2.83 +/- 0.65 pmol/l; p < 0.02). Glyburide 80-93 islet amyloid polypeptide Homo sapiens 270-276 10225476-7 1999 Plasma membrane GLUT4 protein content was significantly augmented by a factor of 1.48-fold (p<0.02) in the glibenclamide-treated group and tended to be increased 1.32 times by administration of metformin (p=0.06). Glyburide 110-123 solute carrier family 2 member 4 Rattus norvegicus 16-21 10342285-9 1999 A blocker of ATP-sensitive K+ channel, glibenclamide (1 microM), partially recovered the interleukin-1 beta-induced inhibition. Glyburide 39-52 interleukin 1 beta Rattus norvegicus 89-107 10087141-0 1999 P-glycoprotein inhibition by glibenclamide and related compounds. Glyburide 29-42 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 10087141-1 1999 Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5"-triphosphate (ATP)-binding cassette] transporters. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 49-71 10087141-1 1999 Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5"-triphosphate (ATP)-binding cassette] transporters. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 73-76 10087141-1 1999 Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5"-triphosphate (ATP)-binding cassette] transporters. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 126-177 10087141-1 1999 Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5"-triphosphate (ATP)-binding cassette] transporters. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 187-191 10087141-2 1999 The effect of glibenclamide and two synthetic sulphonylcyanoguanidine derivatives (dubbed BM-208 and BM-223) was examined on P-glycoprotein, the major ABC transporter responsible for multidrug resistance (MDR) in cancer cells. Glyburide 14-27 ATP binding cassette subfamily B member 1 Homo sapiens 125-139 10087141-5 1999 Furthermore, glibenclamide is itself a substrate for P-glycoprotein, since the cellular accumulation of [3H]glibenclamide was low and substantially increased by addition of P-glycoprotein substrates (e. g., vinblastine and cyclosporine) only in the P-glycoprotein-expressing cell lines. Glyburide 13-26 ATP binding cassette subfamily B member 1 Homo sapiens 53-67 10087141-5 1999 Furthermore, glibenclamide is itself a substrate for P-glycoprotein, since the cellular accumulation of [3H]glibenclamide was low and substantially increased by addition of P-glycoprotein substrates (e. g., vinblastine and cyclosporine) only in the P-glycoprotein-expressing cell lines. Glyburide 13-26 ATP binding cassette subfamily B member 1 Homo sapiens 173-187 10087141-5 1999 Furthermore, glibenclamide is itself a substrate for P-glycoprotein, since the cellular accumulation of [3H]glibenclamide was low and substantially increased by addition of P-glycoprotein substrates (e. g., vinblastine and cyclosporine) only in the P-glycoprotein-expressing cell lines. Glyburide 13-26 ATP binding cassette subfamily B member 1 Homo sapiens 173-187 10087141-6 1999 We conclude that glibenclamide and two sulphonylcyanoguanidine derivatives inhibit P-glycoprotein and that sulphonylurea drugs would appear to be general inhibitors of ABC transporters, suggesting an interaction with some conserved motif. Glyburide 17-30 ATP binding cassette subfamily B member 1 Homo sapiens 83-97 11798656-3 1999 RESULTS: In amylin concentrations of 5 micromol/L and 10 micromol/L, 3 nmol/L glyburide decreased insulin release volume, being (3.8 +/- 1.0) microg/L and (2.1 +/- 1.0) microg/L as compare with (4.9 +/- 0.9) microg/L of the control group (t = 2.313, P < 0.05; t = 5.887, P < 0.01). Glyburide 78-87 islet amyloid polypeptide Rattus norvegicus 12-18 10070091-8 1999 Pretreatment with the ATP-sensitive potassium-channel blocker glibenclamide enhanced epicardial vasodilation in response to BNP. Glyburide 62-75 natriuretic peptides B Sus scrofa 124-127 10193691-5 1999 Serum insulin levels were lower with troglitazone than with glibenclamide. Glyburide 60-73 insulin Homo sapiens 6-13 10369423-3 1999 In this study, we have investigated effects of hypoglycemic sulfonylureas (gliclazide and glibenclamide) and a thiazolidinedione (troglitazone) on lipopolysaccharide-induced TNF-alpha production, which was evaluated by immunoassay and bioassay, in vivo using mice and partly in vitro using human peripheral blood mononuclear cells. Glyburide 90-103 tumor necrosis factor Mus musculus 174-183 10069674-8 1999 Sin-1 produced a significant decrease in calcium transient (by approximately 20%), which was already maximal at 10(-7) M. When given with the potassium channel antagonist glibenclamide (10(-5) M), nicorandil induced the same effects as those observed with Sin-1. Glyburide 171-184 MAPK associated protein 1 Homo sapiens 0-5 10069674-8 1999 Sin-1 produced a significant decrease in calcium transient (by approximately 20%), which was already maximal at 10(-7) M. When given with the potassium channel antagonist glibenclamide (10(-5) M), nicorandil induced the same effects as those observed with Sin-1. Glyburide 171-184 MAPK associated protein 1 Homo sapiens 256-261 10509738-5 1999 These findings suggest a much higher affinity of glibenclamide than S21403 for the artificial phospholipid bilayer, this coinciding with a higher biological potency, as insulin secretagogue, of the hypoglycemic sulfonylurea as compared to meglitinide analog. Glyburide 49-62 insulin Homo sapiens 169-176 9990013-8 1999 This direct biochemical evidence of cooperative interaction in nucleotide binding of the two NBFs of SUR1 suggests that glibenclamide both blocks this cooperative binding of ATP and MgADP and, in cooperation with the MgADP bound at NBF2, causes ATP to be released from NBF1. Glyburide 120-133 ATP binding cassette subfamily C member 8 Homo sapiens 101-105 16801070-0 1999 Inhibitory effect of glyburide on thrombin-induced platelet aggregation and phosphoinositide metabolism in normal human platelets. Glyburide 21-30 coagulation factor II, thrombin Homo sapiens 34-42 10022602-6 1999 The adrenomedullin-induced response in left pulmonary artery blood flow was inhibited by N(omega)-nitro-L-arginine (inhibition rate 99%) and significantly attenuated by glibenclamide (inhibition rate 44%); however, no significant changes were found with CGRP receptor blocker or indomethacin (inhibition rate 0 and 17%, respectively). Glyburide 169-182 pro-adrenomedullin Ovis aries 4-18 9889382-4 1999 6+/-0.2 microM ATP, and that the mechanical stress-induced release of ATP was inhibited by glibenclamide and verapamil, non-specific inhibitors of the cystic fibrosis transmembrane conductance regulator and P-glycoprotein, respectively. Glyburide 91-104 cystic fibrosis transmembrane conductance regulator Mus musculus 151-202 10659155-5 1999 The results show a dose-dependent decline in CBF in normoxia and at the end of reperfusion (after an ischemic period) with glibenclamide treatment compared to control. Glyburide 123-136 CCAAT/enhancer binding protein zeta Rattus norvegicus 45-48 10728789-4 1999 These studies suggest that the K+(ATP) channel blocker, glibenclamide, modulated the adenosine A2A receptor in such a manner that [3H]CGS 21680 alone recognizes a single affinity adenosine receptor, but that the interactions between K+(ATP) channels and adenosine receptors. Glyburide 56-69 adenosine A2a receptor Bos taurus 85-107 10543411-12 1999 Despite this C-peptide was significantly higher (p < 0.002) glibenclamide (5.7 +/- 1.5 ng/ml) compared to glimepiride (5.1 +/- 1.3 ng/ml); the trend was the same for insulin but the results were not significantly different (p = 0.06) In conclusion, in the fasting state, glimepiride and glibenclamide had similar effects on the changes in blood glucose levels after i.v. Glyburide 63-76 insulin Homo sapiens 13-22 9884422-3 1999 Renin activity significantly increased from a basal value of 11.7 +/- 3.6 to a peak value of 20.6 +/- 5.5 ng/Ang I/ml/h with tolbutamide, from 14.4 +/- 4.6 to 32.7 +/- 6.5 ng/Ang I/ml/h with glibenclamide, and from 15.0 +/- 4.9 to 30.4 +/- 6.1 ng/Ang I/ml/h with chlorpropamide. Glyburide 191-204 renin Rattus norvegicus 0-5 9884422-5 1999 In kidneys perfused with a calcium-free medium, glibenclamide produced a significant increase in renin activity from a basal value of 13.4 +/- 2.1 to a peak value of 30.6 +/- 3.4 ng Ang I/ml/h. Glyburide 48-61 renin Rattus norvegicus 97-102 16801070-2 1999 To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. Glyburide 112-121 coagulation factor II, thrombin Homo sapiens 137-145 16801070-3 1999 Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). Glyburide 153-162 coagulation factor II, thrombin Homo sapiens 50-58 16801070-3 1999 Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). Glyburide 153-162 insulin Homo sapiens 193-200 16801070-4 1999 Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. Glyburide 83-92 coagulation factor II, thrombin Homo sapiens 0-8 16801070-5 1999 Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. Glyburide 109-118 coagulation factor II, thrombin Homo sapiens 48-56 16801070-6 1999 These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. Glyburide 27-36 coagulation factor II, thrombin Homo sapiens 60-68 9843850-6 1998 The cystic fibrosis transmembrane conductance regulator channel blocker glibenclamide and the loop diuretic bumetanide partially decreased the forskolin-induced increase in short-circuit current. Glyburide 72-85 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 4-55 9867217-7 1998 Glibenclamide, KCl or corticotropin releasing factor (CRF) stimulated (p < 0.05) insulin secretion both in AtT20HI and AtT20HI-GLUT2-GK-6 cells. Glyburide 0-13 solute carrier family 2 (facilitated glucose transporter), member 2 Mus musculus 130-135 9867217-7 1998 Glibenclamide, KCl or corticotropin releasing factor (CRF) stimulated (p < 0.05) insulin secretion both in AtT20HI and AtT20HI-GLUT2-GK-6 cells. Glyburide 0-13 glucokinase Mus musculus 136-138 9867217-8 1998 Insulin secretion stimulated by glibenclamide, KCl or CRF was further enhanced by the addition of 25 mmol/l glucose in AtT20HI-GLUT2-GK-6 cells but not in AtT20HI cells. Glyburide 32-45 insulin Homo sapiens 0-7 9862440-2 1998 In this paper we show that I(HERG), recorded in neuroblastoma cells and guinea-pig ventricular myocytes, was reversibly inhibited by the K(ATP) channel blocker glibenclamide (IC50 = 74 microM). Glyburide 160-173 potassium voltage-gated channel subfamily H member 2 Homo sapiens 29-33 9600650-7 1998 treatment with glibenclamide (20 mg/kg), the vasodepressor responses not only to adenosine but also to CGRP (0.5 microg/kg) and cromakalim (30 microg/kg) were significantly reduced, while those to acetylcholine and isoproterenol remained unchanged. Glyburide 15-28 calcitonin-related polypeptide alpha Rattus norvegicus 103-107 11091663-4 1998 Insulin therapy was thought to be necessary because treatment with glibenclamide was not effective. Glyburide 67-80 insulin Homo sapiens 0-7 9676714-4 1998 Relaxations to CNP were significantly less in arteries from male compared with female pigs and were significantly attenuated by charybdotoxin and glibenclamide in both sexes. Glyburide 146-159 natriuretic peptide C Sus scrofa 15-18 9658206-11 1998 In normokalemic animals, insulin applied in vitro to the muscles induced a glybenclamide-sensitive hyperpolarization of the fibers and also stimulated the sarcolemmal ATP-sensitive K+ channels. Glyburide 75-88 insulin Homo sapiens 25-32 9618558-7 1998 In contrast, the P-glycoprotein inhibitors tamoxifen and verapamil and the cystic fibrosis transmembrane conductance regulator (CFTR) blockers glybenclamide and diphenylamine-2-carboxylate did not affect ATP release from either cell type. Glyburide 143-156 CF transmembrane conductance regulator Bos taurus 75-126 9618558-7 1998 In contrast, the P-glycoprotein inhibitors tamoxifen and verapamil and the cystic fibrosis transmembrane conductance regulator (CFTR) blockers glybenclamide and diphenylamine-2-carboxylate did not affect ATP release from either cell type. Glyburide 143-156 CF transmembrane conductance regulator Bos taurus 128-132 9603917-4 1998 Similar to the KATP channels in the kidney but different from KATP channels in excitable tissues, the Kir1.1a/CFTR channel was inhibited by glibenclamide with micromolar affinity. Glyburide 140-153 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 110-114 9841499-5 1998 These effects were partially attenuated by 10 microM glibenclamide (62 +/- 16% inhibition, P = 0.025), indicating both KATP-dependent and -independent actions of CGRP. Glyburide 53-66 calcitonin-related polypeptide alpha Rattus norvegicus 162-166 9841499-7 1998 CGRP also inhibited the efferent arteriolar response to angiotensin II in the absence and presence of glibenclamide. Glyburide 102-115 calcitonin-related polypeptide alpha Rattus norvegicus 0-4 9661051-7 1998 Stimulation with a cAMP-elevating agent induces a Isc increase that is inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) blocker glibenclamide. Glyburide 155-168 CF transmembrane conductance regulator Homo sapiens 88-139 9661051-7 1998 Stimulation with a cAMP-elevating agent induces a Isc increase that is inhibited by the cystic fibrosis transmembrane conductance regulator (CFTR) blocker glibenclamide. Glyburide 155-168 CF transmembrane conductance regulator Homo sapiens 141-145 9605159-6 1998 In contrast, increasing concentrations of IL-3 or granulocyte-macrophage CSF overcome glyburide inhibition. Glyburide 86-95 interleukin 3 Homo sapiens 42-46 9575885-7 1998 Enhanced glomerular production of both inactive and active TGF-beta 1 induced by the 8.0% NaCl diet was inhibited by tetraethylammonium (TEA) and not glybenclamide. Glyburide 150-163 transforming growth factor, beta 1 Rattus norvegicus 59-69 9571356-10 1998 Ventricular fibrillation in diabetic patients taking glibenclamide (11.8%) was similar to that of nondiabetic patients (11.0%) but was lower than that for those patients taking either gliclazide (18.0%; 0.1 > P > 0.05) or insulin (22.8%; P < 0.05). Glyburide 53-66 insulin Homo sapiens 228-235 9490811-12 1998 1-transfected cells were not affected by glibenclamide, whereas glibenclamide did inhibit the conductance expressed in cells co-transfected with CFTR (IC50 = 35.9 +/- 6.6 microM). Glyburide 77-90 cystic fibrosis transmembrane conductance regulator Mus musculus 158-162 9490813-13 1998 Experiments with amphotericin B-permeabilized monolayers revealed that the apical PGE2-activated, NPPB- and glibenclamide-sensitive conductance was Cl- dependent and that the current-voltage relationship and anion permeation properties (SCN->Br- > Cl- > I-) were characteristic of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 108-121 CF transmembrane conductance regulator Homo sapiens 294-345 9490813-13 1998 Experiments with amphotericin B-permeabilized monolayers revealed that the apical PGE2-activated, NPPB- and glibenclamide-sensitive conductance was Cl- dependent and that the current-voltage relationship and anion permeation properties (SCN->Br- > Cl- > I-) were characteristic of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 108-121 CF transmembrane conductance regulator Homo sapiens 347-351 9815080-3 1998 Incubation of rabbit RBCs with either of two inhibitors of CFTR activity, glibenclamide (10 microM) or niflumic acid (20 microM), resulted in inhibition of deformation-induced ATP release. Glyburide 74-87 cystic fibrosis transmembrane conductance regulator Oryctolagus cuniculus 59-63 9799404-5 1998 Incubation with 1 microM glibenclamide, a blocker of the ATP-dependent K+ current (IKATP), abolished the swelling-induced shortening of the action potential duration, whereas incubation with 0.5 mM 4, 4"-diisothiocyanatostilbene-2,2"-disulphonic acid (DIDS), a blocker of the swelling-induced Cl- current (ICl,swell), had no effect on the action potential duration in hypotonic solution. Glyburide 25-38 ATP-sensitive inward rectifier potassium channel 11 Cavia porcellus 83-88 9806343-13 1998 Glibenclamide inhibited [3H]-P1075 binding with Ki values of 0.35 and 2.4 microM at 3 Mm and 1 mM free Mg2+, respectively. Glyburide 0-13 mucin 7, secreted Homo sapiens 103-106 9806343-14 1998 Glibenclamide enhanced the dissociation of the [3H]-P1075-SUR2B complex suggesting a negative allosteric coupling between the binding sites for P1075 and the sulphonylureas. Glyburide 0-13 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 58-63 9806343-16 1998 It is concluded that an MgATP site on SUR2B with microM affinity must be occupied to allow opener binding whereas Mg2+ concentrations > or = 10 microM decrease the affinities for openers and glibenclamide. Glyburide 194-207 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 38-43 9806343-16 1998 It is concluded that an MgATP site on SUR2B with microM affinity must be occupied to allow opener binding whereas Mg2+ concentrations > or = 10 microM decrease the affinities for openers and glibenclamide. Glyburide 194-207 mucin 7, secreted Homo sapiens 114-117 11367749-7 1998 (4) Preperfusing with KATP channel antagonist-glibenclamide (10 mumol/L) could also eliminated the effects of ET-1. Glyburide 46-59 endothelin 1 Rattus norvegicus 110-114 9726229-6 1998 Glibenclamide also blocked Kir6.2/SUR1 and Kir6.2/SUR2A currents with high affinity (Kis approximately 4 nmol/l and approximately 27 nmol/l, respectively); however, only for cardiac-type K(ATP) channels was this block reversible. Glyburide 0-13 ATP-binding cassette sub-family C member 8 Xenopus laevis 34-38 9726229-7 1998 Physiological concentrations of MgADP (100 micromol/l) enhanced glibenclamide inhibition of Kir6.2/SUR1 currents but reduced that of Kir6.2/SUR2A currents. Glyburide 64-77 ATP-binding cassette sub-family C member 8 Xenopus laevis 99-103 9699500-5 1998 We also demonstrated that inhibition of CFTR by glibenclamide or diphenylamine-2-carboxylate did not modify the activity of SGLT1 and inhibition of SGLT1 by phlorizin did not modify the activity of CFTR, although it resulted in inhibition of glycoconjugate synthesis. Glyburide 48-61 CF transmembrane conductance regulator Homo sapiens 40-44 9589648-7 1998 Postprandial insulin levels were significantly greater than placebo and miglitol in the glyburide group (P < 0.01). Glyburide 88-97 insulin Homo sapiens 13-20 9589648-11 1998 The greater HbA1c reductions seen with once-a-day glyburide occurred at a cost of significant increases in weight, insulin levels, and the incidences of clinical and subclinical hypoglycemia, which did not occur in the miglitol groups. Glyburide 50-59 insulin Homo sapiens 115-122 9797183-4 1998 RESULTS: Administration of glibenclamide produced significantly better glycaemic control than placebo (fasting blood glucose level 8.5 +/- 2.4 versus 13.5 +/- 4.5 mmol/l, P < 0.001) and plasma insulin levels were significantly higher during glibenclamide treatment than they were with placebo (12.9 +/- 4.4 versus 9.2 +/- 4.1 mU/l, P < 0.05). Glyburide 27-40 insulin Homo sapiens 196-203 9797183-7 1998 Responses of diastolic blood pressure to intravenous infusion of angiotensin II and forearm vascular responses to intra-brachial arterial infusion of angiotensin II were significantly greater during glibenclamide treatment than they were with placebo (P < 0.05). Glyburide 199-212 angiotensinogen Homo sapiens 65-79 9797183-7 1998 Responses of diastolic blood pressure to intravenous infusion of angiotensin II and forearm vascular responses to intra-brachial arterial infusion of angiotensin II were significantly greater during glibenclamide treatment than they were with placebo (P < 0.05). Glyburide 199-212 angiotensinogen Homo sapiens 150-164 9559898-28 1998 It was concluded that circumferential stretch of the proximal RP inhibits the contractility of the distal RP and that a component of this inhibition involves the activation of a glibenclamide-sensitive mechanism via the release of endogenous CGRP, possibly from the varicosities of intramural sensory nerves. Glyburide 178-191 calcitonin related polypeptide alpha Homo sapiens 242-246 9530112-5 1998 Purified CFTR-mediated ATP currents were activated by protein kinase A and ATP (1 mM) from the "intracellular" side of the molecule and were inhibited by diphenylamine-2-carboxylate, glibenclamide, and anti-CFTR antibodies. Glyburide 183-196 CF transmembrane conductance regulator Homo sapiens 9-13 9545119-8 1998 If patients rested after administration of glibenclamide serum insulin levels rose and remained elevated. Glyburide 43-56 insulin Homo sapiens 63-70 9545119-9 1998 When exercise and glibenclamide were combined the rise in serum insulin levels was blunted and insulin levels fell once exercise was begun. Glyburide 18-31 insulin Homo sapiens 64-71 9545119-9 1998 When exercise and glibenclamide were combined the rise in serum insulin levels was blunted and insulin levels fell once exercise was begun. Glyburide 18-31 insulin Homo sapiens 95-102 9545119-10 1998 Thus, exercise attenuates the glibenclamide induced increase in serum insulin in moderately hyperglycaemic Type 2 diabetic patients. Glyburide 30-43 insulin Homo sapiens 70-77 9530990-4 1998 Intravenous treatment with glibenclamide (20 mg kg(-1)) [corrected] significantly attenuated not only the vasodepression caused by VIP and CGRP, but also the enhancement of the effects of the agents by nicorandil. Glyburide 27-40 vasoactive intestinal peptide Rattus norvegicus 131-134 9490826-4 1998 CGRP (50 nM) activated an inward current at -60 mV in symmetrical 140 mM K+ that was blocked by glibenclamide (10 microM), an inhibitor of ATP-sensitive potassium (KATP) channels. Glyburide 96-109 Calcitonin gene-related peptide Sus scrofa 0-4 9486225-3 1998 This AVT-stimulated secretory Cl- current was significantly inhibited by glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 73-86 CF transmembrane conductance regulator Bos taurus 108-159 9486225-3 1998 This AVT-stimulated secretory Cl- current was significantly inhibited by glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 73-86 CF transmembrane conductance regulator Bos taurus 161-165 9517388-7 1998 The CFTR chloride channel activity was blocked by glibenclamide (100 microM) but not by DIDS (100 microM). Glyburide 50-63 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 4-8 9530990-4 1998 Intravenous treatment with glibenclamide (20 mg kg(-1)) [corrected] significantly attenuated not only the vasodepression caused by VIP and CGRP, but also the enhancement of the effects of the agents by nicorandil. Glyburide 27-40 calcitonin-related polypeptide alpha Rattus norvegicus 139-143 9491553-3 1998 The utility of data dependent MS1-MS2-MS3 analyses, where the mass spectrometer makes "real-time" decisions about the experiment to be performed, are described using the characterization of two novel metabolites of glyburide as an example. Glyburide 215-224 MS Homo sapiens 30-33 9491553-3 1998 The utility of data dependent MS1-MS2-MS3 analyses, where the mass spectrometer makes "real-time" decisions about the experiment to be performed, are described using the characterization of two novel metabolites of glyburide as an example. Glyburide 215-224 MS2 Homo sapiens 34-37 9491553-3 1998 The utility of data dependent MS1-MS2-MS3 analyses, where the mass spectrometer makes "real-time" decisions about the experiment to be performed, are described using the characterization of two novel metabolites of glyburide as an example. Glyburide 215-224 MS3 Homo sapiens 38-41 9409470-13 1997 These results show that (i) glibenclamide is one of the most potent inhibitors of guinea-pig atrial ICl,swell, and (ii) atrial ICl,swell and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- currents are almost equally sensitive to inhibition by glibenclamide. Glyburide 28-41 cystic fibrosis transmembrane conductance regulator Cavia porcellus 145-196 9440664-11 1998 Plasma glucose level was decreased (nadir, 4.9 mmol/L [88 mg/dL] for a 20-mg dose of glyburide vs 8.3 mmol/L [150 mg/dL] for placebo; nadir, 5.8 mmol/L [105 mg/dL] for a 20-mg dose of glipizide GITS vs 8.7 mmol/L [157 mg/dL] for placebo), and serum insulin was increased in the sulfonylurea studies compared with placebo (P<.001). Glyburide 85-94 insulin Homo sapiens 249-256 9489857-6 1998 However, glibenclamide reduced the endothelin-1-induced contraction in internal mammary arteries. Glyburide 9-22 endothelin 1 Homo sapiens 35-47 9489857-8 1998 These results suggest that glibenclamide also reduced the endothelin-1-induced contractions by inhibiting a thromboxane A2 receptor-mediated component of the contraction elicited by this peptide. Glyburide 27-40 endothelin 1 Homo sapiens 58-70 18370552-10 1998 Compared with placebo, plasminogen activator inhibitor (PAI) antigen was significantly lower on glibenclamide but not glimepiride [P: 28.8 (19.7) microg/L, glimepiride: 24.4 (15.2) microg/L; p = 0.300, glibenclamide: 20.0 (10.9) microg/L; p = 0.003]. Glyburide 96-109 serpin family E member 1 Homo sapiens 56-59 9428220-8 1998 RESULTS: Y-26763 increased GMBF, which was abolished by glibenclamide, and a CGRP-induced increase in GMBF was attenuated by glibenclamide. Glyburide 125-138 calcitonin-related polypeptide alpha Rattus norvegicus 77-81 9407075-8 1997 ATP acting on both cell types activated at least two channels, the Ca2+-activated Cl- channel and a Ca2+-independent glibenclamide-sensitive Cl--current, possibly cystic fibrosis transmembrane regulator (CFTR). Glyburide 117-130 CF transmembrane conductance regulator Rattus norvegicus 163-202 9407075-8 1997 ATP acting on both cell types activated at least two channels, the Ca2+-activated Cl- channel and a Ca2+-independent glibenclamide-sensitive Cl--current, possibly cystic fibrosis transmembrane regulator (CFTR). Glyburide 117-130 CF transmembrane conductance regulator Rattus norvegicus 204-208 9537814-3 1997 Following an intralobar infusion of glibenclamide (5 mg/kg), vasoconstrictor responses to U46619, prostaglandin F2alpha and prostaglandin D2 were significantly reduced, whereas vasoconstrictor responses to norepinephrine and angiotensin II were not altered and responses to BAY K 8644 were significantly enhanced. Glyburide 36-49 angiotensinogen Homo sapiens 225-239 9435515-7 1997 Sulfonylureas (glibenclamide and LY-295501) inhibited M2-901/ CFTR channel activity by an identical mechanism to that described for wtCFTR. Glyburide 15-28 CF transmembrane conductance regulator Homo sapiens 62-66 9421231-10 1997 Glipizide and Glybenclamide, selective sulfonylureas which can block GK(ATP), dose-dependently enhanced 1,25(OH)2D3-induced OC secretion (p < 0.005). Glyburide 14-27 bone gamma-carboxyglutamate protein Homo sapiens 124-126 9421231-11 1997 Reducing the extracellular calcium concentration with EGTA (microM range) totally inhibited the effect of Glipizide and Glybenclamide on osteocalcin secretion (p < 0.005), which remained at the same levels as controls. Glyburide 120-133 bone gamma-carboxyglutamate protein Homo sapiens 137-148 9444621-8 1997 The SIN-1 DRC was shifted to the right by glibenclamide and not affected by L-NOARG. Glyburide 42-55 MAPK associated protein 1 Homo sapiens 4-9 9409470-13 1997 These results show that (i) glibenclamide is one of the most potent inhibitors of guinea-pig atrial ICl,swell, and (ii) atrial ICl,swell and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- currents are almost equally sensitive to inhibition by glibenclamide. Glyburide 28-41 cystic fibrosis transmembrane conductance regulator Cavia porcellus 198-202 9409470-13 1997 These results show that (i) glibenclamide is one of the most potent inhibitors of guinea-pig atrial ICl,swell, and (ii) atrial ICl,swell and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- currents are almost equally sensitive to inhibition by glibenclamide. Glyburide 263-276 cystic fibrosis transmembrane conductance regulator Cavia porcellus 145-196 9463023-10 1997 As a function of their action period and possibly of intrinsic properties, some sulfonamides more than others (e.g. glibenclamide) affect fasting hepatic glucose production, which is particularly increased early in the day in non-insulin-dependent diabetic patients because of a circadian drop in insulin sensitivity (dawn phenomenon). Glyburide 116-129 insulin Homo sapiens 297-304 9374850-1 1997 In a previous study on inside-out patches of Xenopus oocytes, we demonstrated that the cystic fibrosis transmembrane conductance regulator (CFTR) enhances the glibenclamide sensitivity of a coexpressed inwardly rectifying K+ channel, ROMK2 (C. M. McNicholas, W. B. Guggino, E. M. Schwiebert, S. C. Hebert, G. Giebisch, and M. E. Egan. Glyburide 159-172 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 87-138 9374850-1 1997 In a previous study on inside-out patches of Xenopus oocytes, we demonstrated that the cystic fibrosis transmembrane conductance regulator (CFTR) enhances the glibenclamide sensitivity of a coexpressed inwardly rectifying K+ channel, ROMK2 (C. M. McNicholas, W. B. Guggino, E. M. Schwiebert, S. C. Hebert, G. Giebisch, and M. E. Egan. Glyburide 159-172 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 140-144 9374850-7 1997 In the present study, we used the two-microelectrode voltage-clamp technique to measure whole cell K+ currents in Xenopus oocytes, and we further characterized the enhanced sensitivity of ROMK2 to glibenclamide by CFTR. Glyburide 197-210 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 214-218 9374850-8 1997 Glibenclamide inhibited K+ currents by 56% in oocytes expressing both ROMK2 and CFTR but only 11% in oocytes expressing ROMK2 alone. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 80-84 9374850-10 1997 In oocytes coinjected with ROMK2 and a truncated construct of CFTR with an intact NBF1 (CFTR-K593X), glibenclamide inhibited K+ currents by 46%. Glyburide 101-114 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 62-66 9374850-10 1997 In oocytes coinjected with ROMK2 and a truncated construct of CFTR with an intact NBF1 (CFTR-K593X), glibenclamide inhibited K+ currents by 46%. Glyburide 101-114 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 88-92 9374850-11 1997 However, in oocytes coinjected with ROMK2 and a CFTR mutant truncated immediately before NBF1 (CFTR-K370X), glibenclamide inhibited K+ currents by 12%. Glyburide 108-121 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 48-52 9374850-11 1997 However, in oocytes coinjected with ROMK2 and a CFTR mutant truncated immediately before NBF1 (CFTR-K370X), glibenclamide inhibited K+ currents by 12%. Glyburide 108-121 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 95-99 9374850-12 1997 Also, oocytes expressing both ROMK2 and CFTR mutants with naturally occurring NBF1 point mutations, CFTR-G551D or CFTR-A455E, display glibenclamide-inhibitable K+ currents of only 14 and 25%, respectively. Glyburide 134-147 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 40-44 9374850-13 1997 Because CFTR mutations that alter the NBF1 domain reduce the glibenclamide sensitivity of the coexpressed ROMK2 channel, we conclude that the NBF1 motif is necessary for the CFTR-ROMK2 interaction that confers sulfonylurea sensitivity. Glyburide 61-74 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 8-12 9374850-13 1997 Because CFTR mutations that alter the NBF1 domain reduce the glibenclamide sensitivity of the coexpressed ROMK2 channel, we conclude that the NBF1 motif is necessary for the CFTR-ROMK2 interaction that confers sulfonylurea sensitivity. Glyburide 61-74 cystic fibrosis transmembrane conductance regulator L homeolog Xenopus laevis 174-178 15251771-9 1997 CONCLUSION: In patients with NIDDM and good glycemic control with insulin treatment, a glyburide-related increase in endogenous insulin secretion caused a proportionate decrease in exogenous insulin requirements. Glyburide 87-96 insulin Homo sapiens 66-73 15251771-9 1997 CONCLUSION: In patients with NIDDM and good glycemic control with insulin treatment, a glyburide-related increase in endogenous insulin secretion caused a proportionate decrease in exogenous insulin requirements. Glyburide 87-96 insulin Homo sapiens 128-135 9376570-4 1997 We show here that the sulfonylurea glyburide, currently used in the oral therapy of noninsulin dependent diabetes, is an inhibitor of IL-1beta secretion from human monocytes and mouse macrophages. Glyburide 35-44 interleukin 1 beta Homo sapiens 134-142 9376570-5 1997 Glyburide reduces dramatically the recovery of extracellular 17-kD IL-1beta in the absence of toxic effects on the cells and without affecting the synthesis or processing of the IL-1beta precursor. Glyburide 0-9 interleukin 1 beta Homo sapiens 67-75 9376570-8 1997 Interestingly, glyburide blocks the anion exchanger function of ABC1, a mammalian member of the family of ABC transporters. Glyburide 15-24 ATP binding cassette subfamily A member 1 Homo sapiens 64-68 9376570-8 1997 Interestingly, glyburide blocks the anion exchanger function of ABC1, a mammalian member of the family of ABC transporters. Glyburide 15-24 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 64-67 9375955-0 1997 The effect of glibenclamide on the production of interstitial adenosine by inhibiting ecto-5"-nucleotidase in rat hearts. Glyburide 14-27 5' nucleotidase, ecto Rattus norvegicus 86-106 9375955-14 1997 These results suggest that glibenclamide inhibits the activity of endogenous ecto-5"-nucleotidase and decreases the concentration of adenosine in the interstitial space of rat ventricular muscles in situ. Glyburide 27-40 5' nucleotidase, ecto Rattus norvegicus 77-97 9364411-5 1997 Glibenclamide (2.5, 5.0 and 10.0 mg kg-1) dose-dependently reduced glucose and glucagon levels, and increased that of insulin in normal and diabetic rats. Glyburide 0-13 insulin Homo sapiens 118-125 9364411-6 1997 Simultaneous treatment of normal and diabetic rats with the plant extract (0.5, 2.0 and 5.0 g kg-1) and glibenclamide (5.0 mg kg-1) significantly exacerbated the effects on glucose, insulin and glucagon induced by the extract or by glibenclamide when given separately. Glyburide 104-117 insulin Homo sapiens 182-189 9322807-3 1997 Sulfonylureas (e.g., glyburide), which stimulate insulin secretion, have been reported either to increase or not to affect arterial pressure, whereas nonsulfonylurea agents with insulin-sensitizing properties, the biguanide metformin and various thiazolidinediones (eg, pioglitazone), have been reported to decrease arterial pressure in humans and rodents. Glyburide 21-30 insulin Homo sapiens 49-56 9322807-8 1997 Conversely, glyburide induced an accentuating action of insulin on potassium-mediated contractions. Glyburide 12-21 insulin Homo sapiens 56-63 9337640-10 1997 Although glibenclamide, an inhibitor of KATP channels, inhibited the thrombin-stimulated efflux, it did so only in a high concentration (20 mumol/l). Glyburide 9-22 coagulation factor II, thrombin Homo sapiens 69-77 9283792-0 1997 Glibenclamide, but not acarbose, increases leptin concentrations parallel to changes in insulin in subjects with NIDDM. Glyburide 0-13 insulin Homo sapiens 88-95 9283792-1 1997 OBJECTIVE: To hypothesize if glibenclamide, which increases insulin levels, also increases leptin concentrations. Glyburide 29-42 insulin Homo sapiens 60-67 9283792-5 1997 Differing effects can be expected, since glibenclamide acts via stimulation of insulin secretion, whereas acarbose inhibits alpha-glucosidases of the small intestine and has no direct effect on insulin levels. Glyburide 41-54 insulin Homo sapiens 79-86 9283792-14 1997 CONCLUSIONS: Glibenclamide increases circadian leptin and insulin concentrations, whereas acarbose does not. Glyburide 13-26 insulin Homo sapiens 58-65 9300314-4 1997 Coronary vasodilation in response to AT1 receptor antagonists was blunted by pretreatment with glibenclamide (a specific inhibitor of K+ATP channels; p < 0.01) but not by either an adenosine-receptor antagonist or an inhibitor of nitric oxide synthesis. Glyburide 95-108 angiotensin II receptor type 1 Canis lupus familiaris 37-40 9300319-5 1997 The relaxation caused by CGRP was also slightly inhibited at 2 x 10(-8) M by removal of endothelium and in the presence of methylene blue, NG-nitro-L-arginine methylester (L-NAME), or glibenclamide but was not affected by atropine, propranolol, indomethacin, or tetrodotoxin. Glyburide 184-197 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 25-29 9306276-0 1997 Mechanism of glibenclamide inhibition of cystic fibrosis transmembrane conductance regulator Cl- channels expressed in a murine cell line. Glyburide 13-26 cystic fibrosis transmembrane conductance regulator Mus musculus 41-92 9306276-2 1997 The sulphonylurea drug glibenclamide is a widely used inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 23-36 cystic fibrosis transmembrane conductance regulator Mus musculus 71-122 9306276-2 1997 The sulphonylurea drug glibenclamide is a widely used inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). Glyburide 23-36 cystic fibrosis transmembrane conductance regulator Mus musculus 124-128 9306276-3 1997 To investigate how glibenclamide inhibits CFTR, we studied CFTR Cl- channels using excised inside-out membrane patches from cells expressing wild-type human CFTR. Glyburide 19-32 CF transmembrane conductance regulator Homo sapiens 42-46 9306276-5 1997 Addition of glibenclamide (10-100 microM) to the intracellular solution caused a concentration-dependent decrease in the open time of CFTR Cl- channels, but closed times did not change. Glyburide 12-25 cystic fibrosis transmembrane conductance regulator Mus musculus 134-138 9306276-6 1997 This suggests that glibenclamide is an open-channel blocker of CFTR. Glyburide 19-32 cystic fibrosis transmembrane conductance regulator Mus musculus 63-67 9306276-9 1997 Acidification of the intracellular solution relieved glibenclamide inhibition of CFTR, suggesting that the anionic form of glibenclamide inhibits CFTR. Glyburide 53-66 cystic fibrosis transmembrane conductance regulator Mus musculus 81-85 9306276-9 1997 Acidification of the intracellular solution relieved glibenclamide inhibition of CFTR, suggesting that the anionic form of glibenclamide inhibits CFTR. Glyburide 123-136 cystic fibrosis transmembrane conductance regulator Mus musculus 81-85 9306276-9 1997 Acidification of the intracellular solution relieved glibenclamide inhibition of CFTR, suggesting that the anionic form of glibenclamide inhibits CFTR. Glyburide 123-136 cystic fibrosis transmembrane conductance regulator Mus musculus 146-150 9306276-12 1997 Glibenclamide inhibition of CFTR was unaffected by nucleotide-dependent stimulation of CFTR, suggesting that glibenclamide and intracellular MgATP interact with CFTR at distinct sites. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 28-32 9306276-14 1997 Glibenclamide inhibition of CFTR was voltage dependent and enhanced when the external Cl- concentration was decreased. Glyburide 0-13 cystic fibrosis transmembrane conductance regulator Mus musculus 28-32 9306276-15 1997 The data suggest that glibenclamide and Cl- ions may compete for a common binding site located within a large intracellular vestibule that is part of the CFTR pore. Glyburide 22-35 cystic fibrosis transmembrane conductance regulator Mus musculus 154-158 9201033-0 1997 Inhibitory effects of glibenclamide on cystic fibrosis transmembrane regulator, swelling-activated, and Ca(2+)-activated Cl- channels in mammalian cardiac myocytes. Glyburide 22-35 CF transmembrane conductance regulator Homo sapiens 39-78 9277342-10 1997 Channels activated by all activators were inhibited by glibenclamide and a known inhibitory antiserum [anti-CFTR-(505-511)]. Glyburide 55-68 cystic fibrosis transmembrane conductance regulator Mus musculus 108-112 9279533-0 1997 Effect of glibenclamide on insulin release at moderate and high blood glucose levels in normal man. Glyburide 10-23 insulin Homo sapiens 27-34 9279533-2 1997 We studied the effect of glibenclamide on insulin secretion at submaximally and maximally stimulating blood glucose levels with a primed hyperglycaemic glucose clamp. Glyburide 25-38 insulin Homo sapiens 42-49 9279533-6 1997 However, glibenclamide led to a significantly larger increase in AUC delta insulin from 30 to 120 min (second phase): 16087 +/- 4489 vs. 7107 +/- 1533 pmol L-1 x 90 min (with and without glibenclamide respectively, P < 0.03). Glyburide 9-22 insulin Homo sapiens 75-82 9279533-13 1997 In conclusion, glibenclamide increases second-phase insulin secretion only at a submaximally stimulating blood glucose level without enhancement of first-phase insulin release and has no additive effect on insulin secretion at maximally stimulating blood glucose levels. Glyburide 15-28 insulin Homo sapiens 52-59 9286264-7 1997 RESULTS: Endothelium-dependent relaxations to bradykinin (maximal [max], 99% +/- 3%) were strongly inhibited by L-NAME (max, 39% +/- 4%, P < 0.01) and partially by TEA (max, 62% +/- 3%, P < 0.01) or glibenclamide (max, 77% +/- 4%, P < 0.01). Glyburide 205-218 kininogen 1 Homo sapiens 46-56 9286264-8 1997 Administration of glibenclamide plus L-NAME further suppressed bradykinin-induced relaxation (max, 23% +/- 6%; P < 0.01), whereas TEA and L-NAME (max, 6% +/- 2%; P < 0.01) abolished the relaxation. Glyburide 18-31 kininogen 1 Homo sapiens 63-73 9211801-0 1997 Glibenclamide suppresses stretch-activated ANP secretion: involvements of K+ATP channels and L-type Ca2+ channel modulation. Glyburide 0-13 natriuretic peptide A Rattus norvegicus 43-46 9211801-1 1997 The mechanism by which glibenclamide regulates mechanically activated atrial natriuretic peptide (ANP) secretion was investigated using isolated perfused rat atria. Glyburide 23-36 natriuretic peptide A Rattus norvegicus 70-96 9211801-1 1997 The mechanism by which glibenclamide regulates mechanically activated atrial natriuretic peptide (ANP) secretion was investigated using isolated perfused rat atria. Glyburide 23-36 natriuretic peptide A Rattus norvegicus 98-101 9211801-4 1997 Glibenclamide (1, 10, 100 microM), an ATP-sensitive K+ (K+ATP) channel blocker, had no effect on the basal secretion of ANP, suppressed the stimulation of stretch-activated ANP secretion in a dose-dependent manner, but not the translocation of the ECF. Glyburide 0-13 natriuretic peptide A Rattus norvegicus 173-176 9211801-6 1997 Suppression by glibenclamide (100 microM) of the stretch-induced ANP secretion was not observed in atria that had been pretreated with pinacidil (200 microM), an ATP-sensitive K+ channel opener: pinacidil alone had no effect on ECF translocation and ANP secretion. Glyburide 15-28 natriuretic peptide A Rattus norvegicus 65-68 9211801-6 1997 Suppression by glibenclamide (100 microM) of the stretch-induced ANP secretion was not observed in atria that had been pretreated with pinacidil (200 microM), an ATP-sensitive K+ channel opener: pinacidil alone had no effect on ECF translocation and ANP secretion. Glyburide 15-28 natriuretic peptide A Rattus norvegicus 250-253 9211801-7 1997 Furthermore, blocking Ca2+ influx by using the Ca2+ channel blocker diltiazem (10 nM), or a Ca2+-depleted medium prevented the suppression of stretch-induced ANP secretion by glibenclamide. Glyburide 175-188 natriuretic peptide A Rattus norvegicus 158-161 9211801-10 1997 From these results, we suggest that glibenclamide suppresses atrial release of ANP by blocking K+ATP channels and increasing Ca2+ influx and that the K+ATP channels are associated with the regulation of the mechanically activated ANP secretion from the atria. Glyburide 36-49 natriuretic peptide A Rattus norvegicus 79-82 9253949-3 1997 While the K(ATP) channel blocker, glibenclamide (1 and 3 x 10(-6) M) caused dose-dependent inhibition of vasorelaxations produced by pinacidil (10(-8)-10(-4) M), it had no effect on the vasodilations elicited by SIN-1 (10(-8)-10(-5) M) in the coronary arterial smooth muscle. Glyburide 34-47 MAPK associated protein 1 Homo sapiens 212-217 9201033-4 1997 Glibenclamide markedly inhibited CFTR Cl- currents in a voltage-independent manner at 22 degrees C, with estimated IC50 values of 12.5 and 11.0 mumol/L at +50 and -100 mV, respectively. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 33-37 9201033-8 1997 These results suggest that glibenclamide, an inhibitor of cardiac CFTR Cl- channels, also inhibits swelling-activated and Ca(2+)-activated Cl- channels at higher concentrations. Glyburide 27-40 CF transmembrane conductance regulator Homo sapiens 66-70 9208926-6 1997 Ph2COOH and 4-acetamido-4"-isothiocyanato-stilbene-2,2"-disulfonic acid inhibited the basal Cl(-)-conductive pathways, while PKA-treated microsomes were sensitive also to N(PhPrNH2)BzOH and glybenclamide, suggesting that additional Cl- pathways were activated by phosphorylation. Glyburide 190-203 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 125-128 9200561-5 1997 Glibenclamide (3-10 microM) decreased the effect of human CGRP at a concentration greater than 1 nM whilst glibenclamide did not affect the inhibitory effect of human CGRP on the agonist-induced contractions. Glyburide 0-13 calcitonin related polypeptide alpha Homo sapiens 58-62 9154337-10 1997 Glibenclamide (1 microM), an inhibitor of ATP-sensitive potassium (K+ATP) channels, inhibited responses to bradykinin or A23187 but did not affect relaxations evoked by acetylcholine. Glyburide 0-13 kininogen 1 Canis lupus familiaris 107-117 9154337-13 1997 With bradykinin, glibenclamide attenuated total relaxation by 49 +/- 8%, but did not alter the individual NO and PGI2-mediated components of the response. Glyburide 17-30 kininogen 1 Canis lupus familiaris 5-15 9154337-17 1997 With bradykinin or A23187, this component of relaxation was inhibited by glibenclamide, whereas with acetylcholine, glibenclamide had no effect. Glyburide 73-86 kininogen 1 Canis lupus familiaris 5-15 9135928-9 1997 CONCLUSIONS: Glibenclamide therapy is accompanied by greater systolic BP responses to norepinephrine and angiotensin II and higher plasma norepinephrine levels than those that occur on metformin therapy. Glyburide 13-26 angiotensinogen Homo sapiens 105-119 9137239-12 1997 The KATP channel antagonist glibenclamide enhanced vasoconstriction of NPY, and the agonist pinacidil suppressed it with a predominant effect in the subepicardial region. Glyburide 28-41 neuropeptide Y Canis lupus familiaris 71-74 9159628-6 1997 RESULTS: The endothelium-derived hyperpolarizing factor-mediated relaxation induced by substance P, which could be significantly inhibited by the Ca(2+)-activated K channel blocker tetraethylammonium but only to a lesser extent by the adenosine triphosphate-sensitive K channel blocker glibenclamide, was significantly reduced. Glyburide 286-299 tachykinin precursor 1 Homo sapiens 87-98 9134058-0 1997 Effects of glibenclamide and metformin (alone or in combination) on insulin release from isolated human pancreatic islets. Glyburide 11-24 insulin Homo sapiens 68-75 9175727-0 1997 3-Morpholinosydnonimine as instigator of a glibenclamide-sensitive reduction in the insulin secretory rate. Glyburide 43-56 insulin Homo sapiens 84-91 9175727-2 1997 The negative insulinotropic action of SIN-1 was attenuated by the hypoglycemic sulfonylurea glibenclamide. Glyburide 92-105 MAPK associated protein 1 Homo sapiens 38-43 9105697-13 1997 In conventional whole-cell recordings, inclusion of an NDP in the pipette solution induced a small outward current which slowly reached a maximal amplitude (in 2 to 10 min) and was suppressed by glibenclamide. Glyburide 195-208 norrin cystine knot growth factor NDP Sus scrofa 55-58 9160878-5 1997 The protective effects of both ischaemic preconditioning and A1-adenosine receptor activation were prevented by 6 mg/kg, but not 3 mg/kg, of the K(ATP) channel blocker, glibenclamide, in rabbits anaesthetized with pentobarbital, while these effects were prevented by 3 mg/kg of the blocker in rabbits anaesthetized with ketamine-xylazine. Glyburide 169-182 adenosine receptor A1 Oryctolagus cuniculus 61-82 9134058-2 1997 At 3.3 mmol/l glucose level, the addition of 5.0 mumol/l glibenclamide or 5.0 mumol/l glibenclamide plus 200 mumol/l metformin caused a significant increase of insulin release, compared with glucose alone. Glyburide 57-70 insulin Homo sapiens 160-167 9134058-2 1997 At 3.3 mmol/l glucose level, the