PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8883586-6 1996 In other studies we determined the effect of increasing concentrations of ZDV on production of granulocyte colony-stimulating factor (G-CSF) protein [enzyme-linked immunosorbent assay (ELISA)] and mRNA by fetal and maternal monocytes, and on production of erythropoietin protein (ELISA) and mRNA by Hep3B cells. Zidovudine 74-77 colony stimulating factor 3 Homo sapiens 95-132 8883586-6 1996 In other studies we determined the effect of increasing concentrations of ZDV on production of granulocyte colony-stimulating factor (G-CSF) protein [enzyme-linked immunosorbent assay (ELISA)] and mRNA by fetal and maternal monocytes, and on production of erythropoietin protein (ELISA) and mRNA by Hep3B cells. Zidovudine 74-77 colony stimulating factor 3 Homo sapiens 134-139 8680517-7 1996 Exciting new management strategies appear to be the use of granulocyte colony-stimulating factor to enhance neutrophilia and zidovudine to reduce vertical transmission of HIV infection. Zidovudine 125-135 colony stimulating factor 3 Homo sapiens 59-96 7511543-5 1993 These results suggest that combined therapy with granulocyte colony-stimulating factor and erythropoietin may improve leukopenia and anaemia, which is not zidovudine-related, in children who have AIDS. Zidovudine 155-165 colony stimulating factor 3 Homo sapiens 49-86 1281810-9 1992 G-CSF plays an important role in the treatment of patients with HIV-associated Kaposi sarcoma and enables combined treatment with zidovudine, interferon, and cytostatic drugs. Zidovudine 130-140 colony stimulating factor 3 Homo sapiens 0-5 1279153-2 1992 We evaluated the effect of subcutaneously administered granulocyte colony-stimulating factor (G-CSF) in pediatric patients whose absolute neutrophil count was less than 0.8 x 10(9)/L during AZT therapy despite dosage reductions to 120 mg/m2 every 6 hours. Zidovudine 190-193 colony stimulating factor 3 Homo sapiens 94-99 1279153-9 1992 With doses of G-CSF ranging from 1 to 20 micrograms/kg per day, 17 of 19 patients were able to tolerate AZT at a dose of 120 to 180 mg/m2 every 6 hours. Zidovudine 104-107 colony stimulating factor 3 Homo sapiens 14-19 1279153-10 1992 We conclude that G-CSF therapy enables patients who have had AZT-related neutropenia to receive therapeutic doses of AZT. Zidovudine 61-64 colony stimulating factor 3 Homo sapiens 17-22 1279153-10 1992 We conclude that G-CSF therapy enables patients who have had AZT-related neutropenia to receive therapeutic doses of AZT. Zidovudine 117-120 colony stimulating factor 3 Homo sapiens 17-22 2018046-3 1991 A combination of granulocyte colony-stimulating factor and erythropoietin has also been demonstrated to alleviate both neutropenia and anemia in patients with advanced AIDS or AIDS-related complex receiving zidovudine. Zidovudine 207-217 colony stimulating factor 3 Homo sapiens 17-54 1380256-9 1992 When erythropoietin was added to the regimen, combined G-CSF and EPO corrected both anemia and leukopenia and lessened subsequent zidovudine toxicity. Zidovudine 130-140 colony stimulating factor 3 Homo sapiens 55-60 1385275-0 1992 Efficacy of granulocyte colony-stimulating factor (G-CSF) on neutropenia in zidovudine-treated patients with AIDS and ARC: a preliminary report. Zidovudine 76-86 colony stimulating factor 3 Homo sapiens 12-49 1385275-0 1992 Efficacy of granulocyte colony-stimulating factor (G-CSF) on neutropenia in zidovudine-treated patients with AIDS and ARC: a preliminary report. Zidovudine 76-86 colony stimulating factor 3 Homo sapiens 51-56 1720567-5 1991 The combination of G-CSF and recombinant human erythropoietin completely reversed the zidovudine-induced neutropenia of AIDS patients but was only partially effective in reversing anemia. Zidovudine 86-96 colony stimulating factor 3 Homo sapiens 19-24 1714756-0 1991 Effects of recombinant human granulocyte colony-stimulating factor on leucopenia in zidovudine-treated patients with AIDS and AIDS related complex, a phase I/II study. Zidovudine 84-94 colony stimulating factor 3 Homo sapiens 29-66 1714756-13 1991 We conclude that G-CSF increases the number of circulating neutrophilic granulocytes in zidovudine-treated patients at relatively low doses and with few side-effects. Zidovudine 88-98 colony stimulating factor 3 Homo sapiens 17-22 1709368-0 1991 Combined therapy with recombinant granulocyte colony-stimulating factor and erythropoietin decreases hematologic toxicity from zidovudine. Zidovudine 127-137 colony stimulating factor 3 Homo sapiens 34-71 2022593-2 1991 Both G-CSF and GM-CSF have demonstrated the ability to correct leukopenia related to HIV infection and ameliorate the drug-related myelosuppressive effects of zidovudine, trimethoprim/sulfamethoxazole, ganciclovir, and, in the case of GM-CSF, alpha-interferon, and cancer chemotherapies. Zidovudine 159-169 colony stimulating factor 3 Homo sapiens 5-10 1713806-11 1991 Combined G-CSF and EPO treatment corrected both anemia and leukopenia and reduced zidovudine toxicity. Zidovudine 82-92 colony stimulating factor 3 Homo sapiens 9-14 9571329-10 1998 CONCLUSIONS: Gliclazide administration to NIDDM patients inhibits the increased adhesiveness of diabetic monocytes to endothelial cells and reduces the production of TNF-alpha by these cells. Gliclazide 13-23 tumor necrosis factor Homo sapiens 166-175 9517374-9 1998 RESULTS: In gliclazide-treated NIDDM patients, PDH activity in circulating lymphocytes recovered. Gliclazide 12-22 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 47-50 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 91-94 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 insulin Homo sapiens 182-189 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 203-206 9498623-9 1998 These data indicate that gliclazide, aside from either a direct antioxidant action or an effect on insulin or glucose levels, may ameliorate diabetic endothelial cell dysfunction. Gliclazide 25-35 insulin Oryctolagus cuniculus 99-106 9439551-0 1997 The stimulation of insulin secretion in non-insulin-dependent diabetic patients by amino acids and gliclazide in the basal and hyperglycemic state. Gliclazide 99-109 insulin Homo sapiens 19-26 9439552-0 1997 Gliclazide treatment of streptozotocin diabetic rats restores GLUT4 protein content and basal glucose uptake in skeletal muscle. Gliclazide 0-10 solute carrier family 2 member 4 Rattus norvegicus 62-67 9439552-12 1997 In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content. Gliclazide 15-25 insulin receptor Rattus norvegicus 155-171 9439552-12 1997 In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content. Gliclazide 15-25 solute carrier family 2 member 4 Rattus norvegicus 222-227 9322798-6 1997 In addition, exposure of BAE cells to gliclazide (0 to 10 micrograms/mL) and native LDL (100 micrograms/mL) induced a dose-dependent diminution of the oxidized LDL-induced monocyte adhesion to BAE cells as measured by the myeloperoxidase (MPO) assay. Gliclazide 38-48 myeloperoxidase Bos taurus 222-237 9322798-6 1997 In addition, exposure of BAE cells to gliclazide (0 to 10 micrograms/mL) and native LDL (100 micrograms/mL) induced a dose-dependent diminution of the oxidized LDL-induced monocyte adhesion to BAE cells as measured by the myeloperoxidase (MPO) assay. Gliclazide 38-48 myeloperoxidase Bos taurus 239-242 8843172-0 1996 Gliclazide potentiates suppression of hepatic glucose production in non-insulin-dependent diabetic patients. Gliclazide 0-10 insulin Homo sapiens 72-79 8843172-9 1996 The increase in plasma insulin and C-peptide concentrations was similar with gliclazide and placebo, although the plasma insulin to glucose ratio was increased with gliclazide. Gliclazide 165-175 insulin Homo sapiens 121-128 8867904-2 1996 Having already shown positive effects of sulfonylreas in long-standing IDDM patients, we decided to try the association of gliclazide with insulin in newly diagnosed IDDM patients. Gliclazide 123-133 insulin Homo sapiens 139-146 9711995-2 1998 This study was designed to elucidate the effect of gliclazide, an oral hypoglycemic sulfonylurea, on diabetic neuropathy, because it has been indicated to be a free radical scavenger and TNF-alpha inhibitor. Gliclazide 51-61 tumor necrosis factor Rattus norvegicus 187-196 8920942-4 1996 Gastrocnemius muscles perfused with gliclazide had a significant increase (2.4-fold) in the GLUT4 content in plasma membranes compared to basal conditions (p < 0.05). Gliclazide 36-46 solute carrier family 2 member 4 Rattus norvegicus 92-97 8920942-6 1996 The effect of insulin on the glucose uptake and on the GLUT 4 translocation was significantly enhanced by gliclazide (3.4-fold and 3.7-fold vs basal, respectively). Gliclazide 106-116 solute carrier family 2 member 4 Rattus norvegicus 55-61 7829624-9 1995 In summary, the improvement in glycemic control and glucose disposal in NIDDM subjects receiving gliclazide therapy cannot be explained by increased expression of GLUT4 in muscle. Gliclazide 97-107 solute carrier family 2 (facilitated glucose transporter), member 4 Mus musculus 163-168 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. Gliclazide 66-76 solute carrier family 2 member 1 Homo sapiens 220-225 7988345-7 1994 The amount of administered somatostatin required for inhibiting glucagon secretion was higher than the maximal level obtained from endogenous secretion of somatostatin after gliclazide. Gliclazide 174-184 somatostatin Rattus norvegicus 27-39 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%). Gliclazide 208-218 hemoglobin subunit alpha 1 Homo sapiens 182-186 7833497-1 1994 In circulating lymphocytes from patients with non-insulin-dependent diabetes mellitus (NIDDM) subnormal pyruvate dehydrogenase (PDH) activity returns to normal following patient treatment with sulfonylurea (gliclazide, 80 mg twice daily/5 weeks). Gliclazide 207-217 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 128-131 7833497-3 1994 Therefore, the low PDH activity in cells of NIDDM patients might be caused by defective insulin control on the enzyme and its recovery in gliclazide-treated patients by