addition of 5.0 mumol/l glibenclamide or 5.0 mumol/l glibenclamide plus 200 mumol/l metformin caused a significant increase of insulin release, compared with glucose alone. Glyburide 86-99 insulin Homo sapiens 160-167 9120578-7 1997 In 60-80% of hippocampal CA1 neurons, glibenclamide or tolbutamide (3-100 microM) reduced the amplitude of the hypoxic hyperpolarization in a concentration-dependent manner by up to approximately 70%. Glyburide 38-51 carbonic anhydrase 1 Rattus norvegicus 25-28 9152851-6 1997 The additional ACh2-induced increase in gK+ is selectively blocked by 10 microM glibenclamide, identifying the current as IK,ATP. Glyburide 80-93 acyl-CoA thioesterase 1 Homo sapiens 15-19 9006906-3 1997 We report here that ABC1 generates an anion flux sensitive to glibenclamide, sulfobromophthalein, and blockers of anion transporters. Glyburide 62-75 ATP binding cassette subfamily A member 1 S homeolog Xenopus laevis 20-24 9059770-1 1997 Insulin-requiring diabetes (IRD) is a condition of permanent blood glucose imbalance which occurs despite a regulated diet and treatment with maximum doses of oral anti-diabetic drugs (glibenclamide 15 mg/d + metformin 1,700 mg/d). Glyburide 185-198 insulin Homo sapiens 0-7 9050449-6 1997 We found an apparent rate constant for glibenclamide binding of 9.9 x 10(7) m-1 sec-1 and an unbinding rate of 6.26 sec-1. Glyburide 39-52 secretory blood group 1, pseudogene Homo sapiens 80-85 9050449-8 1997 The glibenclamide concentration within this phase will be greater than that in the aqueous solution and we have taken this into account to estimate a true binding rate constant of 1.66 x 10(6) m-1 sec-1. Glyburide 4-17 secretory blood group 1, pseudogene Homo sapiens 197-202 8996233-5 1997 The periarterial nerve stimulation (10 V, 4-16 Hz, for 45 sec), exogenous CGRP (10(-8) M) or the ATP-sensitive K+ channel opener cromakalim (10(-6) M) produced relaxation of the rings at a stable plateau tension by the addition of norepinephrine (10(-5) M); the relaxations elicited by CGRP and cromakalim were human CGRP-(8-37)- and glibenclamide-abolishable, respectively. Glyburide 334-347 calcitonin related polypeptide alpha Homo sapiens 74-78 9023770-8 1997 The pharmacological properties of Kir6.2-SUR1 currents resembled those of native beta-cell ATP-sensitive K+ channel currents (KATP currents): the currents were > 90% blocked by tolbutamide (500 microM), meglitinide (10 microM) or glibenclamide (100 nM), and activated 1.8-fold by diazoxide (340 microM), 1.4-fold by pinacidil (1 mM) and unaffected by cromakalim (0.5 mM). Glyburide 233-246 ATP-binding cassette sub-family C member 8 Xenopus laevis 41-45 15045239-4 1996 For HPLC analysis, the glibenclamide and internal standard are derivatized to a highly fluorescent amine with 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD-chloride). Glyburide 23-36 OXA1L mitochondrial inner membrane protein Homo sapiens 134-139 8996509-9 1997 Glibenclamide (10(-6) mol/L), an inhibitor of ATP-sensitive K+ channels, reduced the responses to adrenomedullin without attenuating responses to ADP. Glyburide 0-13 adrenomedullin Rattus norvegicus 98-112 8996509-10 1997 Responses to adrenomedullin were 19 +/- 4% and 35 +/- 6% before and 6 +/- 3% and 19 +/- 5% after glibenclamide, respectively (P < .05). Glyburide 97-110 adrenomedullin Rattus norvegicus 13-27 8982501-14 1996 However, in the presence of either ODQ and apamin, or ODQ and glibenclamide, SIN-1-evoked relaxation was significantly attenuated in intact arterial segments and segments in which NO synthesis was blocked. Glyburide 62-75 MAPK associated protein 1 Homo sapiens 77-82 8960854-9 1996 Two thirds of the patients allocated to glibenclamide treatment had to be given insulin due to inadequate glycaemic control. Glyburide 40-53 insulin Homo sapiens 80-87 8944640-7 1996 In transfected cells, blocking the CFTR conductance with high-concentration glibenclamide (100 microM) reduced the K+ current when activated by cAMP but not when activated by Ca2+. Glyburide 76-89 CF transmembrane conductance regulator Homo sapiens 35-39 8944640-7 1996 In transfected cells, blocking the CFTR conductance with high-concentration glibenclamide (100 microM) reduced the K+ current when activated by cAMP but not when activated by Ca2+. Glyburide 76-89 cathelicidin antimicrobial peptide Homo sapiens 144-148 8945908-8 1996 During contraction to either phenylephrine or prostaglandin F2 alpha, relaxations to CNP were inhibited by HS-142-1, methylene blue, TEA, and charybdotoxin, but not by L-NMMA, glibenclamide, or apamin. Glyburide 176-189 natriuretic peptide C Canis lupus familiaris 85-88 8873691-6 1996 Glyburide decreased the venodilator action of a single dose of substance P (1.5 pmol/min) from 81% to 28% of baseline venodilation (p < 0.05), suggesting that substance P acts through release of endothelium-derived hyperpolarizing factor. Glyburide 0-9 tachykinin precursor 1 Homo sapiens 63-74 8873691-6 1996 Glyburide decreased the venodilator action of a single dose of substance P (1.5 pmol/min) from 81% to 28% of baseline venodilation (p < 0.05), suggesting that substance P acts through release of endothelium-derived hyperpolarizing factor. Glyburide 0-9 tachykinin precursor 1 Homo sapiens 162-173 8873691-8 1996 CONCLUSIONS: Unlike in other vessels, substance P-induced venodilation in hand veins is not mediated through nitric oxide but to a significant extent through a glyburide-sensitive pathway. Glyburide 160-169 tachykinin precursor 1 Homo sapiens 38-49 8897447-9 1996 The glyburide sensitivity of the BMS-180448-induced increase in 86Rb efflux from the aortic preparations suggests that this drug activates IKATP in vascular smooth muscle. Glyburide 4-13 ATP-sensitive inward rectifier potassium channel 11 Cavia porcellus 139-144 8885130-3 1996 This elevation in cyclosporine level is possibly due to an interaction between the two drugs resulting from an inhibition of CYP3A4-mediated metabolism of cyclosporine by glibenclamide. Glyburide 171-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 8867099-3 1996 PAF-induced concentration-dependent vasodilatation of the mesentery was inhibited by pretreatment with L-NMMA, oxyhemoglobin, or methylene blue, and slightly but significantly inhibited by tetraethylammonium, whereas indomethacin, glibenclamide, and ouabain had no inhibitory effects. Glyburide 231-244 PCNA clamp associated factor Rattus norvegicus 0-3 8761850-7 1996 In both nitrate-tolerant and nontolerant coronary arteries, glibenclamide (GLI 10(-6) M), a selective KATP channel blocker, caused a parallel rightward shift in the concentration-response curve to cromakalim, but had no effect on responses to NTG or SNP. Glyburide 60-73 GLI family zinc finger 1 Homo sapiens 75-78 9026680-7 1996 These results indicate that in NIDDM patients with secondary failure to glyburide bed-time ultralent insulin administration is a better tool to improve the post prandial plasma glucose. Glyburide 72-81 insulin Homo sapiens 101-108 8928882-6 1996 Ectosolic and cytosolic 5"-nucleotidase activity increased in the ischemic preconditioning group compared with that in the control group; this preconditioning-induced increase in 5"-nucleotidase activity was blunted by glibenclamide (n = 5) and mimicked by cromakalim (n = 5) and nicorandil (n = 5). Glyburide 219-232 5'-nucleotidase ecto Canis lupus familiaris 24-39 8928882-6 1996 Ectosolic and cytosolic 5"-nucleotidase activity increased in the ischemic preconditioning group compared with that in the control group; this preconditioning-induced increase in 5"-nucleotidase activity was blunted by glibenclamide (n = 5) and mimicked by cromakalim (n = 5) and nicorandil (n = 5). Glyburide 219-232 5'-nucleotidase ecto Canis lupus familiaris 179-194 8622600-0 1996 Glyburide increases the secretion, tissue uptake, and action of insulin in conscious normal dogs. Glyburide 0-9 insulin Canis lupus familiaris 64-71 8622600-8 1996 Glyburide increased the insulin secretory response during the late phase of the IGTT and augmented glucose clearance during the IICT. Glyburide 0-9 insulin Canis lupus familiaris 24-31 8622600-9 1996 Hepatic extraction of insulin was also stimulated by glyburide. Glyburide 53-62 insulin Canis lupus familiaris 22-29 8622600-11 1996 In addition, glyburide augments the extraction of insulin by the liver, and such an effect might prevent the development of sustained high levels of insulin in blood perusing peripheral tissues. Glyburide 13-22 insulin Canis lupus familiaris 50-57 8622600-11 1996 In addition, glyburide augments the extraction of insulin by the liver, and such an effect might prevent the development of sustained high levels of insulin in blood perusing peripheral tissues. Glyburide 13-22 insulin Canis lupus familiaris 149-156 8911981-9 1996 Glimepiride and glibenclamide stimulated beta-cell secretion and in the basal state both beta-cell secretory products insulin and C-peptide, were elevated in the plasma (basal C-peptide concentration: glimepiride v. placebo, 0.79 +/- 0.08 v. 0.68 +/- 0.07 nmol/l, p < 0.01; glibenclamide v. placebo, 0.79 +/- 0.07 v. 0.68 +/- 0.07 nmol/l, p < 0.004). Glyburide 16-29 insulin Homo sapiens 118-125 8910849-4 1996 The amount of glibenclamide dissolved from the non-micronized formulation within 2 h, was 1.2, 4.5 and 76% at pH 2, pH 6 and pH 9, respectively (P < 0.01), whereas 21, 29 and 100% was dissolved from the micronized formulation (P < 0.01). Glyburide 14-27 polyhomeotic homolog 2 Homo sapiens 110-114 9072666-4 1996 Glibenclamide stimulates insulin release by pancreatic beta cells (pancreatic attachment point), while metformin acts at a peripheral level by increasing glucose absorption in muscular, fatty and hepatic tissues, thus considerably reducing insulin resistance (extra-pancreatic attachment point). Glyburide 0-13 insulin Homo sapiens 25-32 8770056-0 1996 Glibenclamide blockade of CFTR chloride channels. Glyburide 0-13 CF transmembrane conductance regulator Homo sapiens 26-30 8770056-3 1996 100: 573-591, 1992) showed that glibenclamide, a compound which binds to the sulfonylurea receptor and thus blocks nucleotide-dependent K+ channels, reduced CFTR whole cell current. Glyburide 32-45 CF transmembrane conductance regulator Homo sapiens 157-161 8770056-5 1996 Exposure to gliben-clamide caused a reversible reduction in current carried by CFTR which was paralleled by a decrease in channel open probability (Po). Glyburide 12-26 CF transmembrane conductance regulator Homo sapiens 79-83 8770056-11 1996 Since the initial Po was 0.50 +/- 0.02 (n = 12), we can conclude that glibenclamide blocks CFTR by a closed-open-blocked mechanism. Glyburide 70-83 CF transmembrane conductance regulator Homo sapiens 91-95 8770120-4 1996 After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced. Glyburide 214-227 kininogen 1 Homo sapiens 139-149 8842604-0 1996 Glucagon-like peptide I enhances the insulinotropic effect of glibenclamide in NIDDM patients and in the perfused rat pancreas. Glyburide 62-75 granzyme B Rattus norvegicus 0-23 8842604-7 1996 RESULTS: GLP-I increased the insulinotropic effect of glibenclamide fourfold in the perfused rat pancreas. Glyburide 54-67 granzyme B Rattus norvegicus 9-14 8842604-8 1996 In human experiments, treatment with GLP-I alone and in combination with glibenclamide significantly decreased basal glucose levels (5.1 +/- 0.4 and 4.5 +/- 0.1 vs. 6.0 +/- 0.3 mmol/l, P < 0.01), while with only glibenclamide, glucose concentrations remained unchanged. Glyburide 73-86 granzyme B Rattus norvegicus 37-42 8842604-8 1996 In human experiments, treatment with GLP-I alone and in combination with glibenclamide significantly decreased basal glucose levels (5.1 +/- 0.4 and 4.5 +/- 0.1 vs. 6.0 +/- 0.3 mmol/l, P < 0.01), while with only glibenclamide, glucose concentrations remained unchanged. Glyburide 215-228 granzyme B Rattus norvegicus 37-42 8842604-14 1996 GLP-I, glibenclamide, and combined treat-stimulated meal-induced insulin release as reflected by insulinogenic indexes (control 1.44 +/- 0.4; GLP-I 6.3 +/- 1.6, P < 0.01; glibenclamide 6.8 +/- 2.1, P < 0.01; combination 20.7 +/- 5.0, P < 0.001). Glyburide 174-187 insulin Homo sapiens 65-72 8842604-19 1996 The glucose-lowering effect of GLP-I was further enhanced by glibenclamide. Glyburide 61-74 granzyme B Rattus norvegicus 31-36 8755607-1 1996 We demonstrate here that coexpression of ROMK2, an inwardly rectifying ATP-sensitive renal K+ channel (IKATP) with cystic fibrosis transmembrane regulator (CFTR) significantly enhances the sensitivity of ROMK2 to the sulfonylurea compound glibenclamide. Glyburide 239-252 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 103-108 8755607-1 1996 We demonstrate here that coexpression of ROMK2, an inwardly rectifying ATP-sensitive renal K+ channel (IKATP) with cystic fibrosis transmembrane regulator (CFTR) significantly enhances the sensitivity of ROMK2 to the sulfonylurea compound glibenclamide. Glyburide 239-252 CF transmembrane conductance regulator Homo sapiens 156-160 8755607-3 1996 The interaction between ROMK2, CFTR, and glibenclamide is modulated by altering the phosphorylation state of either ROMK2, CFTR, or an associated protein, as exogenous MgATP and the catalytic subunit of protein kinase A significantly attenuate the inhibitory effect of glibenclamide on ROMK2. Glyburide 41-54 CF transmembrane conductance regulator Homo sapiens 31-35 8755607-3 1996 The interaction between ROMK2, CFTR, and glibenclamide is modulated by altering the phosphorylation state of either ROMK2, CFTR, or an associated protein, as exogenous MgATP and the catalytic subunit of protein kinase A significantly attenuate the inhibitory effect of glibenclamide on ROMK2. Glyburide 41-54 CF transmembrane conductance regulator Homo sapiens 123-127 8755607-3 1996 The interaction between ROMK2, CFTR, and glibenclamide is modulated by altering the phosphorylation state of either ROMK2, CFTR, or an associated protein, as exogenous MgATP and the catalytic subunit of protein kinase A significantly attenuate the inhibitory effect of glibenclamide on ROMK2. Glyburide 269-282 CF transmembrane conductance regulator Homo sapiens 31-35 8901455-6 1996 The K+ channel blocker 4-aminopyridine (1 mM) and the ATP-dependent K+ channel inhibitor glibenclamide (10 microM) prevented the effect of ANP on APD in both ventricular atrial preparations. Glyburide 89-102 natriuretic peptide A Homo sapiens 139-142 8744307-2 1996 Previously, Sheppard and Welsh reported that the sulfonylureas glibenclamide and tolbutamide reduced CFTR whole cell currents. Glyburide 63-76 CF transmembrane conductance regulator Homo sapiens 101-105 8603612-7 1996 In agreement with this hypothesis, the effect of CGRP is blocked by 1 microM glybenclamide, a specific inhibitor of ATP-sensitive potassium (K(ATP)) channels, or by pretreatment of cells with 1 mM iodoacetic acid to deplete intracellular ATP. Glyburide 77-90 calcitonin-related polypeptide alpha Rattus norvegicus 49-53 8542676-4 1995 Pre-treatment with glibenclamide attenuated the analgesic activity of PRL while treatment with minoxidil potentiated the activity. Glyburide 19-32 prolactin Mus musculus 70-73 8758691-5 1996 (3) The negative chronotropic action of ET-1 on the pacemaker cells was totally abolished by pretreatment with a kind of KATP channel blocker glibenclamide (10 mumol/L). Glyburide 142-155 endothelin-1 Oryctolagus cuniculus 40-44 8701024-10 1996 In sucrose gap, brief superfusion with 0.3 microM CGRP produced a TTX (1 microM)- resistant membrane hyperpolarization and relaxation: the hyperpolarization produced by CGRP was inhibited by about 50% by either TEA (10 mM) or CPA (10 microM), while being unaffected by glibenclamide (3 microM). Glyburide 269-282 calcitonin related polypeptide alpha Homo sapiens 50-54 8701024-10 1996 In sucrose gap, brief superfusion with 0.3 microM CGRP produced a TTX (1 microM)- resistant membrane hyperpolarization and relaxation: the hyperpolarization produced by CGRP was inhibited by about 50% by either TEA (10 mM) or CPA (10 microM), while being unaffected by glibenclamide (3 microM). Glyburide 269-282 calcitonin related polypeptide alpha Homo sapiens 169-173 8769733-5 1996 Glibenclamide (10-100 microM intracortically) attenuated [K+]e and CBF during hypoxia (ABP approximately 75 mmHg, P < 0.01). Glyburide 0-13 glutamate receptor interacting protein 2 Rattus norvegicus 87-90 8769767-5 1996 Vasodilation and increase in cAMP production evoked by CGRP were inhibited not only by glibenclamide (ATP-sensitive K+ channel blocker) but also by charybdotoxin (large-conductance Ca(2+)-activated K+ channel blocker), but this was not the case for the isoproterenol-induced vasodilation and cAMP production. Glyburide 87-100 calcitonin-related polypeptide alpha Rattus norvegicus 55-59 8773160-14 1996 Insulin concentrations were increased during the glyburide plus aspirin treatment. Glyburide 49-58 insulin Homo sapiens 0-7 8847337-6 1996 Pretreatment with glibenclamide, TEA, and 4-aminopyridine at elevated vascular tone significantly potentiated the pressor effect of ET-1, and TEA blocked the transient vasodilation to ET-1. Glyburide 18-31 endothelin 1 Canis lupus familiaris 132-136 8847337-6 1996 Pretreatment with glibenclamide, TEA, and 4-aminopyridine at elevated vascular tone significantly potentiated the pressor effect of ET-1, and TEA blocked the transient vasodilation to ET-1. Glyburide 18-31 endothelin 1 Canis lupus familiaris 184-188 8749025-7 1995 Glibenclamide increased the serum insulin level and decreased the blood glucose level. Glyburide 0-13 insulin Canis lupus familiaris 34-41 7589855-0 1995 An ATP-sensitive Cl- channel current that is activated by cell swelling, cAMP, and glyburide in insulin-secreting cells. Glyburide 83-92 insulin Homo sapiens 96-103 8825525-6 1996 Bath additions of NPPB, flufenamate, glibenclamide (all 100 microM) and DIDS (500 microM) produced varying degrees of block of OR currents with NPPB being the most potent (IC50 of approximately 50 microM) while DIDS was the least effective. Glyburide 37-50 natriuretic peptide type B Mus musculus 144-148 7488089-6 1995 The inhibitory effect of galanin was reduced partially by a blocker of ATP-sensitive K+ channel (K+ ATP), glibenclamide, and prevented by pretreatment of the cells with PTX. Glyburide 106-119 galanin and GMAP prepropeptide Mus musculus 25-32 8590976-10 1995 The reduction in infarct size afforded by ET-1 (0.03 nmol kg-1) was abolished by pretreatment of rabbits with the KATP channel inhibitors, glibenclamide (0.3 mg kg-1) and 5-HD (5 mg kg-1), (infarct size 59 +/- 3 and 63 +/- 4% respectively; n = 4-9). Glyburide 139-152 endothelin-1 Oryctolagus cuniculus 42-46 8846678-0 1995 More uniform diurnal blood glucose control and a reduction in daily insulin dosage on addition of glibenclamide to insulin in type 1 diabetes mellitus: role of enhanced insulin sensitivity. Glyburide 98-111 insulin Homo sapiens 68-75 8846678-6 1995 Therefore, it is apparent that the addition of glibenclamide to insulin reduces daily insulin dosage and renders a greater uniformity to diurnal blood glucose control, most probably secondary to enhancement of insulin sensitivity. Glyburide 47-60 insulin Homo sapiens 86-93 8846678-6 1995 Therefore, it is apparent that the addition of glibenclamide to insulin reduces daily insulin dosage and renders a greater uniformity to diurnal blood glucose control, most probably secondary to enhancement of insulin sensitivity. Glyburide 47-60 insulin Homo sapiens 86-93 8744980-8 1995 The early suppressant effect of CGRP or forskolin was inhibited by 1 or 10 microM glibenclamide; about 30% of the effect of CGRP was glibenclamide-resistant. Glyburide 82-95 calcitonin related polypeptide alpha Homo sapiens 32-36 8744980-8 1995 The early suppressant effect of CGRP or forskolin was inhibited by 1 or 10 microM glibenclamide; about 30% of the effect of CGRP was glibenclamide-resistant. Glyburide 133-146 calcitonin related polypeptide alpha Homo sapiens 124-128 8744980-12 1995 Glibenclamide (10 nM-10 microM) concentration-dependently inhibited the effect of CGRP and cromakalim with IC50S of 0.13 and 0.72 microM, respectively. Glyburide 0-13 calcitonin related polypeptide alpha Homo sapiens 82-86 7573545-4 1995 Glibenclamide (10(-6) M), a KATP inhibitor, attenuated the dilation resulting from moderate and severe hypoxia [23 +/- 1 and 33 +/- 2% vs. 7 +/- 1 and 18 +/- 2%, respectively, for moderate and severe hypoxia (arterial PO2 approximately 35 and 25 mmHg, respectively) in the absence vs. presence of glibenclamide]. Glyburide 0-13 PO2 Sus scrofa 218-221 7573545-5 1995 In addition, glibenclamide attenuated the dilation produced by methionine enkephalin (10(-8) and 10(-6) M) (13 +/- 1 vs. 4 +/- 2% and 21 +/- 2 vs. 7 +/- 3%, respectively, for methionine enkephalin in the absence and presence of glibenclamide). Glyburide 13-26 proenkephalin Sus scrofa 74-84 7573545-5 1995 In addition, glibenclamide attenuated the dilation produced by methionine enkephalin (10(-8) and 10(-6) M) (13 +/- 1 vs. 4 +/- 2% and 21 +/- 2 vs. 7 +/- 3%, respectively, for methionine enkephalin in the absence and presence of glibenclamide). Glyburide 13-26 proenkephalin Sus scrofa 186-196 7573545-5 1995 In addition, glibenclamide attenuated the dilation produced by methionine enkephalin (10(-8) and 10(-6) M) (13 +/- 1 vs. 4 +/- 2% and 21 +/- 2 vs. 7 +/- 3%, respectively, for methionine enkephalin in the absence and presence of glibenclamide). Glyburide 228-241 proenkephalin Sus scrofa 74-84 7573545-6 1995 Leucine enkephalin-induced dilation was similarly attenuated by glibenclamide. Glyburide 64-77 proenkephalin Sus scrofa 8-18 7653598-0 1995 Glyburide attenuates calmodulin antagonist-stimulated renin release from isolated mouse juxtaglomerular cells. Glyburide 0-9 calmodulin 2 Mus musculus 21-31 7653598-2 1995 Therefore, we examined whether the K+ channel blocker, glyburide, inhibits basal RR or RR stimulated by elevating cAMP or by inhibiting Ca2+/calmodulin activity in cultures of isolated mouse JG cells. Glyburide 55-64 calmodulin 2 Mus musculus 141-151 7653598-5 1995 In contrast, glyburide significantly attenuated RR stimulated by the calmodulin antagonists, calmidazolium, trifluoperazine, and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). Glyburide 13-22 calmodulin 2 Mus musculus 69-79 7614725-2 1995 Since epithelial cystic fibrosis transmembrane conductance regulator Cl- channels are known to be sensitive to an antidiabetic sulfonylurea, glibenclamide, we tested whether the drug modulates cardiac cAMP-activated Cl- conductance. Glyburide 141-154 cystic fibrosis transmembrane conductance regulator Cavia porcellus 17-68 8846441-7 1995 Using a three-chamber organ bath that enabled the separate perfusion of the renal, middle, and bladder regions of the organ, evidence was obtained that CGRP blocks propagation of impulses along the ureter through a glibenclamide-sensitive mechanism. Glyburide 215-228 calcitonin related polypeptide alpha Homo sapiens 152-156 7584533-12 1995 The results suggest that the growth promoting effect of glibenclamide on isolated human chondrocytes is mediated by IGF-I dependent mechanisms. Glyburide 56-69 insulin like growth factor 1 Homo sapiens 116-121 7544421-7 1995 The demonstrated effect of electrical stimulation was inhibited by glibenclamide (10(-5) M), but not tetraethylammonium (2 x 10(-4) M); glibenclamide abolished the relaxation in response to exogenous CGRP or the ATP-sensitive K+ channel opener cromakalim (10(-6) M) in endothelium-denuded rings. Glyburide 67-80 calcitonin related polypeptide alpha Homo sapiens 200-204 7544421-7 1995 The demonstrated effect of electrical stimulation was inhibited by glibenclamide (10(-5) M), but not tetraethylammonium (2 x 10(-4) M); glibenclamide abolished the relaxation in response to exogenous CGRP or the ATP-sensitive K+ channel opener cromakalim (10(-6) M) in endothelium-denuded rings. Glyburide 136-149 calcitonin related polypeptide alpha Homo sapiens 200-204 7542532-2 1995 We have investigated whether glibenclamide, an inhibitor of ATP-sensitive potassium channels, influences the induction of the