drug-mediated removal of the defect. Gliclazide 138-148 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 19-22 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 35-38 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 212-215 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 insulin Homo sapiens 404-411 8000110-1 1994 We evaluated insulin resistance and assessed the effect of gliclazide on insulin resistance in a patient with diabetes mellitus associated with Turner"s syndrome. Gliclazide 59-69 insulin Homo sapiens 73-80 8000110-3 1994 The insulin dose-response curve of this patient shifted to the right and down, and recovered somewhat after the administration of gliclazide. Gliclazide 130-140 insulin Homo sapiens 4-11 8000110-5 1994 Gliclazide reduced her insulin resistance, which suggests that this agent is suitable for treating the insulin resistance in diabetic patients with Turner"s syndrome. Gliclazide 0-10 insulin Homo sapiens 23-30 8000110-5 1994 Gliclazide reduced her insulin resistance, which suggests that this agent is suitable for treating the insulin resistance in diabetic patients with Turner"s syndrome. Gliclazide 0-10 insulin Homo sapiens 103-110 7988345-7 1994 The amount of administered somatostatin required for inhibiting glucagon secretion was higher than the maximal level obtained from endogenous secretion of somatostatin after gliclazide. Gliclazide 174-184 somatostatin Rattus norvegicus 155-167 8207672-3 1994 Gliclazide crystallizes in the monoclinic space group P2(1)/n, with the unit cell dimensions a = 10.828(2) A, b = 14.342(19) A, c = 11.005(6) A, and with beta = 106.97(2) degrees, V = 1635(12) A3, and Z = 4. Gliclazide 0-10 cyclin dependent kinase inhibitor 1A Homo sapiens 54-59 1788832-5 1991 Studies with Gliclazide, Metformin, Glibenclamide and insulin have shown that while all other drugs tested have no effect, Gliclazide increases fibrin fibre thickness (microT) significantly, diminishes tensile strength and reduces permeability. Gliclazide 123-133 insulin Homo sapiens 54-61 7691511-5 1993 Gradually accumulating evidence suggests that gliclazide may be useful in patients with diabetic retinopathy, due to its haemobiological actions, and that addition of gliclazide to insulin therapy enables insulin dosage to be reduced. Gliclazide 167-177 insulin Homo sapiens 205-212 8415212-3 1993 The association of gliclazide with insulin resulted in better metabolic control expressed by significant decrease of basal and postprandial glycaemia and small (non-significant) decrease of serum triglycerides level--with simultaneous reduction of daily insulin requirement by 34% on the average. Gliclazide 19-29 insulin Homo sapiens 35-42 8415212-3 1993 The association of gliclazide with insulin resulted in better metabolic control expressed by significant decrease of basal and postprandial glycaemia and small (non-significant) decrease of serum triglycerides level--with simultaneous reduction of daily insulin requirement by 34% on the average. Gliclazide 19-29 insulin Homo sapiens 254-261 8415212-5 1993 The improvement of the metabolic state and the increased C-peptide secretion persisted also after gliclazide withdrawal (during the second period of exclusive insulin therapy), although the determined parameters were less favourable than when combined treatment was applied. Gliclazide 98-108 insulin Homo sapiens 159-166 8375268-0 1993 Effect of a sulfonylurea (gliclazide) treatment on insulin sensitivity and glucose-mediated glucose disposal in patients with non-insulin-dependent diabetes mellitus (NIDDM). Gliclazide 26-36 insulin Homo sapiens 51-58 8375268-5 1993 After gliclazide, despite significantly lower (almost normal) plasma glucose, normalization of glycosylated hemoglobin and increased fasting insulin levels, there was a slight but significant increase in SI while SG showed a further reduction, the improvement in glucose control being also associated to the significant increased first and 2nd phase insulin release for the first 20 min after glucose infusion. Gliclazide 6-16 insulin Homo sapiens 141-148 8375268-5 1993 After gliclazide, despite significantly lower (almost normal) plasma glucose, normalization of glycosylated hemoglobin and increased fasting insulin levels, there was a slight but significant increase in SI while SG showed a further reduction, the improvement in glucose control being also associated to the significant increased first and 2nd phase insulin release for the first 20 min after glucose infusion. Gliclazide 6-16 insulin Homo sapiens 350-357 1409040-9 1992 The change of Tolbutamide or Chlorpropamide to Gliclazide increased the therapeutical efficacy only in these patients, in whom such a change was associated with an increase of prandial, reactive serum insulin level (IRI). Gliclazide 47-57 insulin Homo sapiens 201-208 1576681-2 1992 Effects of glycation on gliclazide (oral hypoglycemic drug)-binding with serum albumin in diabetics. Gliclazide 24-34 albumin Homo sapiens 79-86 1576681-4 1992 The binding capacity of the primary binding site for gliclazide in the albumin molecule was increased from 4.5 x 10(-4) to 8.0 x 10(-4) M-1 by glycation of albumin, but not that of the secondary binding site (1.2 x 10(-4) M-1). Gliclazide 53-63 albumin Homo sapiens 71-78 1576681-4 1992 The binding capacity of the primary binding site for gliclazide in the albumin molecule was increased from 4.5 x 10(-4) to 8.0 x 10(-4) M-1 by glycation of albumin, but not that of the secondary binding site (1.2 x 10(-4) M-1). Gliclazide 53-63 albumin Homo sapiens 156-163 1576681-5 1992 This suggests that the glycation of albumin increases its total binding capacity for gliclazide, resulting in a low free gliclazide level. Gliclazide 85-95 albumin Homo sapiens 36-43 1576681-5 1992 This suggests that the glycation of albumin increases its total binding capacity for gliclazide, resulting in a low free gliclazide level. Gliclazide 121-131 albumin Homo sapiens 36-43 1425152-4 1992 An improvement was observed in the beta-cell function of the patients on gliclazide treatment: reduction of fasting plasma glucose associated with a progressive increase in C-peptide level but insulin levels decreased at 12 months, suggesting an increase in hepatic insulin extraction at this time. Gliclazide 73-83 insulin Homo sapiens 173-182 1425152-4 1992 An improvement was observed in the beta-cell function of the patients on gliclazide treatment: reduction of fasting plasma glucose associated with a progressive increase in C-peptide level but insulin levels decreased at 12 months, suggesting an increase in hepatic insulin extraction at this time. Gliclazide 73-83 insulin Homo sapiens 193-200 1425152-7 1992 While the prehepatic insulin secretion rate increased progressively on gliclazide during all glucose challenges, the fractional hepatic insulin extraction fell after 3 and increased at 12 month treatment, with opposite changes in insulin delivered to peripheral tissues. Gliclazide 71-81 insulin Homo sapiens 21-28 1425152-8 1992 Thus the insulinogenic effect of gliclazide could be masked during long-term administration by a concomitant effect of gliclazide which increases hepatic extraction of insulin. Gliclazide 33-43 insulin Homo sapiens 9-16 1860552-0 1991 Release of amylin from perfused rat pancreas in response to glucose, arginine, beta-hydroxybutyrate, and gliclazide. Gliclazide 105-115 islet amyloid polypeptide Rattus norvegicus 11-17 1860552-2 1991 The isolated perfused normal rat pancreas was used to evaluate the effects of glucose and insulin secretagogues, such as arginine, beta-hydroxybutyrate, and gliclazide, on amylin secretion. Gliclazide 157-167 islet amyloid polypeptide Rattus norvegicus 172-178 1649715-5 1991 We assessed the effect of gliclazide on glucose-stimulated insulin secretion in eight healthy volunteers. Gliclazide 26-36 insulin Homo sapiens 59-66 1649715-12 1991 We conclude that gliclazide indeed leads to a shift to the left of the dose-response curve of first-phase insulin release in vivo without a change in Vmax, which indicates an apparent enhancement of B-cell glucose sensitivity. Gliclazide 17-27 insulin Homo sapiens 106-113 1831320-10 1991 After gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (a) in vitro glucose-induced insulin secretion was increased three- to fivefold; (b) the response to arginine, which is increased in diabetic rats, was amplified by two- to threefold; (c) insulin release in response to gliclazide was unchanged. Gliclazide 6-16 insulin Homo sapiens 122-129 1831320-10 1991 After gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (a) in vitro glucose-induced insulin secretion was increased three- to fivefold; (b) the response to arginine, which is increased in diabetic rats, was amplified by two- to threefold; (c) insulin release in response to gliclazide was unchanged. Gliclazide 44-54 insulin Homo sapiens 122-129 1872302-5 1991 Gliclazide is a second-generation sulfonylurea drug whose efficacy in the treatment of NIDDM, alone or in combination with insulin, has been widely demonstrated. Gliclazide 0-10 insulin Homo sapiens 123-130 1872303-0 1991 Effect of 6-month gliclazide treatment on insulin release and sensitivity to endogenous insulin in NIDDM: role of initial continuous subcutaneous insulin infusion-induced normoglycemia. Gliclazide 18-28 insulin Homo sapiens 42-49 1872303-0 1991 Effect of 6-month gliclazide treatment on insulin release and sensitivity to endogenous insulin in NIDDM: role of initial continuous subcutaneous insulin infusion-induced normoglycemia. Gliclazide 18-28 insulin Homo sapiens 88-95 1872303-0 1991 Effect of 6-month gliclazide treatment on insulin release and sensitivity to endogenous insulin in NIDDM: role of initial continuous subcutaneous insulin infusion-induced normoglycemia. Gliclazide 18-28 insulin Homo sapiens 88-95 1908182-9 1991 However, under physiologic hyperinsulinemic conditions gliclazide therapy was associated with an increased sensitivity of glycogen synthase for its allosteric activation by glucose-6-phosphatase (p less than 0.04). Gliclazide 55-65 glucose-6-phosphatase catalytic subunit 