calcium-independent isoform of nitric oxide synthase (iNOS) in cultured J774.2 macrophages activated by bacterial endotoxin (E.coli lipopolysaccharide; LPS), as well as in the lung and aorta of rats with endotoxic shock. Glyburide 29-42 nitric oxide synthase 2 Rattus norvegicus 180-184 7542532-8 1995 The inhibition by glibenclamide (3 microM) of the increase in nitrite induced by LPS in J774.2 macrophages was weaker when glibenclamide was given several hours after LPS, indicating that glibenclamide inhibits the induction, but not the activity, of iNOS. Glyburide 18-31 nitric oxide synthase 2 Rattus norvegicus 251-255 7542532-8 1995 The inhibition by glibenclamide (3 microM) of the increase in nitrite induced by LPS in J774.2 macrophages was weaker when glibenclamide was given several hours after LPS, indicating that glibenclamide inhibits the induction, but not the activity, of iNOS. Glyburide 123-136 nitric oxide synthase 2 Rattus norvegicus 251-255 7542532-8 1995 The inhibition by glibenclamide (3 microM) of the increase in nitrite induced by LPS in J774.2 macrophages was weaker when glibenclamide was given several hours after LPS, indicating that glibenclamide inhibits the induction, but not the activity, of iNOS. Glyburide 123-136 nitric oxide synthase 2 Rattus norvegicus 251-255 7542532-32 1995 Thus, glibenclamide inhibits the induction, but not the activity, of iNOS in vitro and in vivo. Glyburide 6-19 nitric oxide synthase 2 Rattus norvegicus 69-73 7542532-33 1995 This inhibition of iNOS induction may contribute to the beneficial haemodynamic effects of glibenclamide in endotoxic shock. Glyburide 91-104 nitric oxide synthase 2 Rattus norvegicus 19-23 7540745-2 1995 Following the report by Sheppard and Welsh (J Gen Physiol 100: 573, 1992) that glibenclamide inhibits whole-cell Cl- currents in genetically manipulated fibroblasts expressing the cystic fibrosis transmembrane conductance regulator (CFTR), we have studied the effect of glibenclamide on different types of Cl- channels of HT29 and T84 cells at the single-channel level. Glyburide 79-92 CF transmembrane conductance regulator Homo sapiens 180-231 7540745-2 1995 Following the report by Sheppard and Welsh (J Gen Physiol 100: 573, 1992) that glibenclamide inhibits whole-cell Cl- currents in genetically manipulated fibroblasts expressing the cystic fibrosis transmembrane conductance regulator (CFTR), we have studied the effect of glibenclamide on different types of Cl- channels of HT29 and T84 cells at the single-channel level. Glyburide 79-92 CF transmembrane conductance regulator Homo sapiens 233-237 7540745-3 1995 Our results confirm that micromolar concentrations of glibenclamide inhibit the linear, low-conductance Cl-channel, which appears to represent CFTR and show that the inhibition results from a typical flicker block. Glyburide 54-67 CF transmembrane conductance regulator Homo sapiens 143-147 7752646-7 1995 The decrease in mean PAP induced by 4 Ala ET-1 and IRL 1620 was attenuated by N omega-nitro-L-arginine [an inhibitor of endothelium-derived nitric oxide (EDNO) synthesis] (16.6% +/- 3.5 vs. 5.9% +/- 2.3 and 16.2% +/- 3.4 vs. 6.6% +/- 2.8, p < 0.05) and by glybenclamide (a blocker of ATP-dependent potassium channels) (18.2% +/- 7.9 vs. 7.5% +/- 8.3 and 14.7% +/- 3.6 vs. 6.3% +/- 3.2, p < 0.05). Glyburide 259-272 EDN1 Ovis aries 42-46 8001275-11 1995 Expression of TF activity was also inhibited by glibenclamide, an inhibitor of ATP-dependent K+ channels (I50, 25 mumol/L). Glyburide 48-61 coagulation factor III, tissue factor Homo sapiens 14-16 7584533-0 1995 Glibenclamide stimulates growth of human chondrocytes by IGF I dependent mechanisms. Glyburide 0-13 insulin like growth factor 1 Homo sapiens 57-62 7582479-6 1995 The presence of glibenclamide only weakly influenced the vasorelaxant properties of salbutamol, a beta 2-adrenoceptor agonist, while those of verapamil, a beta-adrenoceptor-independent vasorelaxant, were unaffected. Glyburide 16-29 adrenoceptor beta 2 Rattus norvegicus 98-117 7750472-9 1995 We conclude that the stimulation of glucose uptake in L6 cells by gliclazide and glyburide is associated not with a redistribution but, rather, with an increase in the total membrane content and plasma membrane level of GLUT1, which is independent of protein synthesis. Glyburide 81-90 solute carrier family 2 member 1 Homo sapiens 220-225 7755556-0 1995 Effects of glucose refeeding and glibenclamide treatment on glucokinase and GLUT2 gene expression in pancreatic B-cells and liver from rats. Glyburide 33-46 glucokinase Rattus norvegicus 60-71 7755556-0 1995 Effects of glucose refeeding and glibenclamide treatment on glucokinase and GLUT2 gene expression in pancreatic B-cells and liver from rats. Glyburide 33-46 solute carrier family 2 member 2 Rattus norvegicus 76-81 7755556-6 1995 But glibenclamide caused a 4-fold increase of glucokinase mRNA in liver which was abolished by concomitant administration of diazoxide, a drug which antagonizes glibenclamide stimulated insulin secretion. Glyburide 4-17 glucokinase Rattus norvegicus 46-57 7755556-6 1995 But glibenclamide caused a 4-fold increase of glucokinase mRNA in liver which was abolished by concomitant administration of diazoxide, a drug which antagonizes glibenclamide stimulated insulin secretion. Glyburide 161-174 glucokinase Rattus norvegicus 46-57 7737718-8 1995 The intracerebroventricular injections of glibenclamide significantly increased the plasma concentration of vasopressin (P < .05) and significantly decreased the pituitary concentration of vasopressin (P < .05) in rats with bilateral carotid artery ligation. Glyburide 42-55 arginine vasopressin Rattus norvegicus 108-119 7737718-8 1995 The intracerebroventricular injections of glibenclamide significantly increased the plasma concentration of vasopressin (P < .05) and significantly decreased the pituitary concentration of vasopressin (P < .05) in rats with bilateral carotid artery ligation. Glyburide 42-55 arginine vasopressin Rattus norvegicus 192-203 7737718-9 1995 Intravenous pretreatment with the vasopressin V1 receptor antagonist OPC-21268 abolished the vasopressor response to intracerebroventricular glibenclamide (+16 +/- 2 versus +1 +/- 1 mm Hg, P < .01). Glyburide 141-154 arginine vasopressin Rattus norvegicus 34-45 7544471-5 1995 Moreover, ODN inhibited insulin release induced by 0.01 or 1 microM glibenclamide with a similar IC50 (8 to 10 nM) in both isolated pancreatic islets and in HIT-T15 beta-cells. Glyburide 68-81 insulin Mesocricetus auratus 24-31 7544471-9 1995 These results suggest that ODN or ODN-like peptide fragments of DBI, may inhibit glucose or glibenclamide-induced insulin secretion via a signaling pathway that regulate the cytoplasmic free Ca2+ concentration. Glyburide 92-105 acyl-CoA-binding protein Mesocricetus auratus 64-67 7999110-2 1994 Relaxations to CNP in isolated coronary arteries were significantly attenuated with potassium channel antagonists charybdotoxin (10(-7)M) and glibenclamide (10(-7)M). Glyburide 142-155 2',3'-cyclic nucleotide 3' phosphodiesterase Homo sapiens 15-18 7738833-9 1994 Inhibitors of Ca(2+)-activated K+ channels (K+Ca), such as apamin (1 microM) and tetrabutylammonium (TBA, 3 mM), strongly attenuated the EDHF-mediated bradykinin-induced relaxation, while glibenclamide (3 microM), an inhibitor of K+ATP channels, had no effect. Glyburide 188-201 kininogen 1 Bos taurus 151-161 7916303-0 1994 Atrial natriuretic factor potentiates glibenclamide-sensitive K+ currents via the activation of receptor guanylate cyclase in follicle-enclosed Xenopus oocytes. Glyburide 38-51 natriuretic peptide A L homeolog Xenopus laevis 0-25 7870193-3 1994 The effect of CGRP was antagonized in a noncompetitive manner (depression of Emax, no change in EC50) by glibenclamide (1-10 microM), a blocker of ATP-sensitive potassium channels (KATP). Glyburide 105-118 calcitonin related polypeptide alpha Homo sapiens 14-18 7870193-4 1994 A substantial fraction of the inhibitory effect of CGRP was glibenclamide-resistant, however. Glyburide 60-73 calcitonin related polypeptide alpha Homo sapiens 51-55 7870193-9 1994 The inhibitory effect of CGRP on the phasic contraction to KCl was partly glibenclamide-(1 microM) sensitive, while that on the tonic contraction was glibenclamide-resistant. Glyburide 74-87 calcitonin related polypeptide alpha Homo sapiens 25-29 7833494-3 1994 When five groups of type II diabetic patients were treated concurrently with five randomly allocated different sulfonylureas over 1 year, the percentage of patients achieving normal HbA1 levels was best with gliclazide (80%) and glibenclamide (74%), when compared with chlorpropamide (17%), glipizide (40%), and gliquidone (40%). Glyburide 229-242 hemoglobin subunit alpha 1 Homo sapiens 182-186 8082525-8 1994 The mean relative insulin increase (1-h postprandial) was 1.5 in the placebo group, 1.1 in the acarbose group, and 2.5 in the glibenclamide group. Glyburide 126-139 insulin Homo sapiens 18-25 8082525-15 1994 Because postprandial insulin increase has been shown to be associated with increased risk for cardiovascular disease, acarbose, which lowers pp increase, may be superior to glibenclamide, which elevates postprandial insulin increase. Glyburide 173-186 insulin Homo sapiens 216-223 7967225-8 1994 Glibenclamide at either dose decreased the level of blood glucose by 20-30% and increased the blood insulin level twice. Glyburide 0-13 insulin Canis lupus familiaris 100-107 7936815-5 1994 The absolute increase in pulmonary blood flow produced by ET-1 was attenuated by glibenclamide (an ATP-dependent potassium channel blocker) (flow increase of 73.4 +/- 34.1 versus 49.3 +/- 16.8 mL/kg/min, p < 0.05). Glyburide 81-94 EDN1 Ovis aries 58-62 7530840-2 1994 Endogenous vasodilators such as calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2) and adenosine activate glibenclamide-ATP-sensitive K+ (KATP) channels in Xenopus oocyte follicular cells. Glyburide 156-169 vasoactive intestinal peptide L homeolog Xenopus laevis 103-106 7530840-2 1994 Endogenous vasodilators such as calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2) and adenosine activate glibenclamide-ATP-sensitive K+ (KATP) channels in Xenopus oocyte follicular cells. Glyburide 156-169 prostaglandin E synthase 2 S homeolog Xenopus laevis 109-125 7530840-2 1994 Endogenous vasodilators such as calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2) and adenosine activate glibenclamide-ATP-sensitive K+ (KATP) channels in Xenopus oocyte follicular cells. Glyburide 156-169 prostaglandin E synthase 2 S homeolog Xenopus laevis 127-131 7988301-1 1994 OBJECTIVE: To assess the hypoglycemic effect and the insulin-releasing effect of the main glyburide (glibenclamide) metabolites 4-trans-hydroxy-glibenclamide (M1) and 3-cis-hydroxy-glibenclamide (M2) in humans. Glyburide 90-99 insulin Homo sapiens 53-60 7988301-1 1994 OBJECTIVE: To assess the hypoglycemic effect and the insulin-releasing effect of the main glyburide (glibenclamide) metabolites 4-trans-hydroxy-glibenclamide (M1) and 3-cis-hydroxy-glibenclamide (M2) in humans. Glyburide 101-114 insulin Homo sapiens 53-60 7988301-7 1994 Serum insulin levels were significantly increased by Gb as well as by M1 and M2. Glyburide 53-55 insulin Homo sapiens 6-13 7808838-5 1994 In juvenile sheep, the increase in resting pulmonary arterial pressure produced by ET-1 was inhibited by meclofenamic acid, an inhibitor of prostaglandin synthesis (40.3 +/- 9.9% versus 2.3 +/- 4.7%, p < 0.05); during pulmonary hypertension, the decrease in pulmonary arterial pressure produced by ET-1 was inhibited by N omega-nitro-L-arginine, an inhibitor of endothelium-derived nitric oxide synthesis (21.4 +/- 10.7% versus 8.0 +/- 3.6%, p < 0.05) and by glybenclamide, an ATP-dependent potassium-channel blocker (18.8 +/- 8.4% versus 4.0 +/- 4.4%, p < 0.05). Glyburide 465-478 EDN1 Ovis aries 83-87 7972332-5 1994 Glibenclamide significantly inhibited the contractions produced by prostaglandins F2 alpha, E2 and D2 but was without effect on responses to norepinephrine, 5-HT or KCl. Glyburide 0-13 dihydrolipoamide S-succinyltransferase Rattus norvegicus 82-101 7972332-9 1994 Thus, in addition to the effect on ATP-dependent potassium channels, glibenclamide inhibits responses to prostaglandins F2 alpha, E2 and D2 but not to other agents. Glyburide 69-82 dihydrolipoamide S-succinyltransferase Rattus norvegicus 120-139 8093111-0 1994 Stimulation of glucose utilization in 3T3 adipocytes and rat diaphragm in vitro by the sulphonylureas, glimepiride and glibenclamide, is correlated with modulations of the cAMP regulatory cascade. Glyburide 119-132 cathelicidin antimicrobial peptide Rattus norvegicus 172-176 7805761-0 1994 Potentiation by insulin and insulin-like growth factor-1 of glibenclamide-sensitive K+ currents in follicle-enclosed Xenopus oocytes. Glyburide 60-73 insulin S homeolog Xenopus laevis 16-23 7805761-0 1994 Potentiation by insulin and insulin-like growth factor-1 of glibenclamide-sensitive K+ currents in follicle-enclosed Xenopus oocytes. Glyburide 60-73 insulin like growth factor 1 L homeolog Xenopus laevis 28-56 7805761-1 1994 Effects of insulin and IGF-1 (insulin-like growth factor-1) on K+ channel opener-induced/glibenclamide-sensitive K+ currents were studied using follicle-enclosed Xenopus oocytes. Glyburide 89-102 insulin like growth factor 1 L homeolog Xenopus laevis 23-28 7805761-1 1994 Effects of insulin and IGF-1 (insulin-like growth factor-1) on K+ channel opener-induced/glibenclamide-sensitive K+ currents were studied using follicle-enclosed Xenopus oocytes. Glyburide 89-102 insulin like growth factor 1 L homeolog Xenopus laevis 30-58 7805761-6 1994 These results suggest that insulin and IGF-1 potentiate the glibenclamide-sensitive K+ current by activating IGF-1 receptor and that pertussis toxin-sensitive G-protein may be associated with these effects. Glyburide 60-73 insulin S homeolog Xenopus laevis 27-34 7805761-6 1994 These results suggest that insulin and IGF-1 potentiate the glibenclamide-sensitive K+ current by activating IGF-1 receptor and that pertussis toxin-sensitive G-protein may be associated with these effects. Glyburide 60-73 insulin like growth factor 1 L homeolog Xenopus laevis 39-44 7805761-6 1994 These results suggest that insulin and IGF-1 potentiate the glibenclamide-sensitive K+ current by activating IGF-1 receptor and that pertussis toxin-sensitive G-protein may be associated with these effects. Glyburide 60-73 insulin like growth factor 1 L homeolog Xenopus laevis 109-114 7916303-1 1994 The effect of the atrial natriuretic factor (ANF) on K+ channel opener-induced glibenclamide-sensitive K+ currents was studied using follicle-enclosed Xenopus oocytes. Glyburide 79-92 natriuretic peptide A L homeolog Xenopus laevis 18-43 7517882-3 1994 Furthermore, the ATP-sensitive K+ channel blockers glibenclamide (MED = 1 nmol) and gliquidone (10 nmol) both prevented the inhibitory effects of galanin on RS86 induced hypothermia. Glyburide 51-64 mediator complex subunit 1 Rattus norvegicus 66-73 8200602-6 1994 Glibenclamide can be used either alone to treat type 2 diabetes or in combination with other oral antidiabetics or insulin. Glyburide 0-13 insulin Homo sapiens 115-122 7517882-3 1994 Furthermore, the ATP-sensitive K+ channel blockers glibenclamide (MED = 1 nmol) and gliquidone (10 nmol) both prevented the inhibitory effects of galanin on RS86 induced hypothermia. Glyburide 51-64 galanin and GMAP prepropeptide Mus musculus 146-153 7517882-4 1994 Glibenclamide (10 nmol) also reversed the inhibitory effects of galanin on tetrahydroaminoacridine induced hypothermia. Glyburide 0-13 galanin and GMAP prepropeptide Mus musculus 64-71 8123030-0 1994 Glyburide enhances insulin gene expression and glucose-induced insulin release in isolated rat islets. Glyburide 0-9 insulin Homo sapiens 19-26 8123030-0 1994 Glyburide enhances insulin gene expression and glucose-induced insulin release in isolated rat islets. Glyburide 0-9 insulin Homo sapiens 63-70 8123030-3 1994 Incubation with glyburide (500 ng/ml) significantly increased insulin release without affecting the insulin content. Glyburide 16-25 insulin Homo sapiens 62-69 8123030-4 1994 The PPI mRNA level was not increased after incubation for 1 h but was increased after incubation for 20 h. Incubation with 5 ng/ml of glyburide for 1 h or 20 h had no effect on the content or release of insulin, but incubation with 5 ng/ml of glyburide for 20 h significantly increased the PPI mRNA level and enhanced insulin release induced by 11 mM glucose. Glyburide 134-143 insulin Homo sapiens 318-325 8123030-5 1994 These results suggest that a high concentration of glyburide stimulates insulin release directly, while a low concentration of glyburide increases the PPI mRNA level and may thereby enhance glucose-induced insulin release. Glyburide 51-60 insulin Homo sapiens 72-79 8183638-5 1994 In patch-clamp experiments, glibenclamide exerted only weak inhibitory effects on the whole-cell currents through CFTR with an IC50 of around 0.1 mM. Glyburide 28-41 CF transmembrane conductance regulator Homo sapiens 114-118 7508205-7 1994 Suffusion with mock cerebrospinal fluid, containing either CGRP or cromakalim, a K(+)-channel opener, dilated the pial artery in a concentration-dependent manner, and their effects were antagonized by glibenclamide. Glyburide 201-214 calcitonin-related polypeptide alpha Rattus norvegicus 59-63 8112188-2 1994 OBJECTIVE: To examine the long-term (15 months) effects on glycemic control and insulin secretion of glipizide and glyburide treatment in patients with non-insulin-dependent diabetes mellitus (NIDDM). Glyburide 115-124 insulin Homo sapiens 80-87 8112188-5 1994 However, both glipizide and glyburide achieved and maintained lowered postprandial glucose levels and increased fasting and postprandial insulin levels compared with placebo. Glyburide 28-37 insulin Homo sapiens 137-144 8112188-6 1994 CONCLUSIONS: Both glipizide and glyburide may achieve and maintain glycemic reduction and stimulation of insulin secretion during long-term treatment. Glyburide 32-41 insulin Homo sapiens 105-112 7812517-5 1994 After administration of glibenclamide, immunoreactivities for insulin and amylin were diminished in a time-dependent manner, decreasing first in medullary and thereafter in cortical beta cells of larger islets. Glyburide 24-37 islet amyloid polypeptide Rattus norvegicus 74-80 8279573-6 1993 Conversely, the K+ channel blockers glibenclamide (10(-4) M) and tetraethylammonium (10(-4) M) attenuated the vasodilator responses to both ET-1 and ET-3. Glyburide 36-49 endothelin 1 Rattus norvegicus 140-153 8246912-1 1993 In single channel patch-clamp recordings from freshly dissociated rat corpus striatum (caudate-putamen) neurons, the sulfonylurea drugs tolbutamide and glibenclamide caused a concentration-dependent blockade of a K+ channel that is activated by D2 dopamine receptor agonists. Glyburide 152-165 dopamine receptor D2 Rattus norvegicus 245-265 8238420-6 1993 The decrease in pulmonary arterial pressure produced by ET-1 (250 ng/kg) was attenuated by N omega-nitro-L-arginine (an inhibitor of endothelium-derived nitric oxide synthesis, 23.7 +/- 3.4 vs. 12.5 +/- 4.7%; P < 0.05) and by glibenclamide (an ATP-gated potassium-channel blocker, 25.2 +/- 5.0 vs. 9.6 +/- 5.3%; P < 0.05) but not by meclofenamic acid (an inhibitor of prostaglandin synthesis). Glyburide 229-242 EDN1 Ovis aries 56-60 8270912-12 1993 (e) Application of 500 microM glibenclamide reduces whole-cell currents in both single and confluent M-1 cells with a glibenclamide-sensitive fractional conductance of 0.71 and 0.83 in single and confluent cells, respectively. Glyburide 30-43 cholinergic receptor, muscarinic 1, CNS Mus musculus 101-104 8270912-12 1993 (e) Application of 500 microM glibenclamide reduces whole-cell currents in both single and confluent M-1 cells with a glibenclamide-sensitive fractional conductance of 0.71 and 0.83 in single and confluent cells, respectively. Glyburide 118-131 cholinergic receptor, muscarinic 1, CNS Mus musculus 101-104 8270912-13 1993 Glibenclamide inhibition occurs slower in confluent M-1 cells than in single cells, suggesting a basolateral action of this lipophilic drug on ATP-sensitive basolateral K channels in M-1 cells. Glyburide 0-13 cholinergic receptor, muscarinic 1, CNS Mus musculus 52-55 8270912-13 1993 Glibenclamide inhibition occurs slower in confluent M-1 cells than in single cells, suggesting a basolateral action of this lipophilic drug on ATP-sensitive basolateral K channels in M-1 cells. Glyburide 0-13 cholinergic receptor, muscarinic 1, CNS Mus musculus 183-186 8403805-7 1993 During potassium channel blocking with glibenclamide the insulin release was more enhanced in patients than in control subjects. Glyburide 39-52 insulin Homo sapiens 57-64 8405748-8 1993 In contrast, in interleukin 1 beta pre-exposed islets both glucose and glyburide stimulation only slightly modified 86Rb efflux (decrement of -19 +/- 1.9% and -5.3 +/- 3.1%, respectively, n = 5, p < 0.001). Glyburide 71-80 interleukin 1 beta Rattus norvegicus 16-34 8224371-2 1993 The mechanism of action of glyburide (a sulfonylurea) on muscle has been investigated by measuring glucose uptake and glucose transporter (GLUT4) protein levels after chronic glyburide treatment. Glyburide 27-36 solute carrier family 2 member 4 Rattus norvegicus 139-144 8340156-1 1993 Glyburide, an insulin secretagogue and an insulin-sensitizing agent, lowers blood pressure in normal male and female dogs when administered acutely. Glyburide 0-9 insulin Canis lupus familiaris 14-21 8340156-1 1993 Glyburide, an insulin secretagogue and an insulin-sensitizing agent, lowers blood pressure in normal male and female dogs when administered acutely. Glyburide 0-9 insulin Canis lupus familiaris 42-49 8340156-2 1993 Because insulin resistance may contribute to spontaneous hypertension in rats, we sought to determine if long-term administration of glyburide (5 mg/kg per day by diet, age 5 weeks to 5 months) would lower blood pressure in male and female stroke-prone spontaneously hypertensive rats. Glyburide 133-142 insulin Canis lupus familiaris 8-15 8340156-5 1993 Glyburide increased plasma insulin levels (twofold, P < .04) in female but not in male rats. Glyburide 0-9 insulin Canis lupus familiaris 27-34 8340156-7 1993 After incubation with insulin, aortic to rings from glyburide-treated female rats demonstrated more than 40% greater contractile responsiveness the phenylephrine compared with aortic rings from control female rats (P < .04). Glyburide 52-61 insulin Canis lupus familiaris 22-29 8232899-6 1993 The distribution of glibenclamide binding sites in the hippocampus was different between the rodents and marmoset; in rodents, most binding sites were distributed in the fascia dentata and the CA3-CA4 fields of Ammon"s horn, contrasting with a very homogeneous distribution in all subfields of the marmoset hippocampus. Glyburide 20-33 carbonic anhydrase 3 Callithrix jacchus 193-200 7664533-0 1994 Regulation of glucokinase gene expression in cultured rat islet cells: the inhibitory effects of T3 and glucagon, and the stimulatory effect of glibenclamide. Glyburide 144-157 glucokinase Rattus norvegicus 14-25 7664533-8 1994 Furthermore, the islet glucokinase mRNA level increased in response to 1 microM glibenclamide with 5.5 mM glucose and the response was abolished by cycloheximide, which indicates the involvement of protein synthesis in the glibenclamide-induced mRNA change. Glyburide 80-93 glucokinase Rattus norvegicus 23-34 7664533-8 1994 Furthermore, the islet glucokinase mRNA level increased in response to 1 microM glibenclamide with 5.5 mM glucose and the response was abolished by cycloheximide, which indicates the involvement of protein synthesis in the glibenclamide-induced mRNA change. Glyburide 223-236 glucokinase Rattus norvegicus 23-34 7510877-7 1993 These results are consistent with murine CFTR being a cAMP-activated chloride channel inhibited by glibenclamide and resistant to DIDS. Glyburide 99-112 cystic fibrosis transmembrane conductance regulator Mus musculus 