1 Homo sapiens 173-194 1936478-0 1991 Comparative three-month study of the efficacies of metformin and gliclazide in the treatment of NIDD. Gliclazide 65-75 zinc finger DHHC-type palmitoyltransferase 23 Homo sapiens 96-100 1936478-5 1991 The fasting serum insulin level decreased significantly in the group receiving metformin (26.2 +/- 3.2 mlU/L at entry versus 19.8 +/- 2.3 mlU/L after three months: less than 0.01), and increased in a non-significant way in the group receiving gliclazide (21.6 +/- 3 mlU/L versus 26.5 +/- 5 mlU/L after three months: NS). Gliclazide 243-253 insulin Homo sapiens 18-25 1936478-10 1991 On the other hand, fasting serum insulin levels decreased significantly in patients receiving metformin compared to gliclazide. Gliclazide 116-126 insulin Homo sapiens 33-40 1828740-5 1991 This was accompanied by an increase in fasting serum insulin concentrations in the gliclazide treated patients (7.0 +/- 1.3 to 10.1 +/- 1.1 mU l-1, p less than 0.005), but no change in the diet treated patients. Gliclazide 83-93 insulin Homo sapiens 53-60 1794261-9 1991 After three months of treatment with Diamicron, all 10 dietary failure patients improved, as did three of the 10 secondary failure cases and five of the insulin-treated patients. Gliclazide 37-46 insulin Homo sapiens 153-160 1794262-4 1991 Gliclazide stimulates insulin secretion through the beta cell sulphonylurea receptor, and possibly through a direct effect on intracellular calcium transport. Gliclazide 0-10 insulin Homo sapiens 22-29 1794265-0 1991 The effect of Diamicron on the secretion and action of insulin. Gliclazide 14-23 insulin Homo sapiens 55-62 1794265-5 1991 Following the administration of Diamicron, the insulin response to the same glucose load increased two-fold and five-fold for the first and second phases, respectively, and the insulin sensitivity also increased by a factor of 2. Gliclazide 32-41 insulin Homo sapiens 47-54 1794265-5 1991 Following the administration of Diamicron, the insulin response to the same glucose load increased two-fold and five-fold for the first and second phases, respectively, and the insulin sensitivity also increased by a factor of 2. Gliclazide 32-41 insulin Homo sapiens 177-184 1794266-0 1991 The physiological action of gliclazide: beta-cell function and insulin resistance. Gliclazide 28-38 insulin Homo sapiens 63-70 1794267-4 1991 Treatment with gliclazide of patients with NIDDM has been shown to be associated with a potentiation of both insulin-mediated glucose disposal and insulin-stimulated glycogen synthase activity in skeletal muscle. Gliclazide 15-25 insulin Homo sapiens 109-116 1794267-4 1991 Treatment with gliclazide of patients with NIDDM has been shown to be associated with a potentiation of both insulin-mediated glucose disposal and insulin-stimulated glycogen synthase activity in skeletal muscle. Gliclazide 15-25 insulin Homo sapiens 147-154 1794267-6 1991 Whether the improved insulin sensitivity and improved insulin action on skeletal muscle glycogen synthase during gliclazide treatment is due to a direct or an indirect action of the drug is discussed. Gliclazide 113-123 insulin Homo sapiens 54-61 1794267-6 1991 Whether the improved insulin sensitivity and improved insulin action on skeletal muscle glycogen synthase during gliclazide treatment is due to a direct or an indirect action of the drug is discussed. Gliclazide 113-123 glycogen synthase 1 Homo sapiens 72-105 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. Gliclazide 83-93 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. Gliclazide 83-93 hemoglobin subunit alpha 1 Homo sapiens 113-117 1794269-0 1991 Effect of 6 months" gliclazide treatment on insulin release and sensitivity to endogenous insulin in NIDDM: role of initial CSII-induced normoglycemia. Gliclazide 20-30 insulin Homo sapiens 44-51 1794269-0 1991 Effect of 6 months" gliclazide treatment on insulin release and sensitivity to endogenous insulin in NIDDM: role of initial CSII-induced normoglycemia. Gliclazide 20-30 insulin Homo sapiens 90-97 34249701-13 2021 Finally, gliclazide was shown to induce cell cycle arrest and apoptosis in LUAD cells possibly by targeting CCNB1, CCNB2, CDK1 and AURKA. Gliclazide 9-19 aurora kinase A Homo sapiens 131-136 1867120-1 1991 The aim of the study was to assess, in patients with non insulin dependent diabetes mellitus (NIDDM), either with previous failure to sulphonylureas or insulin treated since the disease started, if the combination of gliclazide to insulin therapy might induce a reduction of daily insulin requirement. Gliclazide 217-227 insulin Homo sapiens 152-159 1867120-1 1991 The aim of the study was to assess, in patients with non insulin dependent diabetes mellitus (NIDDM), either with previous failure to sulphonylureas or insulin treated since the disease started, if the combination of gliclazide to insulin therapy might induce a reduction of daily insulin requirement. Gliclazide 217-227 insulin Homo sapiens 152-159 2177368-0 1990 The action of gliclazide on insulin secretion and insulin sensitivity in non-obese non-insulin dependent diabetic patients. Gliclazide 14-24 insulin Homo sapiens 28-35 2177368-1 1990 We evaluated the effects of gliclazide on the secretion and action of insulin in 18 non-obese (BMI 24.09 +/- 0.47 Kg/m2, range 20.89-27.52 Kg/m2) non-insulin dependent diabetic patients (mean age 56.9 +/- 1.8 years, range 39-67 years) by the oral glucose tolerance test (OGTT) and insulin suppression test (IST). Gliclazide 28-38 insulin Homo sapiens 70-77 2177368-4 1990 After gliclazide therapy, fasting and 2 hour post-OGTT plasma glucose significantly decreased (136 vs. 185 mg/dl, P less than 0.005 291 vs. 358 mg/dl, P less than 0.005), 2 hours post-OGTT plasma insulin was significantly increased (79 vs. 59 uU/ml, P less than 0.05) while fasting plasma insulin remained unchanged (21 vs. 19 uU/ml, P greater than 0.1). Gliclazide 6-16 insulin Homo sapiens 196-203 2177368-4 1990 After gliclazide therapy, fasting and 2 hour post-OGTT plasma glucose significantly decreased (136 vs. 185 mg/dl, P less than 0.005 291 vs. 358 mg/dl, P less than 0.005), 2 hours post-OGTT plasma insulin was significantly increased (79 vs. 59 uU/ml, P less than 0.05) while fasting plasma insulin remained unchanged (21 vs. 19 uU/ml, P greater than 0.1). Gliclazide 6-16 insulin Homo sapiens 289-296 2177368-7 1990 The mean incremental areas under the plasma insulin curve during OGTT also increased (4482.0 +/- 637.1 vs. 3167.5 +/- 511.9 uU.min/ml, P less than 0.05) after gliclazide therapy. Gliclazide 159-169 insulin Homo sapiens 44-51 34249701-13 2021 Finally, gliclazide was shown to induce cell cycle arrest and apoptosis in LUAD cells possibly by targeting CCNB1, CCNB2, CDK1 and AURKA. Gliclazide 9-19 cyclin B1 Homo sapiens 108-113 34249701-13 2021 Finally, gliclazide was shown to induce cell cycle arrest and apoptosis in LUAD cells possibly by targeting CCNB1, CCNB2, CDK1 and AURKA. Gliclazide 9-19 cyclin B2 Homo sapiens 115-120 34249701-13 2021 Finally, gliclazide was shown to induce cell cycle arrest and apoptosis in LUAD cells possibly by targeting CCNB1, CCNB2, CDK1 and AURKA. Gliclazide 9-19 cyclin dependent kinase 1 Homo sapiens 122-126 34202801-0 2021 How Does Glycation Affect Binding Parameters of the Albumin-Gliclazide System in the Presence of Drugs Commonly Used in Diabetes? Gliclazide 60-70 albumin Homo sapiens 52-59 34202801-5 2021 The interaction between albumin and gliclazide, with the presence of another drug, was confirmed by calculation of association constants (0.11-1.07 x 104 M-1). Gliclazide 36-46 albumin Homo sapiens 24-31 34063566-0 2021 Interaction between Omeprazole and Gliclazide in Relation to CYP2C19 Phenotype. Gliclazide 35-45 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 61-68 34063566-1 2021 The antidiabetic drug gliclazide is partly metabolized by CYP2C19, the main enzyme involved in omeprazole metabolism. Gliclazide 22-32 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 58-65 34063566-2 2021 The aim of the study was to explore the interaction between omeprazole and gliclazide in relation to CYP2C19 phenotype using physiologically based pharmacokinetic (PBPK) modeling approach. Gliclazide 75-85 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 101-108 34063566-5 2021 The PBPK simulations predicted 1.4-1.6-fold higher gliclazide area under the curve (AUC) after 5-day treatment with 20 mg omeprazole in all CYP2C19 phenotype groups except in poor metabolizers. Gliclazide 51-61 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 140-147 34222087-7 2021 Results: Gliclazide consumption was positively correlated with MMP-9 and Cas-3, but not AGEs levels. Gliclazide 9-19 matrix metallopeptidase 9 Homo sapiens 63-68 34222087-7 2021 Results: Gliclazide consumption was positively correlated with MMP-9 and Cas-3, but not AGEs levels. Gliclazide 9-19 caspase 3 Homo sapiens 73-78 1908183-1 1991 This study examined the effect of gliclazide on tissue-type plasminogen activator (t-PA)-related fibrinolysis in 23 Type I diabetic patients without residual beta-cell function and 17 Type II diabetic patients initially treated with tolbutamide. Gliclazide 34-44 plasminogen activator, tissue type Homo sapiens 48-81 1908183-1 1991 This study examined the effect of gliclazide on tissue-type plasminogen activator (t-PA)-related fibrinolysis in 23 Type I diabetic patients without residual beta-cell function and 17 Type II diabetic patients initially treated with tolbutamide. Gliclazide 34-44 plasminogen activator, tissue type Homo sapiens 83-87 1908183-3 1991 In Type I diabetic patients, after 2-3 months of treatment with gliclazide, we observed a significant increase in plasma concentrations of total t-PA antigen that remained stable until discontinuation of the drug (p less than 0.0002), whereas the plasma concentrations of plasminogen activator inhibitor (PAI) did not change significantly during the study. Gliclazide 64-74 plasminogen activator, tissue type Homo sapiens 145-149 1908183-4 1991 Next, we investigated the possibility of gliclazide inducing t-PA-related fibrinolysis in a subset of Type