41-45 8242233-12 1993 Bath-applied glibenclamide inhibited IK(-Ckm) with an IC50 of 200 nM, a value 8 times higher than that found for inhibition of IK(GDP). Glyburide 13-26 creatine kinase M-type Oryctolagus cuniculus 41-44 8242233-16 1993 In inside-out patch recordings (- )-Ckm (10 microM) applied to the intracellular surface of the membrane potentiated the opening of K channels already stimulated by I mM GDP and all of the channel activity was abolished by 10 microM glibenclamide. Glyburide 233-246 creatine kinase M-type Oryctolagus cuniculus 36-39 8368361-8 1993 Dilator responses of the basilar artery to 10(-9) and 10(-8) M CGRP were inhibited by glibenclamide (10(-6) M), a selective inhibitor of ATP-sensitive K+ channels, by 69 +/- 19 and 41 +/- 9%, respectively. Glyburide 86-99 calcitonin-related polypeptide alpha Rattus norvegicus 63-67 8123030-5 1994 These results suggest that a high concentration of glyburide stimulates insulin release directly, while a low concentration of glyburide increases the PPI mRNA level and may thereby enhance glucose-induced insulin release. Glyburide 127-136 insulin Homo sapiens 206-213 8378743-0 1993 Does glibenclamide influence the clearance of insulin and glucose uptake in patients with type 2 diabetes mellitus? Glyburide 5-18 insulin Homo sapiens 46-53 8319338-0 1993 Glibenclamide antagonizes adenosine A1 receptor-mediated cardioprotection in stunned canine myocardium. Glyburide 0-13 adenosine A1 receptor Canis lupus familiaris 26-47 8378743-3 1993 The aim of this study was to investigate whether glibenclamide affects clearance of insulin in Type 2 diabetic patients. Glyburide 49-62 insulin Homo sapiens 84-91 8511023-4 1993 Plasma insulin responses were markedly increased before glyburide therapy (area under insulin response curve 86 +/- 15 and 96 +/- 15 versus 40 +/- 5 nmol/min/L in normal controls, p < 0.001). Glyburide 56-65 insulin Homo sapiens 86-93 8511023-8 1993 In conclusion, in nondiabetic, hyperinsulinemic, thalassemic patients, chronic glyburide therapy normalizes insulin responses to oral glucose. Glyburide 79-88 insulin Homo sapiens 36-43 8511023-5 1993 However, insulin responses to glucose fell significantly after 3 mo of glyburide (to 52 +/- 7 nmol/min/L, p < 0.05 versus pretreatment) and were normalized after 12 mo (42 +/- 7 nmol/min/L, p = NS versus controls). Glyburide 71-80 insulin Homo sapiens 9-16 8511023-6 1993 The rate of insulin-stimulated glucose metabolism during euglycemic insulin clamps (40 mU/m2/min) was low in the patients before treatment (163 +/- 10 versus 215 +/- 17 mg/m2/min in controls, p < 0.05) and increased to 205 +/- 30 mg/m2/min after 3 mo of glyburide. Glyburide 257-266 insulin Homo sapiens 12-19 1356754-10 1992 In conclusion, our findings show that, in MMQ cells, glibenclamide stimulates PRL release, suggesting an involvement of ATP-sensitive potassium channels in the regulation of PRL secretion. Glyburide 53-66 prolactin Rattus norvegicus 78-81 8454937-0 1993 Insulin and IGF1 receptor function among type II diabetic responders and nonresponders to glyburide. Glyburide 90-99 insulin Homo sapiens 0-7 8454937-7 1993 Iodine 125-labeled insulin binding to intact erythrocytes tended to be higher among responders both before and after glyburide. Glyburide 117-126 insulin Homo sapiens 19-26 1493225-0 1992 Adenosine-induced hyperpolarization is depressed by glibenclamide in rat CA1 neurones. Glyburide 52-65 carbonic anhydrase 1 Rattus norvegicus 73-76 1493225-1 1992 The effect of the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel blocker, glibenclamide, on adenosine-induced postsynaptic hyperpolarization was studied by means of intracellular recording techniques in TTX-treated CA1 neurones in the rat hippocampal slice. Glyburide 91-104 carbonic anhydrase 1 Rattus norvegicus 232-235 8422763-0 1993 The effect of glyburide on beta-cell sensitivity to glucose-dependent insulinotropic polypeptide. Glyburide 14-23 gastric inhibitory polypeptide Homo sapiens 52-96 8422763-1 1993 OBJECTIVE: To assess whether treatment with glyburide alters beta-cell sensitivity to GIP in NIDDM patients. Glyburide 44-53 gastric inhibitory polypeptide Homo sapiens 86-89 8422763-10 1993 CONCLUSIONS: We conclude that glyburide enhances beta-cell sensitivity to GIP. Glyburide 30-39 gastric inhibitory polypeptide Homo sapiens 74-77 8201916-7 1993 The dose of insulin was decreased gradually until its replacement by chloropropamide in 1967 and glibenclamide in 1970. Glyburide 97-110 insulin Homo sapiens 12-19 8201916-14 1993 Insulin levels rose moderately after stimulation with glucagon, and with glibenclamide, with simultaneous marked decrease in glycemia. Glyburide 73-86 insulin Homo sapiens 0-7 8437888-5 1993 Both the outward current and Itail were inhibited nearly completely after application of glibenclamide (1 microM), a specific blocker of IKATP. Glyburide 89-102 ATP-sensitive inward rectifier potassium channel 11 Cavia porcellus 137-142 1301234-6 1992 In addition, the use of L-NG-nitroarginine methyl ester, glibenclamide, and other agents strongly suggests that calcitonin gene related peptide also acts by way of the nonadrenergic noncholinergic nervous system, to induce the relaxation of cholecystokinin-induced contraction observed in the guinea pig gallbladder strips. Glyburide 57-70 calcitonin Cavia porcellus 112-122 1289019-5 1992 A further improvement in metabolic control was observed in both groups after the introduction of GL; the mean reduction in glycosylated HbA1c was 1.4% for BTI and 0.7% for MI (p < 0.01 and 0.05, respectively), In conclusion, a subgroup of poorly controlled elderly Type 2 diabetic patients showed an improvement in metabolic control after a single injection of insulin despite discontinuation of maximal doses of oral antidiabetic agents. Glyburide 97-99 insulin Homo sapiens 364-371 1356754-10 1992 In conclusion, our findings show that, in MMQ cells, glibenclamide stimulates PRL release, suggesting an involvement of ATP-sensitive potassium channels in the regulation of PRL secretion. Glyburide 53-66 prolactin Rattus norvegicus 174-177 1356754-11 1992 The reversal by glibenclamide of the effects of SRIF on calcium homeostasis, membrane potential, and PRL release suggests that this type of potassium channel participates to the somatostatinergic inhibition of PRL secretion. Glyburide 16-29 prolactin Rattus norvegicus 101-104 1356754-11 1992 The reversal by glibenclamide of the effects of SRIF on calcium homeostasis, membrane potential, and PRL release suggests that this type of potassium channel participates to the somatostatinergic inhibition of PRL secretion. Glyburide 16-29 prolactin Rattus norvegicus 210-213 1396327-11 1992 Preexposure to 0.1 microM glyburide did not change calcium uptake at a glucose concentration of 2.8 mM (1.44 +/- 0.45 pmol/islet.2 min) but significantly reduced calcium uptake stimulated by 16.7 mM glucose (3.21 +/- 0.35 pmol/islet.2 min; n = 4; P < 0.005 compared to control islets). Glyburide 26-35 ISL LIM homeobox 2 Rattus norvegicus 123-130 1396327-11 1992 Preexposure to 0.1 microM glyburide did not change calcium uptake at a glucose concentration of 2.8 mM (1.44 +/- 0.45 pmol/islet.2 min) but significantly reduced calcium uptake stimulated by 16.7 mM glucose (3.21 +/- 0.35 pmol/islet.2 min; n = 4; P < 0.005 compared to control islets). Glyburide 26-35 ISL LIM homeobox 2 Rattus norvegicus 227-234 1281220-4 1992 The sulfonylureas, tolbutamide and glibenclamide, inhibited whole-cell CFTR Cl- currents at half-maximal concentrations of approximately 150 and 20 microM, respectively. Glyburide 35-48 CF transmembrane conductance regulator Homo sapiens 71-75 1281220-9 1992 The rank order of potency for inhibition of CFTR Cl- currents was: glibenclamide < BRL 38227 approximately equal to minoxidil sulfate > tolbutamide > diazoxide. Glyburide 67-80 CF transmembrane conductance regulator Homo sapiens 44-48 1281220-12 1992 These agents, especially glibenclamide, which was the most potent, may be of value in identifying CFTR Cl- channels. Glyburide 25-38 CF transmembrane conductance regulator Homo sapiens 98-102 1315978-5 1992 The relaxing capacity of ET-1 was absent when the tissue was precontracted by potassium yet was resistant to pretreatments with tetrodotoxin, capsaicin, propranolol, indomethacin, NG-methyl-L-arginine or glibenclamide. Glyburide 204-217 endothelin 1 Rattus norvegicus 25-29 1510715-3 1992 Glibenclamide and glimepiride in the range of 20-40 microM suppressed Ca2+ release from internal Ca2+ stores induced by thrombin. Glyburide 0-13 coagulation factor II, thrombin Homo sapiens 120-128 1355004-2 1992 Hyperpolarization is caused by an increased potassium conductance that is attenuated by glibenclamide (1-10 microM), a selective antagonist of ATP-sensitive potassium channels; in contrast, diazoxide (0.5 mM), an agonist at this channel, induces a hyperpolarization in CA1 neurons of rat hippocampal slices. Glyburide 88-101 carbonic anhydrase 1 Rattus norvegicus 269-272 1353301-5 1992 In contrast, the combination of glibenclamide with idazoxan markedly antagonised the decrease in insulin release evoked by the latter procedure. Glyburide 32-45 insulin Canis lupus familiaris 97-104 1353301-7 1992 In this preparation, glibenclamide inhibited the decrease in insulin release by 50%. Glyburide 21-34 insulin Canis lupus familiaris 61-68 1611155-11 1992 The average daily insulin dose rose significantly in the glyburide but not the placebo group compared with baseline. Glyburide 57-66 insulin Homo sapiens 18-25 1611155-14 1992 Several patients experienced dramatic improvements in glycemic parameters after the addition of glyburide to their insulin regimens. Glyburide 96-105 insulin Homo sapiens 115-122 1611155-15 1992 CONCLUSIONS: Improvements were observed in the FBG and Hb A1c measurements of this heterogeneous population of patients with type I diabetes after the addition of glyburide to their insulin regimens. Glyburide 163-172 insulin Homo sapiens 182-189 1592734-5 1992 In lungs ventilated with 3% oxygen, 10 nM ET-3 completely reversed the resultant hypoxic vasoconstriction (HPV) by 100 +/- 8%, an effect unchanged by either indomethacin (1 microM) or glibenclamide (10 microM). Glyburide 184-197 endothelin 3 Rattus norvegicus 42-46 1628142-12 1992 The BRL 38227-induced current was blocked by glibenclamide (10 microM) and phentolamine (100 microM), specific blockers of the ATP-sensitive K+ current in single cells. Glyburide 45-58 bromodomain containing 1 Homo sapiens 4-7 1628142-14 1992 In human isolated mesenteric artery cells, BRL 38227 (10 microM) induced a glibenclamide-sensitive current similar to, but smaller than, that observed in the rabbit portal vein. Glyburide 75-88 bromodomain containing 1 Homo sapiens 43-46 1611644-3 1992 In comparison with the first-generation sulfonylureas, glyburide is at least as effective, has a lower incidence of side effects, and may enhance postreceptor insulin activity to a greater degree. Glyburide 55-64 insulin Homo sapiens 159-166 1611644-4 1992 Glyburide can improve glycemic control, as evidenced by reduced fasting blood glucose concentrations and glycohemoglobin levels, without the inconvenience of insulin injections, the higher plasma insulin concentrations, and the additional training required to administer insulin. Glyburide 0-9 insulin Homo sapiens 196-203 1611644-4 1992 Glyburide can improve glycemic control, as evidenced by reduced fasting blood glucose concentrations and glycohemoglobin levels, without the inconvenience of insulin injections, the higher plasma insulin concentrations, and the additional training required to administer insulin. Glyburide 0-9 insulin Homo sapiens 196-203 1611644-5 1992 Because of its ability to enhance target tissue insulin action, glyburide also improves glycemic control in many NIDDM patients who have previously failed therapy with other sulfonylurea agents. Glyburide 64-73 insulin Homo sapiens 48-55 1908960-4 1991 These results suggest that glibenclamide binding sites are mainly localized on the mossy fibers in CA3, and on the granular and pyramidal neurons in the fascia dentata and CA1, respectively. Glyburide 27-40 carbonic anhydrase 3 Rattus norvegicus 99-102 1521183-2 1992 In experiments on hippocampal slices (from Wistar rats) glibenclamide (and possibly gliquidone and tolbutamide) significantly reduced the highly voltage-dependent, 4-aminopyridine-sensitive D-type outward current of CA3 neurons. Glyburide 56-69 carbonic anhydrase 3 Rattus norvegicus 216-219 1542435-6 1992 It is concluded that glibenclamide inhibits a voltage-gated, Ca(2+)- and ATPi-independent K+ current in SH-SY5Y cells. Glyburide 21-34 ATP synthase inhibitory factor subunit 1 Homo sapiens 73-77 1317934-7 1992 Glyburide produced a 34.6% decrease in glucose formation and a 31.3% decrease in PCOX flux, but no change in PK flux. Glyburide 0-9 pyruvate carboxylase Rattus norvegicus 81-85 1317934-11 1992 In addition, F26P may play a larger role in the hypoglycemic mechanism of action of tolbutamide than glyburide, since pyruvate carboxylase accounted for most of the decrease in glucose formation observed with glyburide and because preincubation with tolbutamide resulted in an activation of PK. Glyburide 209-218 pyruvate carboxylase Rattus norvegicus 118-138 1836728-5 1991 Glibenclamid completely abolished the inhibitory effect of cicletanine and ANF on ANG II-induced contraction of glomeruli from low-sodium rats. Glyburide 0-12 natriuretic peptide A Rattus norvegicus 75-78 1836728-5 1991 Glibenclamid completely abolished the inhibitory effect of cicletanine and ANF on ANG II-induced contraction of glomeruli from low-sodium rats. Glyburide 0-12 angiotensinogen Rattus norvegicus 82-88 1682478-7 1991 Nicorandil relaxed ET-1-contracted rings from micropig left circumflex coronary artery with an EC50 of 24 +/- 2.8 microM (n = 7); this effect was antagonized by methylene blue (10 microM) and glibenclamide (3 microM) (2- and 4-fold dextral shift of the control concentration-response curve, respectively). Glyburide 192-205 endothelin 1 Rattus norvegicus 19-23 1786796-4 1991 Glybenclamide had no significant effect on pulmonary vasodilator responses to acetylcholine or vasoactive intestinal peptide (VIP) but decreased responses to calcitonin gene-related peptide (CGRP). Glyburide 0-13 calcitonin related polypeptide alpha Homo sapiens 158-189 1786796-4 1991 Glybenclamide had no significant effect on pulmonary vasodilator responses to acetylcholine or vasoactive intestinal peptide (VIP) but decreased responses to calcitonin gene-related peptide (CGRP). Glyburide 0-13 calcitonin related polypeptide alpha Homo sapiens 191-195 1679326-3 1991 We measured amylin secretion from HIT T15 beta-cells exposed to glucose, arginine, glucagon, somatostatin, tolbutamide, glyburide, or metformin. Glyburide 120-129 islet amyloid polypeptide Mesocricetus auratus 12-18 1773716-6 1991 In the patients on oral agents who had marked fasting hyperglycemia (14.8 +/- 0.8 mmol/l) an only transient reduction (for 90 to 120 min) of postprandial hyperglycemia was achieved when INI (1 U/kg) was given in addition to po glyburide (10 mg) prior to the meal. Glyburide 227-236 PHD finger protein 5A Homo sapiens 186-189 1547684-1 1992 OBJECTIVE: TO investigate the effects of the addition of glyburide to the regimen of insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients with regard to their overall insulin requirement and dosage schedule and to assess persistence of these effects. Glyburide 57-66 insulin Homo sapiens 85-92 1547684-6 1992 RESULTS: Insulin requirements in the glyburide group decreased by 29 U at 14 wk compared with 9 U in the placebo group (P less than 0.05). Glyburide 37-46 insulin Homo sapiens 9-16 1547684-8 1992 The mean +/- SD reduction in insulin requirement in the glyburide group was relatively constant (25 +/- 10 U) and was not related to premedication insulin requirement. Glyburide 56-65 insulin Homo sapiens 29-36 1547684-10 1992 CONCLUSIONS: Glyburide reduces insulin requirements for 20 wk of combination therapy in NIDDM patients. Glyburide 13-22 insulin Homo sapiens 31-38 1547684-11 1992 Patients whose initial insulin requirement is less than or equal to 25 U have a 50% chance of achieving equivalent glycemic control on glyburide alone. Glyburide 135-144 insulin Homo sapiens 23-30 1735599-7 1992 Cromakalim (0.1-3 microM) also relaxed rings constricted with 0.3 nM endothelin-1, and this effect was partially reversed by glibenclamide (3 microM). Glyburide 125-138 endothelin 1 Rattus norvegicus 69-81 1628875-12 1992 Among the various drugs interfering with insulin secretion, sulfonylureas, such as tolbutamide and glibenclamide, directly inhibit ATP-dependent K+ channels in the B cell membrane and thereby initiate insulin release. Glyburide 99-112 insulin Homo sapiens 41-48 1490692-1 1992 Six months monotherapy with Acarbose vs. glibenclamide led to a marked improvement of BG and HbA1 in NIDDM, insufficiently controlled with diet. Glyburide 41-54 hemoglobin subunit alpha 1 Homo sapiens 93-97 1836728-6 1991 These results suggest that glibenclamid-sensitive potassium channels are responsible for ANG II hypersensitive contraction and ANF or cicletanine refractoriness of isolated glomeruli from low-sodium rats. Glyburide 27-39 angiotensinogen Rattus norvegicus 89-95 1836728-6 1991 These results suggest that glibenclamid-sensitive potassium channels are responsible for ANG II hypersensitive contraction and ANF or cicletanine refractoriness of isolated glomeruli from low-sodium rats. Glyburide 27-39 natriuretic peptide A Rattus norvegicus 127-130 1954808-1 1991 OBJECTIVE: To examine the relationship between plasma glyburide concentrations (0, 50, 100, 200, 400, and 800 nM) and the insulin response and glucose metabolism during euglycemic (4.6 +/- 0.1 mM) and hyperglycemic (11.6 +/- 0.2 mM) conditions. Glyburide 54-63 insulin Homo sapiens 122-129 1916009-1 1991 A 41-year old male with insulin-dependent diabetes mellitus previously unsuccessfully treated with a controlled diet and glibenclamide, and subsequently with increasing insulin doses (5 and 20 IU/day) experienced polyuria, glycosuria and loss of weight. Glyburide 121-134 insulin Homo sapiens 24-31 1908182-1 1991 The effect of glibenclamide treatment on insulin action in isolated fat cells was studied in eight moderately obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Glyburide 14-27 insulin Homo sapiens 41-48 1908960-4 1991 These results suggest that glibenclamide binding sites are mainly localized on the mossy fibers in CA3, and on the granular and pyramidal neurons in the fascia dentata and CA1, respectively. Glyburide 27-40 carbonic anhydrase 1 Rattus norvegicus 172-175 2149290-8 1990 Tetrabutylammonium (TBA), a nonselective K+ channel blocker, or glibenclamide, a supposed adenosine 5"-triphosphate (ATP)-sensitive K+ channel blocker, abolished the reduction of [Ca2+]i caused by the three K+ channel openers and the relaxant effect of cromakalim, whereas they only slightly attenuated the relaxant effects of pinacidil and nicorandil. Glyburide 64-77 carbonic anhydrase 2 Canis lupus familiaris 180-183 1905175-1 1991 The density of glibenclamide (GB) binding sites decreases considerably in the dentate gyrus (greater than 80%), the CA1 field (approximately 75%) and the stratum lucidum of CA3 field (approximately 70%) after intradentate colchicine injections in rat hippocampus. Glyburide 15-28 carbonic anhydrase 1 Rattus norvegicus 116-119 1905175-1 1991 The density of glibenclamide (GB) binding sites decreases considerably in the dentate gyrus (greater than 80%), the CA1 field (approximately 75%) and the stratum lucidum of CA3 field (approximately 70%) after intradentate colchicine injections in rat hippocampus. Glyburide 15-28 carbonic anhydrase 3 Rattus norvegicus 173-176 1905175-1 1991 The density of glibenclamide (GB) binding sites decreases considerably in the dentate gyrus (greater than 80%), the CA1 field (approximately 75%) and the stratum lucidum of CA3 field (approximately 70%) after intradentate colchicine injections in rat hippocampus. Glyburide 30-32 carbonic anhydrase 1 Rattus norvegicus 116-119 1905175-1 1991 The density of glibenclamide (GB) binding sites decreases considerably in the dentate gyrus (greater than 80%), the CA1 field (approximately 75%) and the stratum lucidum of CA3 field (approximately 70%) after intradentate colchicine injections in rat hippocampus. Glyburide 30-32 carbonic anhydrase 3 Rattus norvegicus 173-176 1902411-8 1991 Glibenclamide added to the diet further decreased fasting glycemia by improving in vivo insulin action and reduced the magnitude of day-time elevation of plasma glucose by enhancing endogenous insulin secretion. Glyburide 0-13 insulin Homo sapiens 88-95 1846336-4 1991 By studying B-cells of glibenclamide-treated rats, we have found that sustained stimulation of insulin release in vivo is associated with a two-fold increase in the level of connexin 43 gene transcripts and in the incidence of both ionic and dye coupling. Glyburide 23-36 gap junction protein, alpha 1 Rattus norvegicus 174-185 1660613-2 1991 Using HIT cells as a model system, we have established an extremely close correlation between the affinity of binding of glyburide and its analog, iodoglyburide, and the activation of various steps in stimulus-secretion coupling--inhibition of 86Rb+ efflux, increase in [Ca2+]i resulting from gating of voltage-gated calcium channels by cell depolarization, and the exocytosis of insulin. Glyburide 121-130 insulin Homo sapiens 380-387 2126639-10 1990 We conclude from our own experience and the literature that combined insulin-glibenclamide therapy is an efficient and compliant therapeutic regimen. Glyburide 77-90 insulin Homo sapiens 69-76 1847815-7 1991 These findings suggest that glyburide-induced increases in PI hydrolysis account, at least in part, for its acute stimulatory effect on insulin output and its ability to sensitize islets to subsequent stimulation. Glyburide 28-37 insulin Homo sapiens 136-143 1930902-5 1991 The test is specific for albumin failing to cross react with other plasma proteins present in urine, as well as with glibenclamide, chlorpropamide, phenformin, hemoglobin, glucose, urea and thymol. Glyburide 117-130 albumin Homo sapiens 25-32 1907539-4 1991 (2) VWF decreased significantly after administration with glibenclamide for 4 months. Glyburide 58-71 von Willebrand factor Homo sapiens 4-7 1825708-6 1991 These vasodilator and hypotensive effects are accompanied by reflex tachycardia and stimulation of the renin-angiotensin system and they are antagonized by glibenclamide, an antagonist of ATP-dependent potassium channels. Glyburide 156-169 renin Homo sapiens 103-108 2001465-6 1991 Cromakalim, CGRP and other vasodilators hyperpolarize and relax arteries in vitro and these responses are reversed by glibenclamide. Glyburide 118-131 calcitonin related polypeptide alpha Homo sapiens 12-16 1794268-7 1991 On the basis of HbA1 levels, the best results were obtained with glibenclamide and gliclazide, leading to normal HbA1 levels in 74% and 80% of patients, respectively. Glyburide 65-78 hemoglobin subunit alpha 1 Homo sapiens 16-20 1794268-7 1991 On the basis of HbA1 levels, the best results were obtained with glibenclamide and gliclazide, leading to normal HbA1 levels in 74% and 80% of patients, respectively. Glyburide 65-78 hemoglobin subunit alpha 1 Homo sapiens 113-117 1904820-2 1991 The rise in serum insulin levels persisted longer after glibenclamide. Glyburide 56-69 insulin Homo sapiens 18-25 1904820-4 1991 It is concluded that glibenclamide is able to maintain a more prolonged increase in serum insulin levels by inhibiting the degradation of insulin in the vascular endothelial cells of the liver. Glyburide 21-34 insulin Homo sapiens 90-97 1904820-4 1991 It is concluded that glibenclamide is able to maintain a more prolonged increase in serum insulin levels by inhibiting the degradation of insulin in the vascular endothelial cells of the liver. Glyburide 21-34 insulin Homo sapiens 138-145 2125460-11 1990 Glibenclamide produced significant increases