II diabetics without detectable concentrations of t-PA during treatment with tolbutamide. Gliclazide 41-51 plasminogen activator, tissue type Homo sapiens 61-65 1908183-5 1991 The concentrations of active t-PA increased significantly 3 months after a change in treatment to gliclazide, and active t-PA again decreased in one patient to undetectable levels after 12 months with gliclazide. Gliclazide 201-211 plasminogen activator, tissue type Homo sapiens 121-125 1908183-8 1991 We conclude that gliclazide has the potential to exert extrametabolic non-insulin-mediated effects on t-PA-related fibrinolysis in diabetic patients. Gliclazide 17-27 insulin Homo sapiens 74-81 1908183-8 1991 We conclude that gliclazide has the potential to exert extrametabolic non-insulin-mediated effects on t-PA-related fibrinolysis in diabetic patients. Gliclazide 17-27 plasminogen activator, tissue type Homo sapiens 102-106 2199202-0 1990 The effects of ingestion time of gliclazide in relationship to meals on plasma glucose, insulin and C-peptide levels. Gliclazide 33-43 insulin Homo sapiens 88-95 2199202-0 1990 The effects of ingestion time of gliclazide in relationship to meals on plasma glucose, insulin and C-peptide levels. Gliclazide 33-43 insulin Homo sapiens 100-109 21181508-1 2011 The aim of this study was to develop a drug-specific absorption model for gliclazide (GLK) using mechanistic gastrointestinal simulation technology (GIST) implemented in GastroPlus(TM) software package. Gliclazide 74-84 mitogen-activated protein kinase kinase kinase kinase 3 Homo sapiens 86-89 34873451-6 2021 A combined fluorescence potassium ion assay with three channel modulators (4-aminopyridine, emodin-Orf3a channel blocker, and gliclazide-E channel blocker) was developed to detect SARS-CoV-2 Orf3a/E channel activity. Gliclazide 126-136 ORF3a protein Severe acute respiratory syndrome coronavirus 2 191-198 34873451-8 2021 Results: In lentivirus-spiked samples, we detected significant channel activity of Orf3a/E based on increase in fluorescence induced by 4-aminopyridine, and this increase in fluorescence was inhibited by emodin and gliclazide. Gliclazide 215-225 ORF3a protein Severe acute respiratory syndrome coronavirus 2 83-88 2669710-9 1989 It is concluded that both acute and prolonged gliclazide therapy directly or indirectly 1) enhances both meal stimulated and post absorptive insulin secretion and 2) increases insulin sensitivity. Gliclazide 46-56 insulin Homo sapiens 141-148 35401218-0 2022 Combination Therapy of Alpha-Lipoic Acid, Gliclazide and Ramipril Protects Against Development of Diabetic Cardiomyopathy via Inhibition of TGF-beta/Smad Pathway. Gliclazide 42-52 transforming growth factor alpha Homo sapiens 140-148 35401218-13 2022 Conclusion: Triple combination therapy of ALA, gliclazide and ramipril prevented DCM development by inhibiting TGF-beta1/Smad pathway. Gliclazide 47-57 transforming growth factor beta 1 Homo sapiens 111-120 2559864-4 1989 During euglycemic insulin clamps, insulin-inhibited endogenous glucose production was improved after gliclazide therapy. Gliclazide 101-111 insulin Homo sapiens 18-25 2559864-4 1989 During euglycemic insulin clamps, insulin-inhibited endogenous glucose production was improved after gliclazide therapy. Gliclazide 101-111 insulin Homo sapiens 34-41 2498455-0 1989 Rise of plasma t-PA fibrinolytic activity in a group of maturity onset diabetic patients shifted from a first generation (tolbutamide) to a second generation sulphonylurea (gliclazide). Gliclazide 173-183 plasminogen activator, tissue type Homo sapiens 15-19 2498455-2 1989 All 10 patients responded on the change in treatment to gliclazide with an increase in activity of t-PA. Gliclazide 56-66 plasminogen activator, tissue type Homo sapiens 99-103 2498455-4 1989 The concentration in plasma of t-PA antigen under basal conditions and after stimulation (venous occlusion) increased significantly during the period of treatment with gliclazide. Gliclazide 168-178 plasminogen activator, tissue type Homo sapiens 31-35 2498455-6 1989 In contrast to these findings seven patients with marked activities of t-PA during treatment with tolbutamide retained unchanged levels of the variables reported above after a change in treatment to gliclazide. Gliclazide 199-209 plasminogen activator, tissue type Homo sapiens 71-75 3072813-4 1988 Diet and gliclazide treated patients showed a reduced B-cell response during the first hour after the meal as indicated by insulin and C-peptide values and areas (insulin areas 0-60 min: controls 57.9 +/- 10.9; p less than 0.01 vs diet alone 14.2 +/- 2.7 and vs gliclazide 22.1 +/- 2.8 microU/ml/min). Gliclazide 9-19 insulin Homo sapiens 123-130 3072813-4 1988 Diet and gliclazide treated patients showed a reduced B-cell response during the first hour after the meal as indicated by insulin and C-peptide values and areas (insulin areas 0-60 min: controls 57.9 +/- 10.9; p less than 0.01 vs diet alone 14.2 +/- 2.7 and vs gliclazide 22.1 +/- 2.8 microU/ml/min). Gliclazide 9-19 insulin Homo sapiens 135-144 3072813-4 1988 Diet and gliclazide treated patients showed a reduced B-cell response during the first hour after the meal as indicated by insulin and C-peptide values and areas (insulin areas 0-60 min: controls 57.9 +/- 10.9; p less than 0.01 vs diet alone 14.2 +/- 2.7 and vs gliclazide 22.1 +/- 2.8 microU/ml/min). Gliclazide 9-19 insulin Homo sapiens 163-170 3072813-6 1988 The first significant C-peptide increase, detected at 10 min in controls and at 30 min under diet alone, was advanced to 15 min after gliclazide treatment. Gliclazide 134-144 insulin Homo sapiens 22-31 3277013-12 1988 Use of oral agents such as glipizide or gliclazide, which induce less diurnal hyperinsulinemia, may be advantageous when compared to traditional oral agent or insulin therapy. Gliclazide 40-50 insulin Homo sapiens 83-90 3050364-8 1988 It is concluded that gliclazide induces small, but significant, non-insulin-dependent extrametabolic effects on the extrinsic (t-PA) and intrinsic (prekallikrein) system of fibrinolysis. Gliclazide 21-31 insulin Homo sapiens 68-75 3050364-8 1988 It is concluded that gliclazide induces small, but significant, non-insulin-dependent extrametabolic effects on the extrinsic (t-PA) and intrinsic (prekallikrein) system of fibrinolysis. Gliclazide 21-31 plasminogen activator, tissue type Homo sapiens 127-131 3042343-0 1988 A comparison of cellular actions between gliclazide and a hypoglycaemic peptide fragment of human growth hormone (hGH 6-13). Gliclazide 41-51 growth hormone 1 Homo sapiens 98-112 3042343-3 1988 Gliclazide was markedly insulinotropic, as are all hypoglycaemic sulphonylureas, whereas hGH 6-13 had no visible effect on basal levels of plasma insulin. Gliclazide 0-10 insulin Homo sapiens 24-31 3935376-3 1985 In a total of 96 patients assessed after 1 year, gliclazide produced normal HbA1 levels in a significantly greater number of patients than chlorpropamide (p = 0.01) and gliquidone (p = 0.038), and glibenclamide was also significantly better than chlorpropamide (p = 0.02). Gliclazide 49-59 hemoglobin subunit alpha 1 Homo sapiens 76-80 3289948-7 1988 Mean plasma insulin concentration was significantly higher and mean serum lactate was significantly lower during treatment with gliclazide. Gliclazide 128-138 insulin Homo sapiens 12-19 3915271-0 1985 Gliclazide on long-term therapy increases insulin response to glucose of type II diabetics. Gliclazide 0-10 insulin Homo sapiens 42-49 6396398-9 1984 Although there were intersubject variations, the therapeutic effects of oral administration of gliclazide on serum glucose and insulin levels were found in four diabetic patients. Gliclazide 95-105 insulin Homo sapiens 127-134 3388872-0 1988 [Gliclazide in the non-insulin-dependent diabetic patient in geriatrics]. Gliclazide 1-11 insulin Homo sapiens 23-30 3595434-7 1987 These data suggest that gliclazide asserts its hypoglycaemic effects by promoting insulin release, and has no detectable effect on other enteropancreatic hormones. Gliclazide 24-34 insulin Homo sapiens 82-89 3552537-2 1987 A prospective double-blind controlled study was performed over 2 years, comparing gliclazide versus placebo in insulin-treated and gliclazide versus glibenclamide in non-insulin-treated diabetic subjects, after a 1-year run-in period. Gliclazide 82-92 insulin Homo sapiens 111-118 3552537-4 1987 Following treatment with gliclazide in 17/32 insulin-treated and 8/17 non-insulin-treated subjects with Albustix-negative proteinuria, there was no difference in retinopathy score, total proteinuria or the renal clearance of creatinine, albumin, transferrin and immunoglobulin G. In the insulin-treated group, progression of retinopathy was observed in approximately one-third of subjects, but no parameter of proteinuria progressed over 2 years. Gliclazide 25-35 insulin Homo sapiens 45-52 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). Gliclazide 93-103 hemoglobin subunit alpha 1 Homo sapiens 28-32 6369531-6 1984 Glucose oxidation significantly improved after gliclazide treatment (16.9 +/- 2.4 g/3 h vs 7.5 +/- 2.1 g/3 h, p less than 0.02) in parallel with the fall in plasma glucose and the increase in insulin response. Gliclazide 47-57 insulin Homo sapiens 192-199 6373160-0 1984 Effect of middle-term gliclazide treatment on insulin secretion in non-insulin dependent diabetics. Gliclazide 22-32 insulin Homo sapiens 46-53 6373160-3 1984 After 3 months of gliclazide therapy (240 mg/day) in addition to a low carbohydrate diet, the intravenous glucose tolerance test showed a significant reduction in blood sugar levels and in the partial and total areas under the blood sugar curve, as well as an improvement in early insulin secretion, characterized by a significant increase in plasma C-peptide at 4, 10 and 20 minutes. Gliclazide 18-28 insulin Homo sapiens 281-288 6373160-3 1984 After 3 months of gliclazide therapy (240 mg/day) in addition to a low carbohydrate diet, the intravenous glucose tolerance test showed a significant reduction in blood sugar levels and in the partial and total areas under the blood sugar curve, as well as an improvement in early insulin secretion, characterized by a significant increase in plasma C-peptide at 4, 10 and 20 minutes. Gliclazide 18-28 insulin Homo sapiens 350-359 6373160-7 1984 The scarcity of hypoglycaemic episodes during therapy with gliclazide may be related to the selective stimulation of early insulin secretion by this drug. Gliclazide 59-69 insulin Homo sapiens 123-130 6761187-0 1982 Long term improvement in insulin response with gliclazide treatment. Gliclazide 47-57 insulin Homo sapiens 25-32 6308816-3 1983 However, the mode of action of gliclazide, which induces an insulin release resembling physiologic conditions, explains why hypoglycemia is uncommon. Gliclazide 31-41 insulin Homo sapiens 60-67 6409019-0 1983 Gliclazide- and glibenclamide-mediated transport of Pr3+ across an artificial lipid membrane. Gliclazide 0-10 proteinase 3 Homo sapiens 52-55 6320319-3 1983 The capacity of gliclazide to stimulate 45Ca and insulin release persisted, to a limited extent, in islets exposed to 20 mM K+, but was abolished in islets exposed to 50 mM K+. Gliclazide 16-26 insulin Homo sapiens 49-56 6320319-4 1983 At the latter concentration, however, K+ was still able to augment 45Ca outflow and insulin secretion from islets first exposed to gliclazide. Gliclazide 131-141 insulin Homo sapiens 84-91 6761818-0 1982 [Medium term effect (3 months) of hypoglycemic sulfamide treatment (gliclazide) on insulin secretion of the non-insulin dependent diabetic]. Gliclazide 68-78 insulin Homo sapiens 83-90 6761818-0 1982 [Medium term effect (3 months) of hypoglycemic sulfamide treatment (gliclazide) on insulin secretion of the non-insulin dependent diabetic]. Gliclazide 68-78 insulin Homo sapiens 112-119 6987025-0 1980 Effect of prolonged glyclazide treatment on blood glucose and plasma insulin responses in obese patients with maturity-onset diabetes. Gliclazide 20-30 insulin Homo sapiens 69-76 7094168-1 1982 V. Effect of ethyl alcohol on gliclazide-binding with bovine serum albumin. Gliclazide 30-40 albumin Homo sapiens 61-74 6757009-0 1982 Modalities of gliclazide-induced Ca2+ influx into the pancreatic B-cell. Gliclazide 14-24 carbonic anhydrase 2 Rattus norvegicus 33-36 6757009-2 1982 The gliclazide-induced increase in 45Ca efflux is thought to reflect a stimulation of 40Ca influx into islet cells; it is suppressed in the absence of extracellular Ca2+ or in the presence of the organic CA2/-antagonist verapamil. Gliclazide 4-14 carbonic anhydrase 2 Rattus norvegicus 165-168 6757009-2 1982 The gliclazide-induced increase in 45Ca efflux is thought to reflect a stimulation of 40Ca influx into islet cells; it is suppressed in the absence of extracellular Ca2+ or in the presence of the organic CA2/-antagonist verapamil. Gliclazide 4-14 carbonic anhydrase 2 Rattus norvegicus 204-207 6987025-1 1980 The effects of prolonged treatment with glyclazide [methyl-4-fenyl sulfonyl-1(perhydrocyclopenta(c) pyrrolyl-2)-3 urea] on blood glucose and plasma insulin responses to meals was studied in 8 obese patients with maturity-onset diabetes. Gliclazide 40-50 insulin Homo sapiens 148-155 33652124-7 2021 Gliclazide did not affect 1.2B4 cell viability and Ca2+ concentration, however, it downregulated CASP-3 and upregulated TP53. Gliclazide 0-10 caspase 3 Homo sapiens 97-103 7273254-2 1981 Interaction of gliclazide with bovine serum albumin. Gliclazide 15-25 albumin Homo sapiens 38-51 33652124-7 2021 Gliclazide did not affect 1.2B4 cell viability and Ca2+ concentration, however, it downregulated CASP-3 and upregulated TP53. Gliclazide 0-10 tumor protein p53 Homo sapiens 120-124 33693776-10 2021 Beta-cell modelling shows that low plasma concentrations of gliclazide potentiate late phase insulin secretion and increase glucose sensitivity by 50%. Gliclazide 60-70 insulin Homo sapiens 93-100 34003600-0 2021 Alleviation of cisplatin-induced hepatotoxicity by gliclazide: Involvement of oxidative stress and caspase-3 activity. Gliclazide 51-61 caspase 3 Mus musculus 99-108 33460615-0 2021 Gliclazide alters macrophages polarization state in diabetic atherosclerosis in vitro via blocking AGE-RAGE/TLR4-reactive oxygen species-activated NF-kbeta nexus. Gliclazide 0-10 renin binding protein Mus musculus 99-102 33460615-0 2021 Gliclazide alters macrophages polarization state in diabetic atherosclerosis in vitro via blocking AGE-RAGE/TLR4-reactive oxygen species-activated NF-kbeta nexus. Gliclazide 0-10 advanced glycosylation end product-specific receptor Mus musculus 103-107 33460615-0 2021 Gliclazide alters macrophages polarization state in diabetic atherosclerosis in vitro via blocking AGE-RAGE/TLR4-reactive oxygen species-activated NF-kbeta nexus. Gliclazide 0-10 toll-like receptor 4 Mus musculus 108-112 33460615-8 2021 Glz pretreatment significantly (P < 0.05) inhibited the AGEs-induced pro-inflammatory mediators (NO , reactive oxygen species, i-NOS), and production of pro-inflammatory cytokines, including IL-1beta, IL-6, and TNF-alpha. Gliclazide 0-3 nitric oxide synthase 2, inducible Mus musculus 127-132 33460615-8 2021 Glz pretreatment significantly (P < 0.05) inhibited the AGEs-induced pro-inflammatory mediators (NO , reactive oxygen species, i-NOS), and production of pro-inflammatory cytokines, including IL-1beta, IL-6, and TNF-alpha. Gliclazide 0-3 interleukin 1 alpha Mus musculus 191-199 33460615-8 2021 Glz pretreatment significantly (P < 0.05) inhibited the AGEs-induced pro-inflammatory mediators (NO , reactive oxygen species, i-NOS), and production of pro-inflammatory cytokines, including IL-1beta, IL-6, and TNF-alpha. Gliclazide 0-3 interleukin 6 Mus musculus 201-205 33460615-8 2021 Glz pretreatment significantly (P < 0.05) inhibited the AGEs-induced pro-inflammatory mediators (NO , reactive oxygen species, i-NOS), and production of pro-inflammatory cytokines, including IL-1beta, IL-6, and TNF-alpha. Gliclazide 0-3 tumor necrosis factor Mus musculus 211-220 33460615-10 2021 Glz pretreatment also effectively abated the AGEs-induced RAGE (~2-fold decrease), and CD86 surface marker expressions (P < 0.001 at 100 muM) on macrophages by inhibiting the NF-kbeta activation in a concentration dependent manner (1-100 muM) (P < 0.001). Gliclazide 0-3 advanced glycosylation end product-specific receptor Mus musculus 58-62 33460615-10 2021 Glz pretreatment also effectively abated the AGEs-induced RAGE (~2-fold decrease), and CD86 surface marker expressions (P < 0.001 at 100 muM) on macrophages by inhibiting the NF-kbeta activation in a concentration dependent manner (1-100 muM) (P < 0.001). Gliclazide 0-3 CD86 antigen Mus musculus 87-91 33460615-11 2021 In conclusion, our data suggests that Glz alleviates the diabetic atherosclerosis progression by ameliorating the AGEs-mediated M1 pro-inflammatory phenotype via blocking AGE-RAGE/TLR4-reactive oxygen species -activated NF-kbeta nexus in macrophages. Gliclazide 38-41 renin binding protein Mus musculus 114-117 33460615-11 2021 In conclusion, our data suggests that Glz alleviates the diabetic atherosclerosis progression by ameliorating the AGEs-mediated M1 pro-inflammatory phenotype via blocking AGE-RAGE/TLR4-reactive oxygen species -activated NF-kbeta nexus in macrophages. Gliclazide 38-41 advanced glycosylation end product-specific receptor Mus musculus 175-179 33460615-11 2021 In conclusion, our data suggests that Glz alleviates the diabetic atherosclerosis progression by ameliorating the AGEs-mediated M1 pro-inflammatory phenotype via blocking AGE-RAGE/TLR4-reactive oxygen species -activated NF-kbeta nexus in macrophages. Gliclazide 38-41 toll-like receptor 4 Mus musculus 180-184 33629551-12 2020 Conclusion: Gliclazide significantly alleviates myocardial injury and reduces myocardial apoptosis in diabetic rats, and its mechanism may be related to lowering blood glucose, improving oxidative stress and regulating RhoA / ROCK1 / eNOS signaling pathway. Gliclazide 12-22 ras homolog family member A Rattus norvegicus 219-223 32648242-12 2020 Gliclazide and gliclazide + metformin were most added as an adjunct to existing prescriptions of biguanides (83.4%) or insulin (64.3%), respectively. Gliclazide 15-25 insulin Homo sapiens 119-126 32687680-9 2020 Administration of GLZ reduced oxidative stress, caspase-3, and NF-kappaB activity, and improved kidney function markers in CP-treated mice compared with CP alone group. Gliclazide 18-21 caspase 3 Mus musculus 48-57 32687680-9 2020 Administration of GLZ reduced oxidative stress, caspase-3, and NF-kappaB activity, and improved kidney function markers in CP-treated mice compared with CP alone group. Gliclazide 18-21 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 63-72 33511553-4 2021 RESULTS: The Delphi consensus suggests that in drug-naive patients with T2DM, intolerant to metformin or in whom metformin is contraindicated, dual therapy of gliclazide/gliclazide-modified release (MR) should be considered along with a dipeptidyl peptidase 4 (DPP4) inhibitor if glycated hemoglobin A1c level is greater than 7.5% and with insulin if the A1c level is greater than 9%. Gliclazide 170-180 dipeptidyl peptidase 4 Homo sapiens 237-259 33511553-4 2021 RESULTS: The Delphi consensus suggests that in drug-naive patients with T2DM, intolerant to metformin or in whom metformin is contraindicated, dual therapy of gliclazide/gliclazide-modified release (MR) should be considered along with a dipeptidyl peptidase 4 (DPP4) inhibitor if glycated hemoglobin A1c level is greater than 7.5% and with insulin if the A1c level is greater than 9%. Gliclazide 170-180 dipeptidyl peptidase 4 Homo sapiens 261-265 33511553-4 2021 RESULTS: The Delphi consensus suggests that in drug-naive patients with T2DM, intolerant to metformin or in whom metformin is contraindicated, dual therapy of gliclazide/gliclazide-modified release (MR) should be considered along with a dipeptidyl peptidase 4 (DPP4) inhibitor if glycated hemoglobin A1c level is greater than 7.5% and with insulin if the A1c level is greater than 9%. Gliclazide 170-180 insulin Homo sapiens 340-347 32790843-9 2021 In the presence of 1 microM clonidine, to separate insulinotropic from glucagonotropic effects, both 