in insulin concentrations compared with drug-free periods (P less than 0.01). Glyburide 0-13 insulin Homo sapiens 48-55 2122177-0 1990 Skeletal muscle glycogen synthase activity in subjects with non-insulin-dependent diabetes mellitus after glyburide therapy. Glyburide 106-115 glycogen synthase 1 Homo sapiens 0-33 2122177-5 1990 After glyburide treatment, the mean active glycogen synthase increased by 39% (P less than .05) above the fasting value during the high-dose insulin infusion. Glyburide 6-15 insulin Homo sapiens 141-148 2122177-7 1990 Changes of insulin-stimulated active glycogen synthase associated with glyburide treatment correlated with changes in total body glucose disposal rates (r = .70, P less than .05) during euglycemic clamps. Glyburide 71-80 insulin Homo sapiens 11-18 2122177-8 1990 We conclude that glyburide treatment of subjects with NIDDM is associated with an increase in insulin action in vivo and concomitantly with improved insulin action on skeletal muscle glycogen synthase. Glyburide 17-26 insulin Homo sapiens 94-101 2122177-8 1990 We conclude that glyburide treatment of subjects with NIDDM is associated with an increase in insulin action in vivo and concomitantly with improved insulin action on skeletal muscle glycogen synthase. Glyburide 17-26 insulin Homo sapiens 149-156 2122177-8 1990 We conclude that glyburide treatment of subjects with NIDDM is associated with an increase in insulin action in vivo and concomitantly with improved insulin action on skeletal muscle glycogen synthase. Glyburide 17-26 glycogen synthase 1 Homo sapiens 167-200 2117385-2 1990 The early studies, which were performed in patients receiving concomitant insulin therapy, may have underestimated the true effect of glyburide on insulin secretion. Glyburide 134-143 insulin Homo sapiens 147-154 2117385-4 1990 The effects of glyburide on insulin secretory rates calculated from plasma C-peptide levels were recently evaluated using individually derived C-peptide kinetic parameters and a validated open two-compartment model of peripheral C-peptide kinetics. Glyburide 15-24 insulin Homo sapiens 28-35 2117385-8 1990 During that time, insulin secretion rates increased by 221 percent in response to glyburide. Glyburide 82-91 insulin Homo sapiens 18-25 2117385-10 1990 In the patients receiving glyburide, the sluggish insulin secretory response to breakfast persisted, and the insulin secretory response during the hyperglycemic clamping was less than the response normally seen in nondiabetic subjects. Glyburide 26-35 insulin Homo sapiens 50-57 2117385-10 1990 In the patients receiving glyburide, the sluggish insulin secretory response to breakfast persisted, and the insulin secretory response during the hyperglycemic clamping was less than the response normally seen in nondiabetic subjects. Glyburide 26-35 insulin Homo sapiens 109-116 2117386-3 1990 Glyburide, one of the second-generation sulfonylureas, decreases glucose production and enhances insulin action in the liver. Glyburide 0-9 insulin Homo sapiens 97-104 2117386-5 1990 The effect of glyburide on the insulin-signaling mechanism(s) is distal to the insulin binding site of the alpha-subunit of the insulin receptor and the tyrosine kinase activation site of the beta-subunit. Glyburide 14-23 insulin Homo sapiens 31-38 2117386-5 1990 The effect of glyburide on the insulin-signaling mechanism(s) is distal to the insulin binding site of the alpha-subunit of the insulin receptor and the tyrosine kinase activation site of the beta-subunit. Glyburide 14-23 insulin Homo sapiens 79-86 2117386-5 1990 The effect of glyburide on the insulin-signaling mechanism(s) is distal to the insulin binding site of the alpha-subunit of the insulin receptor and the tyrosine kinase activation site of the beta-subunit. Glyburide 14-23 insulin Homo sapiens 79-86 2117387-4 1990 Glyburide is generally thought to exert two major actions: stimulation of pancreatic insulin secretion and enhancement of insulin action in hepatic and extrahepatic tissues. Glyburide 0-9 insulin Homo sapiens 85-92 2117389-0 1990 Effects of glyburide on in vivo insulin-mediated glucose disposal. Glyburide 11-20 insulin Homo sapiens 32-39 2117389-6 1990 In protocol 1, glyburide significantly improved insulin sensitivity (p less than 0.01) and insulin secretion (p less than 0.01) in the NIDDM patients. Glyburide 15-24 insulin Homo sapiens 48-55 2117389-8 1990 Insulin sensitivity also improved in the young healthy control subjects after glyburide therapy (6.5 +/- 0.5 to 7.6 +/- 0.7 mg/kg.min; p less than 0.05). Glyburide 78-87 insulin Homo sapiens 0-7 2117400-5 1990 The hypoxia-contracted SPA and LPA were relaxed by 2-4 microM cromakalim; these relaxations were reversed by 2 microM glibenclamide. Glyburide 118-131 surfactant protein A1 Rattus norvegicus 23-26 2123183-10 1990 This study shows that addition of glibenclamide to insulin treatment is advantageous in NIDDM patients showing secondary failure to OHA. Glyburide 34-47 insulin Homo sapiens 51-58 2119677-2 1990 In a single-blind, placebo controlled study the influence of tenoxicam on responses of glucose, insulin and C-peptide to oral doses of glucose and glibenclamide was examined in 16 healthy male volunteers. Glyburide 147-160 insulin Homo sapiens 108-117 2115686-9 1990 The combination of glibenclamide and insulin (administered with the Novo Pen injector) is a safe and effective form of therapy in secondary failure of sulfonylurea, and is well accepted due to the mild start into insulin therapy. Glyburide 19-32 proprotein convertase subtilisin/kexin type 1 inhibitor Homo sapiens 73-76 2115686-9 1990 The combination of glibenclamide and insulin (administered with the Novo Pen injector) is a safe and effective form of therapy in secondary failure of sulfonylurea, and is well accepted due to the mild start into insulin therapy. Glyburide 19-32 insulin Homo sapiens 213-220 33767884-2 2021 Glibenclamide, also known as glyburide, RP-1127, Cirara, and BIIB093, is a second-generation sulfonylurea that binds SUR1 at potassium channels and may significantly reduce cerebral edema following stroke, as evidenced by recent clinical trials. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 117-121 2143093-0 1990 Glibenclamide is a competitive antagonist of the thromboxane A2 receptor in dog coronary artery in vitro. Glyburide 0-13 thromboxane A2 receptor Canis lupus familiaris 49-72 2110711-3 1990 A statistically significant decrease of blood glucose and glycosylated hemoglobin values was found under the combination of glibenclamide-phenformin contained in the same tablet in contrast to the values obtained with the treatment with glibenclamide, gliclazide, chlorpropamide, combination of glibenclamide and biguanides, metformin, and insulin. Glyburide 124-137 insulin Homo sapiens 340-347 2171690-5 1990 Glibenclamide reduced blood glucose and plasma insulin levels indicating improved insulin sensitivity in the mice. Glyburide 0-13 insulin Homo sapiens 47-54 2171690-5 1990 Glibenclamide reduced blood glucose and plasma insulin levels indicating improved insulin sensitivity in the mice. Glyburide 0-13 insulin Homo sapiens 82-89 2171690-8 1990 Treatment with glibenclamide seems to reduce serum immunoreactive insulin levels, microsomal enzyme function and NADPH generating enzyme activities in genetically obese mice. Glyburide 15-28 insulin Homo sapiens 66-73 12106103-0 1990 Galanin and Glibenclamide Modulate the Anoxic Release of Glutamate in Rat CA3 Hippocampal Neurons. Glyburide 12-25 carbonic anhydrase 3 Rattus norvegicus 74-77 2110977-5 1990 BRL 34915 and P 1060 specifically increase the open-state probability of the Ca+(+)-activated K+ (maxi-K+) channel, and these actions are blocked by glyburide and also by charybdotoxin. Glyburide 149-158 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 98-114 2110977-7 1990 Thus, the membrane channel in rat portal vein affected by glyburide, BRL 34915 and P 1060 appears to be the Ca+(+)-activated maxi-K+ channel (that does not show ATP dependence under the conditions of these experiments). Glyburide 58-67 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 125-140 2109832-5 1990 Here, we report that arterial dilations in response to CGRP are partially reversed by blockers of the ATP-sensitive potassium channel (K(ATP)), glibenclamide and barium. Glyburide 144-157 calcitonin related polypeptide alpha Homo sapiens 55-59 1691378-4 1990 The effect was reversible upon addition of glyburide, a known IKATP blocker. Glyburide 43-52 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 62-67 33767884-2 2021 Glibenclamide, also known as glyburide, RP-1127, Cirara, and BIIB093, is a second-generation sulfonylurea that binds SUR1 at potassium channels and may significantly reduce cerebral edema following stroke, as evidenced by recent clinical trials. Glyburide 29-38 ATP binding cassette subfamily C member 8 Homo sapiens 117-121 33767884-2 2021 Glibenclamide, also known as glyburide, RP-1127, Cirara, and BIIB093, is a second-generation sulfonylurea that binds SUR1 at potassium channels and may significantly reduce cerebral edema following stroke, as evidenced by recent clinical trials. Glyburide 40-47 ATP binding cassette subfamily C member 8 Homo sapiens 117-121 33767884-2 2021 Glibenclamide, also known as glyburide, RP-1127, Cirara, and BIIB093, is a second-generation sulfonylurea that binds SUR1 at potassium channels and may significantly reduce cerebral edema following stroke, as evidenced by recent clinical trials. Glyburide 49-55 ATP binding cassette subfamily C member 8 Homo sapiens 117-121 33763207-0 2020 Glibenclamide, ATP and metformin increases the expression of human bile salt export pump ABCB11. Glyburide 0-13 ATP binding cassette subfamily B member 11 Homo sapiens 67-88 33763207-0 2020 Glibenclamide, ATP and metformin increases the expression of human bile salt export pump ABCB11. Glyburide 0-13 ATP binding cassette subfamily B member 11 Homo sapiens 89-95 33763207-2 2020 Drugs such as rifampicin and glibenclamide inhibit BSEP. Glyburide 29-42 ATP binding cassette subfamily B member 11 Homo sapiens 51-55 33763207-16 2020 Western blot and real-time PCR analysis confirmed the upregulation of BSEP on the treatment of HepG2 cells with glibenclamide, ATP, and metformin. Glyburide 112-125 ATP binding cassette subfamily B member 11 Homo sapiens 70-74 33763207-18 2020 We have found glibenclamide, ATP, and metformin upregulates BSEP. Glyburide 14-27 ATP binding cassette subfamily B member 11 Homo sapiens 60-64 34668144-12 2021 It was noted that Hdac1 inhibition significantly decreased placental Bcrp expression, with markedly increases of GLB concentrations and area under the concentration-time curve (AUC) in fetal-units. Glyburide 113-116 histone deacetylase 1 Mus musculus 18-23 18086811-10 2008 In addition, H-89, a cAMP-dependent protein kinase A (PKA) inhibitor, and glibenclamide, a CFTR inhibitor, inhibited fluid accumulation. Glyburide 74-87 cystic fibrosis transmembrane conductance regulator Mus musculus 91-95 34956587-11 2021 9-Oxabicyclo(3.3.1)nonane-2,6-diol and 1,2,3-Benzenetriol bound comparably to glibenclamide in Nrf-2, IL-6, and TNF-alpha binding pockets. Glyburide 78-91 NFE2 like bZIP transcription factor 2 Rattus norvegicus 95-100 34956587-11 2021 9-Oxabicyclo(3.3.1)nonane-2,6-diol and 1,2,3-Benzenetriol bound comparably to glibenclamide in Nrf-2, IL-6, and TNF-alpha binding pockets. Glyburide 78-91 interleukin 6 Rattus norvegicus 102-106 34956587-11 2021 9-Oxabicyclo(3.3.1)nonane-2,6-diol and 1,2,3-Benzenetriol bound comparably to glibenclamide in Nrf-2, IL-6, and TNF-alpha binding pockets. Glyburide 78-91 tumor necrosis factor Rattus norvegicus 112-121 34907818-9 2022 Glyburide is behind metformin and insulin, and more RCTs are needed to verify its safety. Glyburide 0-9 insulin Homo sapiens 34-41 34825567-7 2021 We show that both trans- and cis-JB253 bind to the same SUR1 cavity as antidiabetic sulfonylurea glibenclamide (GBM). Glyburide 112-115 ATP binding cassette subfamily C member 8 Homo sapiens 56-60 34668144-13 2021 Particularly, the ratios of fetal-unit/maternal plasma GLB concentrations were also significantly elevated following Hdac1 repression. Glyburide 55-58 histone deacetylase 1 Mus musculus 117-122 34324857-5 2021 We also show how diazoxide and glibenclamide compete for the same binding site in mitoSUR. Glyburide 31-44 ATP binding cassette subfamily B member 8 Rattus norvegicus 82-89 34912223-8 2021 Both glibenclamide and SA extract significantly decreased levels of TLR-4, MYD88, pro-inflammatory cytokines TNF-alpha, and TRAF-6 in pancreatic tissue homogenates, which correlated well with minimal pancreatic inflammatory cell infiltration. Glyburide 5-18 toll-like receptor 4 Rattus norvegicus 68-73 34869071-9 2021 Inhibition assays with glyburide and CA-074 methyl ester (K+ outflow inhibitor and cathepsin B inhibitor) blocked IL-1beta secretion, which demonstrated the essential role of the NLRP3 inflammasome in inflammatory response. Glyburide 23-32 interleukin 1 alpha Mus musculus 114-122 34869071-9 2021 Inhibition assays with glyburide and CA-074 methyl ester (K+ outflow inhibitor and cathepsin B inhibitor) blocked IL-1beta secretion, which demonstrated the essential role of the NLRP3 inflammasome in inflammatory response. Glyburide 23-32 NLR family, pyrin domain containing 3 Mus musculus 179-184 34844502-8 2021 Inhibition of SUR1-TRPM4 (glyburide/glibenclamide) and VEGF (bevacizumab) are currently closest to translation based on advances in clinical trials. Glyburide 26-35 ATP binding cassette subfamily C member 8 Homo sapiens 14-18 34844502-8 2021 Inhibition of SUR1-TRPM4 (glyburide/glibenclamide) and VEGF (bevacizumab) are currently closest to translation based on advances in clinical trials. Glyburide 36-49 ATP binding cassette subfamily C member 8 Homo sapiens 14-18 34569600-5 2021 Using glibenclamide as a pharmacological inhibitor of PEPT1, we demonstrate in cell lines in vitro and mouse xenografts in vivothat inh--ibition of PEPT1 reduces the proliferation of the cancer cells. Glyburide 6-19 solute carrier family 15 (oligopeptide transporter), member 1 Mus musculus 54-59 34569600-5 2021 Using glibenclamide as a pharmacological inhibitor of PEPT1, we demonstrate in cell lines in vitro and mouse xenografts in vivothat inh--ibition of PEPT1 reduces the proliferation of the cancer cells. Glyburide 6-19 solute carrier family 15 (oligopeptide transporter), member 1 Mus musculus 148-153 34664134-4 2022 Anti-diabetic drug glibenclamide (GLB) possesses anti-inflammatory properties and inhibits NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation. Glyburide 19-32 NLR family, pyrin domain containing 3 Mus musculus 91-139 34664134-4 2022 Anti-diabetic drug glibenclamide (GLB) possesses anti-inflammatory properties and inhibits NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation. Glyburide 19-32 NLR family, pyrin domain containing 3 Mus musculus 141-146 34664134-4 2022 Anti-diabetic drug glibenclamide (GLB) possesses anti-inflammatory properties and inhibits NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation. Glyburide 34-37 NLR family, pyrin domain containing 3 Mus musculus 91-139 34664134-4 2022 Anti-diabetic drug glibenclamide (GLB) possesses anti-inflammatory properties and inhibits NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation. Glyburide 34-37 NLR family, pyrin domain containing 3 Mus musculus 141-146 34664134-10 2022 In contrast, the clinical drug GLB and DMF have several other beneficial effects, which are independent of NLRP3 inhibition and Nrf2 activation. Glyburide 31-34 nuclear factor, erythroid derived 2, like 2 Mus musculus 128-132 34324857-12 2021 Using the molecular structure of the ATP binding protein ABCB8 (pointed by others as the mitoSUR) we demonstrate that glibenclamide competitively inhibits diazoxide actions. Glyburide 118-131 ATP binding cassette subfamily B member 8 Rattus norvegicus 57-62 34324857-12 2021 Using the molecular structure of the ATP binding protein ABCB8 (pointed by others as the mitoSUR) we demonstrate that glibenclamide competitively inhibits diazoxide actions. Glyburide 118-131 ATP binding cassette subfamily B member 8 Rattus norvegicus 89-96 34116285-6 2021 The expression of NLRP3 in the EAM + glyburide group was lower than in the EAM2 group (P < 0.05). Glyburide 37-46 NLR family pyrin domain containing 3 Homo sapiens 18-23 34494549-6 2021 Moreover, when cerebral edema was alleviated by glibenclamide treatment or genetic deletion of Trpm4, post-SE glymphatic system function recovered earlier, along with fewer p-tau-deposited neurons and neuronal degeneration and better cognitive function. Glyburide 48-61 microtubule associated protein tau Homo sapiens 175-178 34116285-8 2021 NLRP3 was expressed at lower levels in the EAM + glyburide group than in the EAM2 group (P < 0.05). Glyburide 49-58 NLR family pyrin domain containing 3 Homo sapiens 0-5 34116285-9 2021 Lower serum IL-1beta levels were detected in the EAM + BBG group than in the EAM1 group (P < 0.05), and serum IL-1beta and IL-18 levels in the EAM + glyburide group were lower than those in the EAM2 group (P < 0.05). Glyburide 149-158 interleukin 1 alpha Homo sapiens 12-20 34116285-9 2021 Lower serum IL-1beta levels were detected in the EAM + BBG group than in the EAM1 group (P < 0.05), and serum IL-1beta and IL-18 levels in the EAM + glyburide group were lower than those in the EAM2 group (P < 0.05). Glyburide 149-158 interleukin 1 alpha Homo sapiens 110-118 34116285-9 2021 Lower serum IL-1beta levels were detected in the EAM + BBG group than in the EAM1 group (P < 0.05), and serum IL-1beta and IL-18 levels in the EAM + glyburide group were lower than those in the EAM2 group (P < 0.05). Glyburide 149-158 interleukin 18 Homo sapiens 123-128 34290084-7 2021 Additionally, the MAO-B inhibition-induced increase in alpha-syn secretion was unaffected by brefeldin A, which inhibits endoplasmic reticulum/Golgi transport, but was blocked by probenecid and glyburide, which inhibit ATP-binding cassette (ABC) transporter function. Glyburide 194-203 monoamine oxidase B Homo sapiens 18-23 34290084-7 2021 Additionally, the MAO-B inhibition-induced increase in alpha-syn secretion was unaffected by brefeldin A, which inhibits endoplasmic reticulum/Golgi transport, but was blocked by probenecid and glyburide, which inhibit ATP-binding cassette (ABC) transporter function. Glyburide 194-203 synuclein alpha Homo sapiens 55-64 34081746-3 2021 Glibenclamide blocks the sulfonylurea 1 transient receptor potential melastatin 4 (Sur1-Trpm4) channel implicated in edema formation. Glyburide 0-13 ATP binding cassette subfamily C member 8 Rattus norvegicus 83-87 34512312-9 2021 In addition, GLC increased the expression of brain-derived neurotrophic factors and decreased the expression of proinflammatory factors (tumor necrosis factor (TNF)-alpha,interleukin (IL)-1, and IL-6). Glyburide 13-16 tumor necrosis factor Rattus norvegicus 137-170 34512312-9 2021 In addition, GLC increased the expression of brain-derived neurotrophic factors and decreased the expression of proinflammatory factors (tumor necrosis factor (TNF)-alpha,interleukin (IL)-1, and IL-6). Glyburide 13-16 interleukin 6 Rattus norvegicus 195-199 34512312-12 2021 In part, GLC may exert these effects by regulating the NF-kappaB signaling pathway through the Sur1-Trpm4 channel. Glyburide 9-12 ATP binding cassette subfamily C member 8 Rattus norvegicus 95-99 34512312-12 2021 In part, GLC may exert these effects by regulating the NF-kappaB signaling pathway through the Sur1-Trpm4 channel. Glyburide 9-12 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 100-105 34233693-11 2021 The expression level of testicular FGF21 gene increased in diabetic rats, which intensified after treatment with HESS as well as glibenclamide. Glyburide 129-142 fibroblast growth factor 21 Rattus norvegicus 35-40 34400867-1 2021 The aim of the present research was to describe the consequences of hyperlipidemia (HL) on the pharmacokinetics of glibenclamide (Gb) in poloxamer 407-induced hyperlipidemic rats. Glyburide 115-128 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 84-86 34400867-1 2021 The aim of the present research was to describe the consequences of hyperlipidemia (HL) on the pharmacokinetics of glibenclamide (Gb) in poloxamer 407-induced hyperlipidemic rats. Glyburide 130-132 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 84-86 34400867-5 2021 Whereas, the Cmax and tmax after oral dose of Gb in HL rats were noted as 773.39 microg/ml and 2.50 h respectively. Glyburide 46-48 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 52-54 34400867-7 2021 While the plasma clearance (CL) after oral dose of Gb was 2.53 ml/h and 1.39 ml/h in normal and HL rats respectively. Glyburide 51-53 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 96-98 34400867-8 2021 The improved plasma concentration of Gb following oral dosing in rats with HL seems to be due to a direct influence on hepatic clearance or metabolizing enzymes. Glyburide 37-39 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 75-77 34400867-9 2021 In conclusion, the Gb pharmacokinetics was considerably affected by the HL in rats. Glyburide 19-21 3-hydroxy-3-methylglutaryl-CoA lyase Rattus norvegicus 72-74 34177610-0 2021 The Effect of K ATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers. Glyburide 36-49 calcitonin related polypeptide alpha Homo sapiens 53-57 34177610-3 2021 Here, we investigated the effect of the K ATP channel blocker glibenclamide on CGRP-induced headache and vascular changes in healthy volunteers. Glyburide 62-75 calcitonin related polypeptide alpha Homo sapiens 79-83 34177610-4 2021 Methods: In a randomized, double-blind, placebo-controlled, cross-over study, 20 healthy volunteers aged 18-27 years were randomly allocated to receive an intravenous infusion of 1.5 mug/min CGRP after oral pretreatment with glibenclamide (glibenclamide-CGRP day) or placebo (placebo-CGRP day). Glyburide 240-253 calcitonin related polypeptide alpha Homo sapiens 254-258 34177610-7 2021 Results: We found no significant difference in the incidence of headache between glibenclamide-CGRP day (14/20, 70%) and placebo-CGRP day (19/20, 95%) (P = 0.06). Glyburide 81-94 calcitonin related polypeptide alpha Homo sapiens 95-99 34440028-0 2021 Possible Synergistic Antidiabetic Effects of Quantified Artemisia judaica Extract and Glyburide in Streptozotocin-Induced Diabetic Rats via Restoration of PPAR-alpha mRNA Expression. Glyburide 86-95 peroxisome proliferator activated receptor alpha Rattus norvegicus 155-165 34349235-3 2022 However, it is unclear whether and how glibenclamide can alleviate cardiac inflammatory injury induced by beta-AR overactivation. Glyburide 39-52 adrenergic receptor, beta 1 Mus musculus 106-113 34349235-5 2022 The results indicated that glibenclamide alleviated ISO-induced macrophage infiltration in the heart, as determined by Mac-3 staining. Glyburide 27-40 lysosomal-associated membrane protein 2 Mus musculus 119-124 34349235-9 2022 ISO activated the NLRP3 inflammasome in both cardiomyocytes and mouse hearts, but this effect was alleviated by glibenclamide pretreatment. Glyburide 112-125 NLR family, pyrin domain containing 3 Mus musculus 18-23 34349235-12 2022 Moreover, glibenclamide inhibited the cAMP/PKA signalling pathway, which is downstream of beta-AR, by increasing phosphodiesterase activity in mouse hearts and cardiomyocytes. Glyburide 10-23 adrenergic receptor, beta 1 Mus musculus 90-97 34349235-13 2022 In conclusion, glibenclamide alleviates beta-AR overactivation-induced cardiac inflammation by inhibiting the NLRP3 inflammasome. Glyburide 15-28 adrenergic receptor, beta 1 Mus musculus 40-47 34349235-13 2022 In conclusion, glibenclamide alleviates beta-AR overactivation-induced cardiac inflammation by inhibiting the NLRP3 inflammasome. Glyburide 15-28 NLR family, pyrin domain containing 3 Mus musculus 110-115 34081746-3 2021 Glibenclamide blocks the sulfonylurea 1 transient receptor potential melastatin 4 (Sur1-Trpm4) channel implicated in edema formation. Glyburide 0-13 