500 microM tolbutamide and 30 microM gliclazide increased glucagon secretion significantly, but transiently. Gliclazide 138-148 glucagon Mus musculus 71-79 32687680-0 2020 Gliclazide attenuates cisplatin-induced nephrotoxicity through inhibiting NF-kappaB and caspase-3 activity. Gliclazide 0-10 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 74-83 32687680-0 2020 Gliclazide attenuates cisplatin-induced nephrotoxicity through inhibiting NF-kappaB and caspase-3 activity. Gliclazide 0-10 caspase 3 Mus musculus 88-97 33629551-12 2020 Conclusion: Gliclazide significantly alleviates myocardial injury and reduces myocardial apoptosis in diabetic rats, and its mechanism may be related to lowering blood glucose, improving oxidative stress and regulating RhoA / ROCK1 / eNOS signaling pathway. Gliclazide 12-22 Rho-associated coiled-coil containing protein kinase 1 Rattus norvegicus 226-231 33629551-12 2020 Conclusion: Gliclazide significantly alleviates myocardial injury and reduces myocardial apoptosis in diabetic rats, and its mechanism may be related to lowering blood glucose, improving oxidative stress and regulating RhoA / ROCK1 / eNOS signaling pathway. Gliclazide 12-22 nitric oxide synthase 3 Rattus norvegicus 234-238 32360661-6 2020 Gliclazide sustained release microparticles were produced by fluidized bed coating using Eudragit NM 30 D and achieved 99% production yield and final coated particle size (D50) of 198 +- 4.3 mum. Gliclazide 0-10 latexin Homo sapiens 192-195 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. Gliclazide 89-99 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 142-148 32347481-10 2020 mRNA expression of INS, IRA, GK, and GLUT2 significantly upregulated in diabetic rats received nanoCUR and GLZ. Gliclazide 107-110 glucokinase Rattus norvegicus 29-31 32347481-10 2020 mRNA expression of INS, IRA, GK, and GLUT2 significantly upregulated in diabetic rats received nanoCUR and GLZ. Gliclazide 107-110 solute carrier family 2 member 2 Rattus norvegicus 37-42 32092333-8 2020 KEY FINDINGS: Treatment with gliclazide alone decreased serum glucose, total cholesterol, triglycerides, malondialdehyde, tumor necrosis factor-alpha and nuclear factor kappa-Beta while increased serum C-peptide, superoxide dismutase, reduced glutathione and adiponectin levels. Gliclazide 29-39 tumor necrosis factor Rattus norvegicus 122-149 32092333-8 2020 KEY FINDINGS: Treatment with gliclazide alone decreased serum glucose, total cholesterol, triglycerides, malondialdehyde, tumor necrosis factor-alpha and nuclear factor kappa-Beta while increased serum C-peptide, superoxide dismutase, reduced glutathione and adiponectin levels. Gliclazide 29-39 insulin 2 Rattus norvegicus 202-211 32092333-8 2020 KEY FINDINGS: Treatment with gliclazide alone decreased serum glucose, total cholesterol, triglycerides, malondialdehyde, tumor necrosis factor-alpha and nuclear factor kappa-Beta while increased serum C-peptide, superoxide dismutase, reduced glutathione and adiponectin levels. Gliclazide 29-39 adiponectin, C1Q and collagen domain containing Rattus norvegicus 259-270 32308446-5 2020 We have chosen gliclazide, as a sulfonylurea and Abasaglar , the less expensive among basal insulin analogues. Gliclazide 15-25 insulin Homo sapiens 92-99 31816432-9 2020 RESULTS: While dapagliflozin and gliclazide similarly improved glycaemic control, dapagliflozin reduced and gliclazide increased fasting insulin. Gliclazide 108-118 insulin Homo sapiens 137-144 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Gliclazide 237-247 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Gliclazide 485-495 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 32114843-2 2020 The purpose of the present study was to assess the possible modulatory effect of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor lovastatin on therapeutic efficiency of traditional antidiabetics, as metformin and gliclazide, regarding hepatic complications in streptozotocin (STZ)-induced diabetes in rats.Methods: Animals were divided into seven groups; normal control group, STZ control group (50 mg/kg, i.p., single dose), lovastatin group, metformin group, gliclazide group, lovastatin plus metformin group and lovastatin plus gliclazide group. Gliclazide 485-495 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-142 32045587-0 2020 Gliclazide attenuates acetic acid-induced colitis via the modulation of PPARgamma, NF-kappaB and MAPK signaling pathways. Gliclazide 0-10 peroxisome proliferator activated receptor gamma Homo sapiens 72-81 32045587-0 2020 Gliclazide attenuates acetic acid-induced colitis via the modulation of PPARgamma, NF-kappaB and MAPK signaling pathways. Gliclazide 0-10 nuclear factor kappa B subunit 1 Homo sapiens 83-92 32045587-9 2020 Gliclazide (10 mg/kg; p.o) prominently decreased colon tissue injury as assessed by the histopathological analysis, myeloperoxidase, and intercellular adhesion molecule-1 levels. Gliclazide 0-10 myeloperoxidase Homo sapiens 116-170 31380248-1 2019 Purpose: In the current study, electrospraying was directed as a novel alternative approach to improve the physicochemical attributes of gliclazide (GLC), as a poorly water-soluble drug, by creating nanocrystalline/amorphous solid dispersions (ESSs). Gliclazide 137-147 NADH:ubiquinone oxidoreductase subunit B11 Homo sapiens 244-248 32045587-10 2020 Gliclazide significantly alleviated the proinflammatory mediator, IL-6, promoted the anti-inflammatory cytokine, IL-10 and, withheld oxidative stress in the injured colon tissues. Gliclazide 0-10 interleukin 6 Homo sapiens 66-70 32045587-10 2020 Gliclazide significantly alleviated the proinflammatory mediator, IL-6, promoted the anti-inflammatory cytokine, IL-10 and, withheld oxidative stress in the injured colon tissues. Gliclazide 0-10 interleukin 10 Homo sapiens 113-118 32045587-11 2020 The protective effect of gliclazide was mediated through the upregulation of PPARgamma and downregulation of NF-kappaB expression. Gliclazide 25-35 peroxisome proliferator activated receptor gamma Homo sapiens 77-86 32045587-11 2020 The protective effect of gliclazide was mediated through the upregulation of PPARgamma and downregulation of NF-kappaB expression. Gliclazide 25-35 nuclear factor kappa B subunit 1 Homo sapiens 109-118 31696501-0 2019 Protective effects of gliclazide on high glucose and AGEs-induced damage of glomerular mesangial cells and renal tubular epithelial cells via inhibiting RAGE-p22phox-NF-kB pathway. Gliclazide 22-32 long intergenic non-protein coding RNA 914 Homo sapiens 153-157 31696501-0 2019 Protective effects of gliclazide on high glucose and AGEs-induced damage of glomerular mesangial cells and renal tubular epithelial cells via inhibiting RAGE-p22phox-NF-kB pathway. Gliclazide 22-32 cytochrome b-245 alpha chain Homo sapiens 158-165 31696501-4 2019 Therefore, the aim of this study was to explore whether gliclazide had protective effects on high glucose and advanced glycation end products (AGEs)-induced injury of human mesangial cells (HMCs) and renal tubular epithelial cells. Gliclazide 56-66 molybdenum cofactor sulfurase Homo sapiens 190-194 31696501-14 2019 CONCLUSIONS: Gliclazide has protective effects on high glucose and AGEs-induced damage of glomerular mesangial cells and renal tubular epithelial cells via inhibiting RAGE-NADPH oxidase-NF-kB pathway. Gliclazide 13-23 long intergenic non-protein coding RNA 914 Homo sapiens 167-171 30663560-4 2020 Regarding antidiabetic medication, metformin, gliclazide, pioglitazone, exenatide and dapagliflozin exert a beneficial effect on Endothelial Function (EF); glimepiride and glibenclamide, dipeptidyl peptidase-4 inhibitors and liraglutide have a neutral effect, while studies examining the effect of insulin analogues, empagliflozin and canagliflozin on EF are limited. Gliclazide 46-56 dipeptidyl peptidase 4 Homo sapiens 187-209 30663560-4 2020 Regarding antidiabetic medication, metformin, gliclazide, pioglitazone, exenatide and dapagliflozin exert a beneficial effect on Endothelial Function (EF); glimepiride and glibenclamide, dipeptidyl peptidase-4 inhibitors and liraglutide have a neutral effect, while studies examining the effect of insulin analogues, empagliflozin and canagliflozin on EF are limited. Gliclazide 46-56 insulin Homo sapiens 298-305 32099442-0 2019 CYP2C19*2 Polymorphism Is Associated with Impaired Oral Clearance of Gliclazide in Healthy Chinese. Gliclazide 69-79 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 0-7 32099442-1 2019 Background: Previous studies suggest gliclazide is metabolised primarily by CYP2C19 rather than CYP2C9, unlike other sulphonylureas. Gliclazide 37-47 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 76-83 32099442-3 2019 Methods: We investigated the effect of CYP2C19 polymorphisms on gliclazide pharmacokinetics in 15 healthy male Chinese subjects after a single 80mg oral dose. Gliclazide 64-74 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 39-46 32099442-6 2019 Conclusion: CYP2C19*2 polymorphism is associated with increased total gliclazide concentration and reduced oral clearance. Gliclazide 70-80 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 12-19 31257474-12 2019 In conclusion, it can be speculated that gliclazide may have a similar mechanism to MSC as a potential therapeutic agent for cisplatin-induced AKI, by regulating miR-210/Serpine1 and miR-378-/Fos-mediated inflammation and cell apoptosis. Gliclazide 41-51 microRNA 210 Homo sapiens 162-169 31257474-12 2019 In conclusion, it can be speculated that gliclazide may have a similar mechanism to MSC as a potential therapeutic agent for cisplatin-induced AKI, by regulating miR-210/Serpine1 and miR-378-/Fos-mediated inflammation and cell apoptosis. Gliclazide 41-51 serpin family E member 1 Homo sapiens 170-178 31257474-12 2019 In conclusion, it can be speculated that gliclazide may have a similar mechanism to MSC as a potential therapeutic agent for cisplatin-induced AKI, by regulating miR-210/Serpine1 and miR-378-/Fos-mediated inflammation and cell apoptosis. Gliclazide 41-51 microRNA 378a Homo sapiens 183-190 31257474-12 2019 In