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 88-93 35397639-0 2022 A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis. Glyburide 2-15 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 26-31 34254494-2 2021 CASE: In this report, we describe a 10-year-old girl who is heterozygous for a new missense mutation in the KCNJ11 gene and whose treatment was successfully switched from insulin to sulfonylurea (glibenclamide) therapy when she was one month old. Glyburide 196-209 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 108-114 35240233-9 2022 Glibenclamide, which targets SUR1, restrained CAFs and suppressed tumor growth in patient-derived xenograft models. Glyburide 0-13 ATP binding cassette subfamily C member 8 Homo sapiens 29-33 35141913-14 2022 Glyburide, an NOD-like receptor pyrin domain containing protein 3 (NLRP3)inhibitor, reduced the expression of pyroptosis markers induced by occlusal trauma with periodontitis and reversed bone resorption. Glyburide 0-9 NLR family, pyrin domain containing 3 Rattus norvegicus 67-72 35612844-5 2022 This case report describes the use of iCGM in the transition from insulin treatment to glibenclamide in a patient with TNDM caused by a pathogenic variant of KCNJ11. Glyburide 87-100 TNDM Homo sapiens 119-123 35612844-5 2022 This case report describes the use of iCGM in the transition from insulin treatment to glibenclamide in a patient with TNDM caused by a pathogenic variant of KCNJ11. Glyburide 87-100 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 158-164 35612844-6 2022 This is the first report of a successful outpatient transition from insulin to glibenclamide, in a Brazilian child with TNDM using iCGM (FreeStyle Libre@). Glyburide 79-92 TNDM Homo sapiens 120-124 35578855-9 2022 Tetraethylammonium, iberiotoxin, 4-Aminopyridine, glyburide, anandamide, and BaCl2 statistically significantly decreased the vasorelaxant effect level of (Pyr1)apelin-13 (p < 0.001). Glyburide 50-59 apelin Homo sapiens 160-166 35491519-6 2022 Glibenclamide at 0.3mg/day reduced glucagon by 32% in the four participants with fasting hyperglucagonemia (25.6pmol/L vs 17.4pmol/L; p<0.05) but not in those with normal levels. Glyburide 0-13 glucagon Homo sapiens 35-43 35017714-6 2022 Post-doxycycline feeding, insulin and glucagon secretion in response to glibenclamide or phenylephrine were compared between the two groups. Glyburide 72-85 glucagon Mus musculus 38-46 35017714-8 2022 RESULTS: In response to glibenclamide, E4orf1 mice secreted more insulin and exhibited lower blood glucose compared to control (47.4 +- 4.4 vs 27.4 +- 3.7 mg/dl, p < 0.003), but showed no difference in glucagon secretion. Glyburide 24-37 glucagon Mus musculus 202-210 35397639-0 2022 A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis. Glyburide 2-15 carbonic anhydrase 1 Mus musculus 54-57 35397639-5 2022 We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE. Glyburide 91-104 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 17-22 35397639-5 2022 We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE. Glyburide 91-104 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 115-120 35463001-12 2022 Furthermore, the potassium (K+) channel inhibitor glyburide decreased LDH release and suppressed NLRP3 inflammasome activation and pyroptosis in HCECs exposed to HKCA. Glyburide 50-59 NLR family, pyrin domain containing 3 Mus musculus 97-102 35380195-13 2022 IL-1beta and TNFalpha in the cortex were significantly decreased in the SAH-glibenclamide group compared to the SAH-control group. Glyburide 76-89 interleukin 1 alpha Rattus norvegicus 0-8 35380195-13 2022 IL-1beta and TNFalpha in the cortex were significantly decreased in the SAH-glibenclamide group compared to the SAH-control group. Glyburide 76-89 tumor necrosis factor Rattus norvegicus 13-21 34841901-9 2022 FUTURE DIRECTIONS: Among strategies to inhibit the NLRP3 inflammasome, Glyburide, Metformin, PPAR agonists and the DPP-4 inhibitor saxagliptin appear to be closest to clinical translation, as these drugs are already FDA approved for other indications. Glyburide 71-80 NLR family pyrin domain containing 3 Homo sapiens 51-56 35212627-3 2022 Antidiabetic sulfonylureas such as glibenclamide target SUR1 and indirectly suppress Kir6.2 activity. Glyburide 35-48 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 56-60 35212627-3 2022 Antidiabetic sulfonylureas such as glibenclamide target SUR1 and indirectly suppress Kir6.2 activity. Glyburide 35-48 potassium inwardly rectifying channel, subfamily J, member 11 Mus musculus 85-91 35221708-5 2022 The applicability and effectiveness of the CASPorter cell line were tested by co-treatment with Dox and four known CASP1/NLRP3 inhibitors (MCC950, Glyburide, VX-765 and VRT-043198). Glyburide 147-156 caspase 1 Homo sapiens 115-120 35221708-5 2022 The applicability and effectiveness of the CASPorter cell line were tested by co-treatment with Dox and four known CASP1/NLRP3 inhibitors (MCC950, Glyburide, VX-765 and VRT-043198). Glyburide 147-156 NLR family pyrin domain containing 3 Homo sapiens 121-126 35185385-0 2022 Glibenclamide Alleviates LPS-Induced Acute Lung Injury through NLRP3 Inflammasome Signaling Pathway. Glyburide 0-13 NLR family, pyrin domain containing 3 Mus musculus 63-68 35185385-4 2022 Meanwhile, the increased proteins of NLRP3 and Caspase-1/p20 after LPS instillation in lungs were downregulated by glibenclamide. Glyburide 115-128 NLR family, pyrin domain containing 3 Mus musculus 37-42 35185385-4 2022 Meanwhile, the increased proteins of NLRP3 and Caspase-1/p20 after LPS instillation in lungs were downregulated by glibenclamide. Glyburide 115-128 caspase 1 Mus musculus 47-56 35185385-4 2022 Meanwhile, the increased proteins of NLRP3 and Caspase-1/p20 after LPS instillation in lungs were downregulated by glibenclamide. Glyburide 115-128 demilune cell and parotid protein 1 Mus musculus 57-60 35185385-5 2022 Similarly, in vitro experiments also found that glibenclamide administration inhibited the LPS-induced upregulations in cytokine secretions of IL-1beta and IL-18, as well as in the expression of components in NLRP3 inflammasome in mouse peritoneal macrophages. Glyburide 48-61 interleukin 1 alpha Mus musculus 143-151 35185385-5 2022 Similarly, in vitro experiments also found that glibenclamide administration inhibited the LPS-induced upregulations in cytokine secretions of IL-1beta and IL-18, as well as in the expression of components in NLRP3 inflammasome in mouse peritoneal macrophages. Glyburide 48-61 interleukin 18 Mus musculus 156-161 35185385-5 2022 Similarly, in vitro experiments also found that glibenclamide administration inhibited the LPS-induced upregulations in cytokine secretions of IL-1beta and IL-18, as well as in the expression of components in NLRP3 inflammasome in mouse peritoneal macrophages. Glyburide 48-61 NLR family, pyrin domain containing 3 Mus musculus 209-214 35185385-7 2022 In conclusion, glibenclamide alleviates the development of LPS-induced ALI in a mouse model via inhibiting the NLRP3/Caspase-1/IL-1beta signaling pathway, which might provide a new strategy for the treatment of LPS-induced ALI. Glyburide 15-28 NLR family, pyrin domain containing 3 Mus musculus 111-116 35185385-7 2022 In conclusion, glibenclamide alleviates the development of LPS-induced ALI in a mouse model via inhibiting the NLRP3/Caspase-1/IL-1beta signaling pathway, which might provide a new strategy for the treatment of LPS-induced ALI. Glyburide 15-28 caspase 1 Mus musculus 117-126 35185385-7 2022 In conclusion, glibenclamide alleviates the development of LPS-induced ALI in a mouse model via inhibiting the NLRP3/Caspase-1/IL-1beta signaling pathway, which might provide a new strategy for the treatment of LPS-induced ALI. Glyburide 15-28 interleukin 1 alpha Mus musculus 127-135 2559356-0 1989 Insulin and IGF-I receptors in neuroblastoma cells: increases in mRNA and binding produced by glyburide. Glyburide 94-103 insulin Homo sapiens 0-7 2513734-2 1989 If the cytosolic ATP concentration is greater than 0 but less than 500 microM, pinacidil increases the activity of a channel identified as the ATP-sensitive K channel (IKATP) by its single-channel conductance, its inhibition by ATP, and its sensitivity to glybenclamide. Glyburide 256-269 ATP-sensitive inward rectifier potassium channel 11 Cavia porcellus 168-173 35261444-1 2022 Insulin is recommended as first-line pharmacologic therapy for gestational diabetes (GDM); however, glyburide and metformin are often used. Glyburide 100-109 insulin Homo sapiens 0-7 2559356-0 1989 Insulin and IGF-I receptors in neuroblastoma cells: increases in mRNA and binding produced by glyburide. Glyburide 94-103 insulin like growth factor 1 Homo sapiens 12-17 2505990-0 1989 Low-dose bedtime NPH insulin in treatment of secondary failure to glyburide. Glyburide 66-75 insulin Homo sapiens 21-28 2544783-4 1989 Glyburide"s actions were mediated without altering the following: (1) 125I-insulin binding; (2) the electrophoretic mobility of the affinity labeled alpha-subunit or the autophosphorylated beta-subunit of the insulin receptor; and (3) the insulin-stimulated insulin receptor kinase activity using histone or the beta-subunit of the insulin receptor as phosphoacceptors. Glyburide 0-9 insulin receptor Rattus norvegicus 209-225 2504288-1 1989 Drugs which influence the electrical activity of insulin-secreting B cells of mammalian islets of Langerhans by closing (tolbutamide and glibenclamide) or opening (diazoxide) ATP-sensitive potassium channels were applied to the ventricular muscle of the rat. Glyburide 137-150 insulin Homo sapiens 49-56 2544783-4 1989 Glyburide"s actions were mediated without altering the following: (1) 125I-insulin binding; (2) the electrophoretic mobility of the affinity labeled alpha-subunit or the autophosphorylated beta-subunit of the insulin receptor; and (3) the insulin-stimulated insulin receptor kinase activity using histone or the beta-subunit of the insulin receptor as phosphoacceptors. Glyburide 0-9 insulin receptor Rattus norvegicus 258-274 2544783-4 1989 Glyburide"s actions were mediated without altering the following: (1) 125I-insulin binding; (2) the electrophoretic mobility of the affinity labeled alpha-subunit or the autophosphorylated beta-subunit of the insulin receptor; and (3) the insulin-stimulated insulin receptor kinase activity using histone or the beta-subunit of the insulin receptor as phosphoacceptors. Glyburide 0-9 insulin receptor Rattus norvegicus 258-274 2499443-2 1989 Glyburide (15 mg/day) or placebo was added to the treatment regimen of 31 insulin-treated type II (non-insulin-dependent) diabetic subjects. Glyburide 0-9 insulin Homo sapiens 74-81 2495353-11 1989 infusion of vasopressin and could be prevented by glibenclamide. Glyburide 50-63 arginine vasopressin Rattus norvegicus 12-23 2497930-4 1989 In hippocampal formation the stratum lucidum and the stratum lacunosum moleculare of CA3 show an important density of glibenclamide binding sites. Glyburide 118-131 carbonic anhydrase 3 Rattus norvegicus 85-88 2524334-5 1989 Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Glyburide 163-176 insulin Homo sapiens 14-21 2524334-5 1989 Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Glyburide 163-176 insulin Homo sapiens 201-208 2524334-6 1989 Hepatic glucose production was also lower following glibenclamide treatment at both the lower (56 +/- 5 vs 68 +/- 5 mg m-2 min-1) and higher 22 +/- 4 vs 32 +/- 6 mg m-2 min-1) insulin levels. Glyburide 52-65 insulin Homo sapiens 176-183 2494027-7 1989 Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Glyburide 0-13 GLI family zinc finger 1 Rattus norvegicus 110-113 2494027-7 1989 Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Glyburide 0-13 vasoactive intestinal peptide Rattus norvegicus 124-127 2494027-7 1989 Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Glyburide 0-13 gastric inhibitory polypeptide Rattus norvegicus 243-246 3149105-1 1988 Insulin binding to erythrocyte receptors was studied in 36 newly diagnosed male subjects with NIDDM, treated with diet alone (Group I; n = 10) or diet + glibenclamide (Group II; n = 12) or diet + glibenclamide + metformin (Group III; n = 14). Glyburide 153-166 insulin Homo sapiens 0-7 3138409-1 1988 The effect of oral hypoglycemic sulfonylureas, tolbutamide and glyburide, on metabolic flux through the pyruvate carboxylase reaction was evaluated in liver mitochondria isolated from 24-hr fasted rats. Glyburide 63-72 pyruvate carboxylase Rattus norvegicus 104-124 2904889-0 1988 Somatostatin activates glibenclamide-sensitive and ATP-regulated K+ channels in insulinoma cells via a G-protein. Glyburide 23-36 somatostatin Rattus norvegicus 0-12 2904889-4 1988 Somatostatin-induced 86Rb+ efflux is abolished by the hypoglycemia-inducing sulfonylurea, glibenclamide, a known blocker of ATP-regulated K+ channels. Glyburide 90-103 somatostatin Rattus norvegicus 0-12 3143744-5 1988 After 3 h of insulin infusion, basal [Ca2+]i rose to 234 +/- 21 nM, but the responses to insulin and glyburide were completely abolished. Glyburide 101-110 insulin Homo sapiens 13-20 3149105-1 1988 Insulin binding to erythrocyte receptors was studied in 36 newly diagnosed male subjects with NIDDM, treated with diet alone (Group I; n = 10) or diet + glibenclamide (Group II; n = 12) or diet + glibenclamide + metformin (Group III; n = 14). Glyburide 196-209 insulin Homo sapiens 0-7 2454858-2 1988 The most potent second-generation drugs, glyburide and glipizide, bind to the receptor and trigger insulin release at nanomolar concentrations. Glyburide 41-50 Insulin-like receptor Drosophila melanogaster 99-106 3147830-0 1988 In vivo action of glibenclamide in obese subjects with mild type 2 (non-insulin dependent) diabetes. Glyburide 18-31 insulin Homo sapiens 72-79 3119405-9 1987 The results indicate that the glycemic effect of glyburide represents enhancement of insulin action and occurs independently of membrane insulin receptors. Glyburide 49-58 insulin Homo sapiens 85-92 3133266-7 1988 Addition of glibenclamide to insulin resulted in a further reduction of the fasting plasma glucose (7.9 +/- 0.5 mmol/l) and HbA1 (8.3 +/- 0.2%) concentration whereas the basal (0.21 +/- 0.03 nmol/l) and glucagon-stimulated C-peptide concentrations (0.34 +/- 0.06 nmol/l) increased again. Glyburide 12-25 insulin Homo sapiens 29-36 3133266-7 1988 Addition of glibenclamide to insulin resulted in a further reduction of the fasting plasma glucose (7.9 +/- 0.5 mmol/l) and HbA1 (8.3 +/- 0.2%) concentration whereas the basal (0.21 +/- 0.03 nmol/l) and glucagon-stimulated C-peptide concentrations (0.34 +/- 0.06 nmol/l) increased again. Glyburide 12-25 hemoglobin subunit alpha 1 Homo sapiens 124-128 3133266-9 1988 The daily insulin dose could be reduced by 25% after addition of glibenclamide to insulin, while it remained unchanged when insulin was combined with placebo. Glyburide 65-78 insulin Homo sapiens 10-17 3133266-9 1988 The daily insulin dose could be reduced by 25% after addition of glibenclamide to insulin, while it remained unchanged when insulin was combined with placebo. Glyburide 65-78 insulin Homo sapiens 82-89 3133266-9 1988 The daily insulin dose could be reduced by 25% after addition of glibenclamide to insulin, while it remained unchanged when insulin was combined with placebo. Glyburide 65-78 insulin Homo sapiens 82-89 3126626-0 1988 Glibenclamide improves the response to insulin treatment in non-insulin-dependent diabetics with second failure to sulfonylurea therapy. Glyburide 0-13 insulin Homo sapiens 39-46 3126626-5 1988 This was observed in spite of the fact that the daily insulin dose was reduced by approximately 30% in the glibenclamide-treated group of patients. Glyburide 107-120 insulin Homo sapiens 54-61 3126626-6 1988 It is concluded that in NIDDM patients with second failure to glibenclamide ot glipizide therapy, the responsiveness to glibenclamide may be at least partially restored by a short period of insulin treatment. Glyburide 120-133 insulin Homo sapiens 190-197 3140992-0 1988 The effects of glibenclamide treatment on insulin secretion and on insulin binding to erythrocytes in type II diabetes mellitus. Glyburide 15-28 insulin Homo sapiens 42-49 3152618-5 1988 After combined dietary and glyburide treatment and normalization of blood sugar, apolipoprotein A1 and A2, HDL-C levels, and HDL-C% increased significantly. Glyburide 27-36 apolipoprotein A1 Homo sapiens 81-98 3126291-2 1988 A system approach to the analysis of pharmacodynamic systems is applied to the relationship between the glyburide serum concentration (Cd) and a resulting pharmacologic effect response, that is, the C-peptide serum concentration (Cc) in patients with non-insulin dependent diabetes mellitus (NIDDM). Glyburide 104-113 insulin Homo sapiens 199-208 3119407-0 1987 Glyburide modulates insulin-mediated locomotor response of confluent cell cultures to wounding. Glyburide 0-9 insulin Homo sapiens 20-27 3119407-1 1987 We determined whether the sulfonylurea glyburide could modify the insulin-induced locomotor response to wounding of bovine aortic, pulmonary artery endothelial, and gerbil fibroma cells. Glyburide 39-48 insulin Bos taurus 66-73 3119407-4 1987 Glyburide enhanced the effect of insulin on both parameters of the locomotor response and also sensitized the cells to a previously ineffective concentration of insulin (10(-12) M). Glyburide 0-9 insulin Homo sapiens 33-40 3119407-4 1987 Glyburide enhanced the effect of insulin on both parameters of the locomotor response and also sensitized the cells to a previously ineffective concentration of insulin (10(-12) M). Glyburide 0-9 insulin Homo sapiens 161-168 2894389-1 1987 The acute effect of glibenclamide, a hypoglycemic sulfonylurea, upon transglutaminase activity was investigated in 6 type II diabetic patients by perfusing 1 mg glibenclamide during 1 h. Blood samples were drawn 0, 10, 20, 30, 60 min during and 30 and 60 min after perfusion to determine insulin, glucose and transglutaminase activity. Glyburide 20-33 insulin Homo sapiens 288-295 3117833-0 1987 Acute effect of glyburide on insulin sensitivity in type I diabetic patients. Glyburide 16-25 insulin Homo sapiens 29-36 3126223-0 1987 Effects of metformin and glibenclamide on insulin receptors in fibroblasts and tumor cells in vitro. Glyburide 25-38 insulin Homo sapiens 42-49 3126223-1 1987 The effects of the oral hypoglycemic agents metformin and glibenclamide on receptor binding of insulin and insulin-induced receptor down-regulation were studied in cultured normal human fibroblasts, human breast tumors (cell lines MCF-7 and T-47D) and a human colon tumor (cell line HCT-8) in order to identify differences in receptor regulation between normal and transformed cells. Glyburide 58-71 insulin Homo sapiens 95-102 3126223-1 1987 The effects of the oral hypoglycemic agents metformin and glibenclamide on receptor binding of insulin and insulin-induced receptor down-regulation were studied in cultured normal human fibroblasts, human breast tumors (cell lines MCF-7 and T-47D) and a human colon tumor (cell line HCT-8) in order to identify differences in receptor regulation between normal and transformed cells. Glyburide 58-71 insulin Homo sapiens 107-114 3126223-3 1987 Glibenclamide (2 microM) and metformin (1-10 microM) induced a 13-28% reduction in insulin receptor down regulation in fibroblasts exposed to 1.7 x 10(-8)M-insulin, the loss of binding on exposure to insulin decreasing from 55% to 40-48%. Glyburide 0-13 insulin receptor Homo sapiens 83-99 3126223-3 1987 Glibenclamide (2 microM) and metformin (1-10 microM) induced a 13-28% reduction in insulin receptor down regulation in fibroblasts exposed to 1.7 x 10(-8)M-insulin, the loss of binding on exposure to insulin decreasing from 55% to 40-48%. Glyburide 0-13 insulin Homo sapiens 83-90 3126223-3 1987 Glibenclamide (2 microM) and metformin (1-10 microM) induced a 13-28% reduction in insulin receptor down regulation in fibroblasts exposed to 1.7 x 10(-8)M-insulin, the loss of binding on exposure to insulin decreasing from 55% to 40-48%. Glyburide 0-13 insulin Homo sapiens 156-163 3117609-7 1987 During the hyperglycemic-clamp studies performed in normal subjects, both GB and GZ increased the first- (1.6-fold) and second- (2.2-fold) phase plasma insulin responses more than hyperglycemia alone. Glyburide 74-76 insulin Homo sapiens 152-159 3117609-10 1987 In both NIDDM and control subjects, the effects of hyperglycemia and sulfonylurea drugs (both GB and GZ) on the first- and second-phase plasma insulin responses were simply additive. Glyburide 94-96 insulin Homo sapiens 143-150 3123184-8 1987 Insulin sensitivity, assessed by an insulin tolerance test, was more improved with glyburide than with glipizide. Glyburide 83-92 insulin Homo sapiens 0-7 3123184-8 1987 Insulin sensitivity, assessed by an insulin tolerance test, was more improved with glyburide than with glipizide. Glyburide 83-92 insulin Homo sapiens 36-43 3117833-1 1987 Possible extrapancreatic effects of glyburide on insulin action were studied in six patients with insulin-dependent diabetes mellitus. Glyburide 36-45 insulin Homo sapiens 49-56 3117833-5 1987 During the glyburide infusion, the Biostator-determined insulin delivery rate was similar to that during the NaCl infusion for the first 6 h after the meal, but it decreased by 32% between the 6th and 12th hours after the meal. Glyburide 11-20 insulin Homo sapiens 56-63 3117833-6 1987 During the hyperinsulinemic clamp studies, glucose was delivered at a significantly higher rate when glyburide was infused; this was true for both rates of insulin infusion [5.6 +/- 1.9 (+/- SD) vs. 3.6 +/- 1.4 mg/kg.min and 12.1 +/- 2.4 vs. 9.1 +/- 2.1 mg/kg.min; P less than 0.05, glyburide vs. NaCl, respectively]. Glyburide 101-110 insulin Homo sapiens 16-23 3117833-8 1987 These results indicate that 1) glyburide has an acute effect on insulin action in insulin-dependent diabetic patients; and 2) this effect occurs at physiological as well as pharmacological insulin concentrations. Glyburide 31-40 insulin Homo sapiens 64-71 3117833-8 1987 These results indicate that 1) glyburide has an acute effect on insulin action in insulin-dependent diabetic patients; and 2) this effect occurs at physiological as well as pharmacological insulin concentrations. Glyburide 31-40 insulin Homo sapiens 82-89 3116364-5 1987 Glyburide increased sensitivity to insulin (ie, shifted the dose-response curve to the left) without affecting either responsiveness or insulin binding. Glyburide 0-9 insulin Homo sapiens 35-42 3115853-4 1987 Serum glibenclamide levels rose to similar levels (160 ng/ml) with protocols A and C. Heart rate, blood pressure, and blood lactate levels increased immediately after onset of exercise and were comparable under conditions of protocols B and C. Serum insulin levels fell during protocol B from 6.1 +/- 0.6 to 4.0 +/- 0.3 microU/ml (P less than .001) but increased from 6.5 +/- 0.6 to 12.3 +/- 2.8 microU/ml during protocol A and from 6.6 +/- 0.6 to 12.7 +/- 4.3 microU/ml during protocol C, P less than .001. Glyburide 6-19 insulin Homo sapiens 250-257 3116364-11 1987 In conclusion, glyburide directly inhibited glycogenolysis, stimulated glycogen synthesis and glycogen synthase, and potentiated the action of insulin on glycogen synthesis at a postbinding site in cultured rat hepatocytes. Glyburide 15-24 insulin Homo sapiens 143-150 3106656-4 1987 Treatment with glyburide, 20 mg/d (plus insulin), compared with placebo (plus insulin) resulted in a significant reduction in mean basal glucose (232 +/- 12 vs 262 +/- 11 mg/dL [12.8 vs 14.4 mmol/L]) and hemoglobin A1C (10.2% +/- 0.5% vs 10.9% +/- 03%) concentrations. Glyburide 15-24 insulin Homo sapiens 40-47 3118579-0 1987 [Long-term effect of combination glibenclamide-insulin treatment in the secondary failure of sulfonylurea therapy--results of a one-year double blind study]. Glyburide 33-46 insulin Homo sapiens 47-54 3118579-2 1987 During a one-year follow-up period the patients on insulin plus glibenclamide required significantly lower exogenous insulin doses. Glyburide 64-77 insulin Homo sapiens 117-124 3118579-5 1987 Glibenclamide withdrawal after six and again after twelve months of the combined therapy provoked a deterioration of glycaemic control, as well as a lowering of the C-peptide concentrations. Glyburide 0-13 insulin Homo sapiens 165-174 2890501-0 1987 Glyburide decreases insulin requirement, increases beta-cell response to mixed meal, and does not affect insulin sensitivity: effects of short- and long-term combined treatment in secondary failure to sulfonylurea. Glyburide 0-9 insulin Homo sapiens 20-27 2890501-12 1987 Glyburide increased basal and meal-but not glucagon-stimulated insulin and C-peptide levels, and also augmented the effect of meals on somatostatin release. Glyburide 0-9 insulin Homo sapiens 63-70 3034949-6 1987 In the absence of glucose, 1 microgram/mL glibenclamide increased insulin release. Glyburide 42-55 insulin Homo sapiens 66-73 3111514-11 1987 Plasma insulin concentrations were significantly elevated when H2-receptor antagonists and glibenclamide were administered concurrently. Glyburide 91-104 insulin Homo sapiens 7-14 3106656-4 1987 Treatment with glyburide, 20 mg/d (plus insulin), compared with placebo (plus insulin) resulted in a significant reduction in mean basal glucose (232 +/- 12 vs 262 +/- 11 mg/dL [12.8 vs 14.4 mmol/L]) and hemoglobin A1C (10.2% +/- 0.5% vs 10.9% +/- 03%) concentrations. Glyburide 15-24 insulin Homo sapiens 78-85 3106656-5 1987 Concomitant with this change, basal C-peptide and free insulin values increased with glyburide therapy, but this pharmacological agent did not alter the ability of the patient"s erythrocytes to bind insulin. Glyburide 85-94 insulin Homo sapiens 55-62 3106656-6 1987 We conclude that in type II diabetic subjects receiving more than 28 units of insulin per day, the addition of glyburide results in a marginal, but statistically significant improvement in basal glucose concentration, but not in glucose tolerance as assessed by integrated glucose concentration. Glyburide 111-120 insulin Homo sapiens 78-85 3091033-0 1986 Glibenclamide induces glucokinase in rat pancreatic islets and liver. Glyburide 0-13 glucokinase Rattus norvegicus 22-33 2878704-4 1986 The patient with impaired glucose tolerance due to insulin deficiency developed diabetes mellitus after four months" treatment; concomitant treatment with glibenclamide resulted in a decreased glucose concentration and increased insulin concentration. Glyburide 155-168 insulin Homo sapiens 51-58 3019808-7 1986 Calmodulin and calmodulin-like activity (PDE-activator activity) in the liver and fat was decreased in diabetes and restored toward normal after glyburide treatment (P less than .05). Glyburide 145-154 calmodulin 1 Rattus norvegicus 0-10 3019808-7 1986 Calmodulin and calmodulin-like activity (PDE-activator activity) in the liver and fat was decreased in diabetes and restored toward normal after glyburide treatment (P less than .05). Glyburide 145-154 calmodulin 1 Rattus norvegicus 15-25 3535793-5 1986 Both glibenclamide and chlorpropamide stimulated insulin release from HIT-T15 cells. Glyburide 5-18 insulin Mesocricetus auratus 49-56 3535793-9 1986 The stimulation of phase I by glibenclamide alone and the inhibition of phase II of glucose induced insulin release by colchicine suggested the presence of a readily available pool of insulin granules which was not rapidly restored by insulin biosynthesis and granule margination. Glyburide 30-43 insulin Mesocricetus auratus 184-191 3535793-9 1986 The stimulation of phase I by glibenclamide alone and the inhibition of phase II of glucose induced insulin release by colchicine suggested the presence of a readily available pool of insulin granules which was not rapidly restored by insulin biosynthesis and granule margination. Glyburide 30-43 insulin Mesocricetus auratus 184-191 3097384-12 1986 The inhibition of insulin secretion (measured by C-peptide) caused by exogenous insulin administration is largely abolished by glibenclamide. Glyburide 127-140 insulin Homo sapiens 18-25 3097384-12 1986 The inhibition of insulin secretion (measured by C-peptide) caused by exogenous insulin administration is largely abolished by glibenclamide. Glyburide 127-140 insulin Homo sapiens 80-87 2879004-3 1986 The capacity of tolbutamide and glibenclamide to relax vanadate-induced contraction of rat uterus in Ca-free medium suggests that sulphonylureas may have an intracellular site of action related to cytosolic free Ca levels, or effect a reduction in Ca action. Glyburide 32-45 neurogenin 3 Rattus norvegicus 49-54 3095909-0 1986 Potentiation by previous nutrients of glibenclamide-induced insulin release in man. Glyburide 38-51 insulin Homo sapiens 60-67 3095909-8 1986 We conclude that nutrients sensitize insulin-releasing cells to subsequent stimulation by glibenclamide, thereby aggravate a blood-glucose-lowering effect of the drug. Glyburide 90-103 insulin Homo sapiens 37-44 3100365-8 1987 In contrast to the IDDM patients, the insulin-treated NIDDM subjects exhibited significant reductions in daily insulin requirement (72 +/- 6 vs. 58 +/- 9 U/day), mean 24-h plasma glucose concentration (153 +/- 10 vs. 131 +/- 5 mg/dl), glucosuria (14 +/- 5 vs. 4 +/- 1 g/day), and glycosylated hemoglobin (10.3 +/- 0.7 vs. 8.0 +/- 0.4%) after glyburide treatment (all P less than or equal to .05). Glyburide 342-351 insulin Homo sapiens 38-45 3104218-0 1987 Pharmacokinetics and pharmacological properties of two galenical preparations of glibenclamide, HB419 and HB420, in non insulin-dependent (type 2) diabetes. Glyburide 81-94 insulin Homo sapiens 120-127 2876707-1 1986 During adipocyte differentiation of 3T3-L1 cells, glyburide increased the specific activity (mU/mg protein) of glycerol-3-P dehydrogenase (by at least 14-fold) and glutamine synthetase (by 5-fold). Glyburide 50-59 glutamate-ammonia ligase (glutamine synthetase) Mus musculus 164-184 3092851-0 1986 Effect of oral verapamil on glibenclamide stimulated insulin secretion. Glyburide 28-41 insulin Homo sapiens 53-60 3092851-1 1986 In order to study the effect of the calcium antagonist, verapamil, on glibenclamide stimulated insulin release, nine healthy fasted male volunteers were given 5 mg oral glibenclamide with either 120 mg oral verapamil or placebo in a double-blind crossover manner 1 week apart. Glyburide 70-83 insulin Homo sapiens 95-102 3016235-3 1986 Crystals of glyburide belong to space group P2(1)/n with a = 9.414(3)A, b = 17.591(5)A, c = 14.410(4)A, beta = 93.42(3) degrees, V = 2382(1)A3, R = 0.0694, Z = 4. Glyburide 12-21 cyclin dependent kinase inhibitor 1A Homo sapiens 44-49 3098013-0 1986 Changes in insulin receptor functions of the erythrocyte by treatment of non-insulin-dependent diabetes mellitus (NIDDM) patients with glibenclamide and diet control. Glyburide 135-148 insulin receptor Homo sapiens 11-27 3098013-1 1986 The insulin binding of erythrocytes from: (i) fifteen age-matched normal subjects, (ii) ten untreated NIDDM patients and (iii) fifteen treated (glibenclamide + hypocaloric diet) NIDDM patients (all males) has been studied. Glyburide 144-157 insulin Homo sapiens 4-11 3085419-5 1986 Plasma glucose and insulin response to glibenclamide was also delayed in the delayed absorption group. Glyburide 39-52 insulin Homo sapiens 19-26 3091112-5 1986 Both glibenclamide and high concentrations of K+ decreased pHi. Glyburide 5-18 glucose-6-phosphate isomerase 1 Mus musculus 59-62 2951088-0 1985 The effect of glibenclamide administration on insulin sensitivity and insulin binding to monocytes in normal subjects. Glyburide 14-27 insulin Homo sapiens 46-53 3935405-6 1985 The blood glucose level during insulin-glibenclamide therapy was 35-45 mg/dl below that during insulin-placebo treatment at all time points investigated. Glyburide 39-52 insulin Homo sapiens 31-38 3934920-0 1985 Release of an insulin-like peptide from perfused extirpated cat legs in response to electrical stimulation of the sciatic and brachial nerves and to administration of ACh, bombesin, oxytocin and glibenclamide. Glyburide 195-208 insulin Bos taurus 14-21 3934920-6 1985 When subjected to high-performance liquid chromatography (HPLC) the insulin-like peptide detected in the cat leg perfusate following nervous stimulation, or administration of oxytocin and glibenclamide, co-eluted with a bovine insulin standard. Glyburide 188-201 insulin Bos taurus 68-75 3934920-6 1985 When subjected to high-performance liquid chromatography (HPLC) the insulin-like peptide detected in the cat leg perfusate following nervous stimulation, or administration of oxytocin and glibenclamide, co-eluted with a bovine insulin standard. Glyburide 188-201 insulin Bos taurus 227-234 3931459-4 1985 Glyburide therapy increased endogenous insulin secretion, increased adipocyte insulin binding after 18 but not three months of therapy, enhanced peripheral insulin action by acting primarily at a post-receptor site, and reduced basal hepatic glucose output. Glyburide 0-9 insulin Homo sapiens 39-46 3931459-4 1985 Glyburide therapy increased endogenous insulin secretion, increased adipocyte insulin binding after 18 but not three months of therapy, enhanced peripheral insulin action by acting primarily at a post-receptor site, and reduced basal hepatic glucose output. Glyburide 0-9 insulin Homo sapiens 78-85 3931462-0 1985 Effect of glyburide on in vivo recycling of the hepatic insulin receptor. Glyburide 10-19 insulin receptor Rattus norvegicus 56-72 3931462-2 1985 In these studies, a novel technique was used to examine the influence of glyburide on in vivo cycling of the hepatic insulin receptor. Glyburide 73-82 insulin receptor Rattus norvegicus 117-133 3931464-5 1985 Distribution of glyburide is affected by high affinity for serum albumin (99 percent bound), and elimination of the drug appears to be evenly divided between biliary and renal routes. Glyburide 16-25 albumin Homo sapiens 59-72 3931466-3 1985 Glyburide lowered plasma glucose and raised plasma insulin concentrations in non-insulin-dependent diabetes mellitus. Glyburide 0-9 insulin Homo sapiens 51-58 3931466-4 1985 Patients with type IV hyperlipoproteinemia had higher fasting free insulin concentrations before and after therapy than patients without hyperlipoproteinemia and may have a slightly reduced hypoglycemic response to glyburide therapy. Glyburide 215-224 insulin Homo sapiens 67-74 3081293-5 1986 One subject with severe renal impairment (CLCR = 5 ml/min/1.7 m2) had decreased glyburide clearance that resulted in a t1/2 of 11 hours. Glyburide 80-89 interleukin 1 receptor like 1 Homo sapiens 119-129 3084315-4 1986 In the glibenclamide group, a significant increase in the number of hypoglycemic episodes was observed in spite of a 8 to 10% reduction in insulin requirements. Glyburide 7-20 insulin Homo sapiens 139-146 2951088-0 1985 The effect of glibenclamide administration on insulin sensitivity and insulin binding to monocytes in normal subjects. Glyburide 14-27 insulin Homo sapiens 70-77 2951088-2 1985 Glibenclamide administration produced a 60% increase in maximal specific insulin binding to monocytes. Glyburide 0-13 insulin Homo sapiens 73-80 3924948-1 1985 The effect of glibenclamide treatment on insulin-mediated glucose disposal was studied in eight C-peptide-negative type I diabetic patients. Glyburide 14-27 insulin Homo sapiens 41-48 3934860-6 1985 These results suggest that a combination with glibenclamide leads to a decrease of insulin-requirement. Glyburide 46-59 insulin Homo sapiens 83-90 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glyburide 60-73 insulin Homo sapiens 4-11 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glyburide 60-73 insulin Homo sapiens 91-98 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glyburide 60-73 insulin Homo sapiens 91-98 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glyburide 224-237 insulin Homo sapiens 4-11 3924948-6 1985 The insulin-mediated glucose disposal rate was greater with glibenclamide during the first insulin infusion period (which generated plasma free insulin levels within the physiological range) 2.68 +/- 0.32 mg kg-1 min-1 with glibenclamide vs. 1.97 +/- 0.20 mg kg-1 min-1 without glibenclamide (P less than 0.005). Glyburide 224-237 insulin Homo sapiens 4-11 3924948-8 1985 These results provide evidence for an extrapancreatic effect of glibenclamide at low insulin concentrations during euglycemic clamping in patients with insulin-dependent diabetes mellitus. Glyburide 64-77 insulin Homo sapiens 85-92 3923961-6 1985 The glyburide-induced fall in plasma glucose concentration was associated with improvements in both insulin secretion and insulin action, but only the enhanced insulin action correlated with the reduction in fasting and postprandial glucose levels. Glyburide 4-13 insulin Homo sapiens 100-107 3923833-4 1985 GL and CP produced essentially the same effects on serum levels of glucose, insulin, glucagon (IRG), growth hormone (GH), cholesterol, and triglyceride. Glyburide 0-2 growth hormone 1 Homo sapiens 117-119 3923453-11 1985 Although glyburide is a potent stimulator of pancreatic insulin secretion after short-term administration, an additional mechanism of action during long-term administration is to decrease the resistance of muscle and liver to the action of insulin. Glyburide 9-18 insulin Homo sapiens 56-63 3923833-4 1985 GL and CP produced essentially the same effects on serum levels of glucose, insulin, glucagon (IRG), growth hormone (GH), cholesterol, and triglyceride. Glyburide 0-2 insulin Homo sapiens 76-83 3923833-4 1985 GL and CP produced essentially the same effects on serum levels of glucose, insulin, glucagon (IRG), growth hormone (GH), cholesterol, and triglyceride. Glyburide 0-2 growth hormone 1 Homo sapiens 101-115 3931537-0 1985 Combination of insulin and glibenclamide in the treatment of elderly non-insulin dependent (type 2) diabetic patients. Glyburide 27-40 insulin Homo sapiens 73-80 3919531-0 1985 Transient effect of the combination of insulin and sulfonylurea (glibenclamide) on glycemic control in non-insulin dependent diabetics poorly controlled with insulin alone. Glyburide 65-78 insulin Homo sapiens 107-114 3931537-5 1985 The level of haemoglobin A, (HbA1) decreased significantly from 13.8 +/- 0.6% (mean +/- SE) to 12.4 +/- 0.6% during the insulin + glibenclamide period (p less than 0.01); in contrast, there was no change during the insulin + placebo period. Glyburide 130-143 hemoglobin subunit alpha 1 Homo sapiens 29-33 3931537-5 1985 The level of haemoglobin A, (HbA1) decreased significantly from 13.8 +/- 0.6% (mean +/- SE) to 12.4 +/- 0.6% during the insulin + glibenclamide period (p less than 0.01); in contrast, there was no change during the insulin + placebo period. Glyburide 130-143 insulin Homo sapiens 120-127 3931537-8 1985 The results suggest that glibenclamide can improve the glycaemic control in insulin-treated elderly diabetics by mechanisms which still are to be elucidated. Glyburide 25-38 insulin Homo sapiens 76-83 3935120-1 1985 The effects of single oral dose of glibenclamide (Gilemid 5 mg) and chlorpropamide (250 mg) on serum insulin and glucose levels and electrolyte (sodium, potassium) balance were studied, in a cross-over double-blind manner, in 11 patients with non-insulin-dependent diabetes. Glyburide 35-48 insulin Homo sapiens 101-108 3935120-2 1985 Both drugs increased serum insulin for more than 8 h but less than 24 h. The effect of glibenclamide was slightly stronger than that of chlorpropamide. Glyburide 87-100 insulin Homo sapiens 27-34 3935376-4 1985 Significant improvements in HbA1 were produced overall in the gliquidone (p less than 0.01), gliclazide (p less than 0.01) and glibenclamide (p less than 0.02) groups and the gliquidone and gliclazide groups were significantly better than the glipizide group (p less than 0.01 in both cases). Glyburide 127-140 hemoglobin subunit alpha 1 Homo sapiens 28-32 6136627-3 1983 Basal levels of growth hormone and of pancreatic and gastric hormones were reduced and the response of growth hormone, insulin and C-peptide to stimuli such as arginine, glucose, glibenclamide and calcium was virtually abolished. Glyburide 179-192 insulin Homo sapiens 119-126 3933984-7 1985 Insulin sensitivity was increased by glibenclamide but not by glipizide. Glyburide 37-50 insulin Homo sapiens 0-7 3933984-10 1985 Only glibenclamide improved insulin sensitivity and was slightly more active than glipizide on fasting blood glucose levels. Glyburide 5-18 insulin Homo sapiens 28-35 6435371-0 1984 Improved diabetic control in insulin-dependent diabetics treated with insulin and glibenclamide. Glyburide 82-95 insulin Homo sapiens 29-36 6435371-5 1984 Combined insulin and glibenclamide treatment may produce a useful improvement of diabetic control in insulin-dependent diabetics who still secrete some endogenous insulin, although further studies are required. Glyburide 21-34 insulin Homo sapiens 101-108 6432610-9 1984 After glyburide, insulin-mediated glucose metabolism increased by 26% to 3.67 mg/kg X min (P less than 0.01). Glyburide 6-15 insulin Homo sapiens 17-24 6376033-7 1984 Thus, after 3 mo of glyburide treatment, glycemic control is markedly improved and this is accompanied by an increase in insulin secretion, no change in cellular insulin receptors, decreased hepatic glucose production rates, and an increase in overall insulin-mediated glucose disposal. Glyburide 20-29 insulin Homo sapiens 121-128 6376033-8 1984 After 18 mo of glyburide treatment, an increase in insulin secretion can no longer be demonstrated, whereas insulin binding to receptors is now significantly increased. Glyburide 15-24 insulin Homo sapiens 51-58 6439409-8 1984 While glyburide produces an insulin release response to glucose that parallels a normal physiological response, it appears to also decrease resistance to insulin and sensitize the receptors while utilizing the patient"s available endogenous insulin. Glyburide 6-15 insulin Homo sapiens 28-35 6439409-8 1984 While glyburide produces an insulin release response to glucose that parallels a normal physiological response, it appears to also decrease resistance to insulin and sensitize the receptors while utilizing the patient"s available endogenous insulin. Glyburide 6-15 insulin Homo sapiens 154-161 6439409-8 1984 While glyburide produces an insulin release response to glucose that parallels a normal physiological response, it appears to also decrease resistance to insulin and sensitize the receptors while utilizing the patient"s available endogenous insulin. Glyburide 6-15 insulin Homo sapiens 154-161 6437842-3 1984 The combined administration of glibenclamide and acarbose resulted in a modest improvement in the blood glucose profile after breakfast and lunch, together with a significant diminution in plasma insulin. Glyburide 31-44 insulin Homo sapiens 196-203 6415086-0 1983 The effect of glibenclamide on insulin receptors in normal man: comparative studies of insulin binding to monocytes and erythrocytes. Glyburide 14-27 insulin Homo sapiens 31-38 6415086-2 1983 To further elucidate the mechanisms of this action, we studied the effect of glibenclamide on in vivo and in vitro cellular insulin receptor binding in normal subjects. Glyburide 77-90 insulin receptor Homo sapiens 124-140 6415086-3 1983 Oral administration of glibenclamide in dose of 2.5 mg/day increased insulin binding to monocytes by 70% (P less than 0.001), in spite of increased postprandial serum insulin levels. Glyburide 23-36 insulin Homo sapiens 69-76 6415086-3 1983 Oral administration of glibenclamide in dose of 2.5 mg/day increased insulin binding to monocytes by 70% (P less than 0.001), in spite of increased postprandial serum insulin levels. Glyburide 23-36 insulin Homo sapiens 167-174 6428843-3 1984 Insulin receptors of peripheral monocytes were initially normal in both number and affinity in this group of insulin-dependent diabetic patients, but, after 6 mo of glyburide therapy, binding to insulin receptors declined at the lower insulin concentration range without falling out of the normal range. Glyburide 165-174 insulin Homo sapiens 0-7 6428843-3 1984 Insulin receptors of peripheral monocytes were initially normal in both number and affinity in this group of insulin-dependent diabetic patients, but, after 6 mo of glyburide therapy, binding to insulin receptors declined at the lower insulin concentration range without falling out of the normal range. Glyburide 165-174 insulin Homo sapiens 195-202 6429023-0 1984 Hyperglycaemic clamp and insulin binding to isolated monocytes before and after glibenclamide treatment of mild type II diabetics. Glyburide 80-93 insulin Homo sapiens 25-32 6432273-0 1984 [Effect of glibenclamide therapy on the plasma insulin level in non-insulin-dependent diabetes]. Glyburide 11-24 insulin Homo sapiens 47-54 6424413-4 1984 The results indicate that the glibenclamide-induced insulin release can be resolved in a "high-affinity" component, which correlates with increased osmotic resistance in the beta-cells and a "low-affinity" component not associated with increased osmotic resistance. Glyburide 30-43 insulin Homo sapiens 52-59 6415086-6 1983 The in vitro studies with monocytes revealed a dose-related insulin receptor stimulatory effect of glibenclamide (P less than 0.05), with a maximal effect of 20% above basal level. Glyburide 99-112 insulin Homo sapiens 60-67 6415086-7 1983 These data indicate that glibenclamide increases the insulin-binding ability of monocytes but not of erythrocytes. Glyburide 25-38 insulin Homo sapiens 53-60 6413265-3 1983 Glibenclamide plus diet succeeded in improving glucose tolerance only in low insulin responders whereas glucose tolerance remained unchanged in normal insulin responders. Glyburide 0-13 insulin Homo sapiens 77-84 6413265-4 1983 There was a significant decrease in fasting and glucose-stimulated insulin levels after two years of glibenclamide treatment in both the normal and low insulin-responders. Glyburide 101-114 insulin Homo sapiens 67-74 6413265-4 1983 There was a significant decrease in fasting and glucose-stimulated insulin levels after two years of glibenclamide treatment in both the normal and low insulin-responders. Glyburide 101-114 insulin Homo sapiens 152-159 6401923-5 1983 Therapy with the second-generation sulfonylurea compound glyburide enhances overall insulin responsiveness without altering insulin binding. Glyburide 57-66 insulin Homo sapiens 84-91 6409019-0 1983 Gliclazide- and glibenclamide-mediated transport of Pr3+ across an artificial lipid membrane. Glyburide 16-29 proteinase 3 Homo sapiens 52-55 6401923-6 1983 Prevailing insulin levels are increased markedly during glyburide therapy but do not correlate with the clinical response, which suggests that the improvement in target tissue insulin action is the critical determinant in terms of the clinical response to the drug. Glyburide 56-65 insulin Homo sapiens 11-18 6401923-6 1983 Prevailing insulin levels are increased markedly during glyburide therapy but do not correlate with the clinical response, which suggests that the improvement in target tissue insulin action is the critical determinant in terms of the clinical response to the drug. Glyburide 56-65 insulin Homo sapiens 176-183 6401923-7 1983 In vitro studies utilizing cultured human fibroblasts indicate that glyburide increases the number of cell-surface insulin receptors and opposes insulin-mediated down-regulation. Glyburide 68-77 insulin Homo sapiens 115-122 6401923-7 1983 In vitro studies utilizing cultured human fibroblasts indicate that glyburide increases the number of cell-surface insulin receptors and opposes insulin-mediated down-regulation. Glyburide 68-77 insulin Homo sapiens 145-152 6818080-4 1982 There was a significant increase in serum apolipoprotein A-I in obese females treated with calorie restriction and metformin and in non-obese females treated with carbohydrate restriction and glibenclamide. Glyburide 192-205 apolipoprotein A1 Homo sapiens 42-60 6858544-5 1983 In particular, a significant reduction of alpha 2M was observed in patients on glibenclamide therapy. Glyburide 79-92 alpha-2-macroglobulin Homo sapiens 42-50