conclusion, it can be speculated that gliclazide may have a similar mechanism to MSC as a potential therapeutic agent for cisplatin-induced AKI, by regulating miR-210/Serpine1 and miR-378-/Fos-mediated inflammation and cell apoptosis. Gliclazide 41-51 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 192-195 31380248-1 2019 Purpose: In the current study, electrospraying was directed as a novel alternative approach to improve the physicochemical attributes of gliclazide (GLC), as a poorly water-soluble drug, by creating nanocrystalline/amorphous solid dispersions (ESSs). Gliclazide 149-152 NADH:ubiquinone oxidoreductase subunit B11 Homo sapiens 244-248 31380248-4 2019 Furthermore, GLC dissolution behaviors from ESSs were fitted to various models in order to realize the drug release mechanism. Gliclazide 13-16 NADH:ubiquinone oxidoreductase subunit B11 Homo sapiens 44-48 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 myeloperoxidase Rattus norvegicus 42-57 30981189-12 2019 The combination of mangiferin with metformin was insulin dependent (Akt pathway) whereas the combination of mangiferin and gliclazide was insulin independent (AMPK pathway). Gliclazide 123-133 insulin Homo sapiens 138-145 30971955-0 2019 Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules. Gliclazide 0-10 selectin P Homo sapiens 96-106 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 myeloperoxidase Homo sapiens 43-46 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 nuclear factor kappa B subunit 1 Homo sapiens 115-118 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 184-189 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 nitric oxide synthase 2 Homo sapiens 191-195 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 RELA proto-oncogene, NF-kB subunit Homo sapiens 211-223 30971955-11 2019 Treatment with gliclazide 10 mg/kg reduced MPO activity (p < 0.001), MDA levels (p < 0.001) and NFkappaB NLS P50 (p < 0.05) protein levels, resulting in low immunostaining to Cox-2, iNOS (p < 0.05), NFkappaB P65 (p < 0.05), and negative immunoreaction to MMP-2 (p < 0.001). Gliclazide 15-25 matrix metallopeptidase 2 Homo sapiens 270-275 30971955-13 2019 Immunofluorescence revealed decreased levels of P-selectin (p < 0.001) after treatment with gliclazide 10 mg/kg (p < 0.05). Gliclazide 95-105 selectin P Homo sapiens 48-58 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 interleukin 1 beta Rattus norvegicus 85-93 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 tumor necrosis factor Rattus norvegicus 99-108 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 164-169 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 cathepsin K Rattus norvegicus 171-182 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 matrix metallopeptidase 2 Rattus norvegicus 184-189 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 TNF superfamily member 11 Rattus norvegicus 197-202 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 superoxide dismutase 1 Rattus norvegicus 204-209 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 glutathione peroxidase 1 Rattus norvegicus 211-216 30810635-9 2019 Treatment with 1 mg/kg gliclazide reduced myeloperoxidase activity, malondialdehyde, IL-1beta, and TNF-alpha levels (p<=0.05), and resulted in weak staining for COX-2, cathepsin k, MMP-2, RANK, RANKL, SOD-1, GPx-1,MIF and PI3k. Gliclazide 23-33 macrophage migration inhibitory factor Rattus norvegicus 217-220 30810635-10 2019 In addition, down-regulation of NF-kappaB p50, PI3k, AKT, and F4/80 were observed, and OPG staining was strong after the 1 mg/kg gliclazide treatment. Gliclazide 129-139 AKT serine/threonine kinase 1 Rattus norvegicus 53-56 30810635-10 2019 In addition, down-regulation of NF-kappaB p50, PI3k, AKT, and F4/80 were observed, and OPG staining was strong after the 1 mg/kg gliclazide treatment. Gliclazide 129-139 TNF receptor superfamily member 11B Rattus norvegicus 87-90 30597970-0 2018 Influence of Piracetam on Gliclazide-Glycated Human Serum Albumin Interaction. Gliclazide 26-36 albumin Homo sapiens 52-65 30597970-5 2018 The aim of the present study was to analyze in vitro glycation of serum albumin in the presence of piracetam (PIR) and the gliclazide (GLZ)-glycated albumin interaction. Gliclazide 135-138 albumin Homo sapiens 66-79 30597970-7 2018 On the basis of obtained data we concluded that under the influence of glycation, association constant ( K a ) of gliclazide to human serum albumin decreases and GLZ binds to HSA with less strength than under physiological conditions. Gliclazide 114-124 albumin Homo sapiens 134-147 28951332-0 2018 Involvement of glucose-regulated protein 78 and spliced X-box binding protein 1 in the protective effect of gliclazide in diabetic nephropathy. Gliclazide 108-118 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 15-43 28951332-0 2018 Involvement of glucose-regulated protein 78 and spliced X-box binding protein 1 in the protective effect of gliclazide in diabetic nephropathy. Gliclazide 108-118 X-box binding protein 1 Rattus norvegicus 56-79 28951332-15 2018 Gliclazide treatment lessens diabetic nephropathy, probably partially by suppressing the GRP78- and sXBP1-mediated ER response. Gliclazide 0-10 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 89-94 29802958-4 2018 This review examines the differences between currently available sulfonylureas with a focus on how gliclazide modified release (MR) differs from other members of this class and from newer oral antihyperglycemic agents in the form of dipeptidyl peptidase-4 (DPP4) and sodium- glucose cotransporter 2 (SGLT2) inhibitors. Gliclazide 99-109 dipeptidyl peptidase 4 Homo sapiens 257-261 30119196-10 2018 The correlation between the minimum concentration of gliclazide and insulin level might be a potential predictor of patients compliance. Gliclazide 53-63 insulin Homo sapiens 68-75 29802958-4 2018 This review examines the differences between currently available sulfonylureas with a focus on how gliclazide modified release (MR) differs from other members of this class and from newer oral antihyperglycemic agents in the form of dipeptidyl peptidase-4 (DPP4) and sodium- glucose cotransporter 2 (SGLT2) inhibitors. Gliclazide 99-109 solute carrier family 5 member 2 Homo sapiens 267-298 29802958-4 2018 This review examines the differences between currently available sulfonylureas with a focus on how gliclazide modified release (MR) differs from other members of this class and from newer oral antihyperglycemic agents in the form of dipeptidyl peptidase-4 (DPP4) and sodium- glucose cotransporter 2 (SGLT2) inhibitors. Gliclazide 99-109 solute carrier family 5 member 2 Homo sapiens 300-305 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. Gliclazide 236-246 solute carrier organic anion transporter family member 1B3 Homo sapiens 178-185 29498478-7 2018 We demonstrated that gliclazide and glimepiride are substrates of OATP1B1 and glibenclamide and glipizide are substrates of OATP1B3. Gliclazide 21-31 solute carrier organic anion transporter family member 1B1 Homo sapiens 66-73 29498478-7 2018 We demonstrated that gliclazide and glimepiride are substrates of OATP1B1 and glibenclamide and glipizide are substrates of OATP1B3. Gliclazide 21-31 solute carrier organic anion transporter family member 1B3 Homo sapiens 124-131 30030468-6 2018 The clearance of glimepiride and gliclazide in CYP2C9*2 and *3 was significantly reduced compared to the wild-type. Gliclazide 33-43 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 47-53 30030468-7 2018 These findings collectively indicate that OATP1B1*5 and *15 and CYP2C9*2 and *3 have a significant effect on the transport and metabolism of glimepiride and gliclazide. Gliclazide 157-167 solute carrier organic anion transporter family member 1B1 Homo sapiens 42-49 30030468-0 2018 CYP2C9 and OATP1B1 genetic polymorphisms affect the metabolism and transport of glimepiride and gliclazide. Gliclazide 96-106 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 30030468-0 2018 CYP2C9 and OATP1B1 genetic polymorphisms affect the metabolism and transport of glimepiride and gliclazide. Gliclazide 96-106 solute carrier organic anion transporter family member 1B1 Homo sapiens 11-18 30030468-7 2018 These findings collectively indicate that OATP1B1*5 and *15 and CYP2C9*2 and *3 have a significant effect on the transport and metabolism of glimepiride and gliclazide. Gliclazide 157-167 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 64-70 30030468-2 2018 The aim of this study was to assess the effect of CYP2C9 and OATP1B1 genetic polymorphisms on the metabolism and transport of glimepiride and gliclazide. Gliclazide 142-152 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 50-56 27694910-3 2017 In the present study, we examined the effects of KCNQ1 variants on the therapeutic response to modified-release gliclazide (gliclazide MR) treatment in Chinese patients newly diagnosed with T2DM. Gliclazide 112-122 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 49-54 30030468-2 2018 The aim of this study was to assess the effect of CYP2C9 and OATP1B1 genetic polymorphisms on the metabolism and transport of glimepiride and gliclazide. Gliclazide 142-152 solute carrier organic anion transporter family member 1B1 Homo sapiens 61-68 30030468-4 2018 The clearance of glimepiride and gliclazide in OATP1B1*5 and *15 was significantly reduced compared to the wild-type. Gliclazide 33-43 solute carrier organic anion transporter family member 1B1 Homo sapiens 47-54 30030468-5 2018 Glimepiride in the presence of CYP2C9*1, *2 and *3 recombinase had Vmax values of 21.58 +- 7.78, 15.69 +- 5.59, and 9.17 +- 3.03 nmol/min/mg protein, while gliclazide had Vmax values of 15.73 +- 3.11, 10.53 +- 4.06, and 6.21 +- 2.94 nmol/min/mg protein, respectively. Gliclazide 156-166 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 31-37 29651307-11 2018 Conclusions: Progressive gliclazide MR 60 mg uptitration was well tolerated and lowered HbA1c across a broad range of HbA1c, BMI and background glucose-lowering therapy. Gliclazide 25-35 lectin, mannose binding 1 Homo sapiens 36-41 29337033-0 2018 Gliclazide, a KATP channel blocker, inhibits vascular smooth muscle cell proliferation through the CaMKKbeta-AMPK pathway. Gliclazide 0-10 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 99-108 29337033-1 2018 Gliclazide, a sulfonylurea that is widely used to treat type II-diabetes, specifically blocks KATP channels and recombinant smooth muscle (SUR2B/Kir6.1) KATP channels with high potency. Gliclazide 0-10 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 145-151 29337033-6 2018 However, KATP channel openers and Kir6.1 siRNA prevented gliclazide-mediated inhibition of VSMC proliferation. Gliclazide 57-67 potassium inwardly rectifying channel subfamily J member 8 Homo sapiens 34-40 29337033-7 2018 Gliclazide also increased the levels of Ca2+/calmodulin-dependent protein kinase kinase beta (CaMKKbeta), an upstream kinase of AMPK. Gliclazide 0-10 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 94-103 29337033-9 2018 Oral administration of 2mg/kg gliclazide resulted in the activation of CaMKKbeta and AMPK in vivo, suggesting that gliclazide suppressed VSMC proliferation via the CaMKKbeta-AMPK signaling pathway. Gliclazide 30-40 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 71-80 29337033-9 2018 Oral administration of 2mg/kg gliclazide resulted in the activation of CaMKKbeta and AMPK in vivo, suggesting that gliclazide suppressed VSMC proliferation via the CaMKKbeta-AMPK signaling pathway. Gliclazide 30-40 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 164-173 29337033-9 2018 Oral administration of 2mg/kg gliclazide resulted in the activation of CaMKKbeta and AMPK in vivo, suggesting that gliclazide suppressed VSMC proliferation via the CaMKKbeta-AMPK signaling pathway. Gliclazide 115-125 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 71-80 29337033-9 2018 Oral administration of 2mg/kg gliclazide resulted in the activation of CaMKKbeta and AMPK in vivo, suggesting that gliclazide suppressed VSMC proliferation via the CaMKKbeta-AMPK signaling pathway. Gliclazide 115-125 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 164-173 28513070-0 2017 Influence of quercetin on the interaction of gliclazide with human serum albumin - spectroscopic and docking approaches. Gliclazide 45-55 albumin Homo sapiens 67-80 28513070-2 2017 Thus, the aim of presented study was to analyse human serum albumin-binding displacement interaction between two ligands, hypoglycaemic drug gliclazide and widely distributed plant flavonoid quercetin. Gliclazide 141-151 albumin Homo sapiens 54-67 28513070-6 2017 According to the fluorescence data analysis, gliclazide presents a substance with a lower binding capacity towards HSA compared with quercetin. Gliclazide 45-55 albumin Homo sapiens 115-118 28513070-7 2017 Results also showed that the presence of quercetin hindered the interaction between HSA and gliclazide, as the binding constant for gliclazide in the ternary system was remarkably lower compared with the binary system. Gliclazide 92-102 albumin Homo sapiens 84-87 28513070-7 2017 Results also showed that the presence of quercetin hindered the interaction between HSA and gliclazide, as the binding constant for gliclazide in the ternary system was remarkably lower compared with the binary system. Gliclazide 132-142 albumin Homo sapiens 84-87 29844963-12 2018 Results: The pharmacodynamic activity (blood glucose reduction and insulin levels) of gliclazide was significantly (p < 0.05) influenced by aprepitant in normal and diabetic condition without any convulsions in animals. Gliclazide 86-96 insulin Oryctolagus cuniculus 67-74 28888191-0 2018 The effect of glycation on bovine serum albumin conformation and ligand binding properties with regard to gliclazide. Gliclazide 106-116 albumin Homo sapiens 34-47 28888191-6 2018 Structural changes of albumin after interaction with gliclazide (0-14muM) were determined using fluorescence quenching and circular dichroism spectroscopy. Gliclazide 53-63 albumin Homo sapiens 22-29 28888191-8 2018 Calculated Stern-Volmer quenching constants, as well as binding constants for the BSA-gliclazide complex, were lower for the glycated form of albumin than for the unmodified protein. Gliclazide 86-96 albumin Homo sapiens 142-149 27694910-3 2017 In the present study, we examined the effects of KCNQ1 variants on the therapeutic response to modified-release gliclazide (gliclazide MR) treatment in Chinese patients newly diagnosed with T2DM. Gliclazide 124-134 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 49-54 27694910-12 2017 KCNQ1 polymorphisms are associated with gliclazide MR efficacy in Chinese patients with type 2 diabetes. Gliclazide 40-50 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 0-5 26663583-0 2016 Using resonance light scattering and UV/vis absorption spectroscopy to study the interaction between gliclazide and bovine serum albumin. Gliclazide 101-111 albumin Homo sapiens 123-136 27181593-1 2016 AIMS/INTRODUCTION: The objective of the present study was to investigate the effects of CYP2C9*3 polymorphisms on the therapeutic response to gliclazide in type 2 diabetes patients. Gliclazide 142-152 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 88-94 26663583-1 2016 At different temperatures (298, 310 and 318 K), the interaction between gliclazide and bovine serum albumin (BSA) was investigated using fluorescence quenching spectroscopy, resonance light scattering spectroscopy and UV/vis absorption spectroscopy. Gliclazide 72-82 albumin Homo sapiens 94-107 26866747-0 2016 Association of KCNQ1 polymorphisms with gliclazide efficacy in Chinese type 2 diabetic patients. Gliclazide 40-50 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 15-20 27499787-0 2016 Inhibition of P-glycoprotein expression and function by anti-diabetic drugs gliclazide, metformin, and pioglitazone in vitro and in situ. Gliclazide 76-86 ATP binding cassette subfamily B member 1 Homo sapiens 14-28 27499787-5 2016 This study investigated the effects of gliclazide, metformin, and pioglitazone on the function and expression of P-gp. Gliclazide 39-49 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 27499787-11 2016 P-gp expression was decreased by gliclazide, metformin and pioglitazone. Gliclazide 33-43 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 27499787-13 2016 It was found that gliclazide, metformin, and pioglitazone inhibited P-gp efflux activity in situ and down-regulated P-gp expression in vitro. Gliclazide 18-28 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 27499787-13 2016 It was found that gliclazide, metformin, and pioglitazone inhibited P-gp efflux activity in situ and down-regulated P-gp expression in vitro. Gliclazide 18-28 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 26866747-1 2016 OBJECTIVES: To investigate the effects of KCNQ1 polymorphisms on the efficacy of gliclazide in type 2 diabetic patients. Gliclazide 81-91 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 42-47 26866747-10 2016 CONCLUSION: Our results indicated that a common variant of KCNQ1, rs2237897, was associated with the efficacy of gliclazide after 8-week monotherapy in Chinese newly diagnosed type 2 diabetic patients. Gliclazide 113-123 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 59-64 26653612-13 2016 Most (95.5%) indicated a greater likelihood of adherence with the gliclazide MR 60 mg regime relative to their previous therapy. Gliclazide 66-76 lectin, mannose binding 1 Homo sapiens 77-82 27042415-3 2016 AIM OF THE STUDY: To investigate the influence of metformin alone or in combination with gliclazide on the level of serum omentin among patients with type 2 diabetes mellitus (T2DM). Gliclazide 89-99 intelectin 1 Homo sapiens 122-129 27042415-6 2016 RESULT: Use of gliclazide as an add-on therapy to metformin in patients with T2DM result in better glycemic control evidenced by significant reductions in the levels of blood glucose levels and HbA1C and much more improvement in insulin sensitivity evidenced by significant decreased in insulin resistance index, whereas it has adverse impact on serum omentin-1 levels evidenced by significant decrement in omentin-1 level in comparison to their pretreatment levels among Group 2 patients. Gliclazide 15-25 insulin Homo sapiens 229-236 27042415-6 2016 RESULT: Use of gliclazide as an add-on therapy to metformin in patients with T2DM result in better glycemic control evidenced by significant reductions in the levels of blood glucose levels and HbA1C and much more improvement in insulin sensitivity evidenced by significant decreased in insulin resistance index, whereas it has adverse impact on serum omentin-1 levels evidenced by significant decrement in omentin-1 level in comparison to their pretreatment levels among Group 2 patients. Gliclazide 15-25 insulin Homo sapiens 287-294 27042415-6 2016 RESULT: Use of gliclazide as an add-on therapy to metformin in patients with T2DM result in better glycemic control evidenced by significant reductions in the levels of blood glucose levels and HbA1C and much more improvement in insulin sensitivity evidenced by significant decreased in insulin resistance index, whereas it has adverse impact on serum omentin-1 levels evidenced by significant decrement in omentin-1 level in comparison to their pretreatment levels among Group 2 patients. Gliclazide 15-25 intelectin 1 Homo sapiens 352-359 27042415-6 2016 RESULT: Use of gliclazide as an add-on therapy to metformin in patients with T2DM result in better glycemic control evidenced by significant reductions in the levels of blood glucose levels and HbA1C and much more improvement in insulin sensitivity evidenced by significant decreased in insulin resistance index, whereas it has adverse impact on serum omentin-1 levels evidenced by significant decrement in omentin-1 level in comparison to their pretreatment levels among Group 2 patients. Gliclazide 15-25 intelectin 1 Homo sapiens 407-414 27042415-7 2016 CONCLUSIONS: Adding of gliclazide to metformin in treatment of patients with T2DM might extend the therapeutic action of metformin in regarding much better controlling of glycemic indices, but, at the same time, it might attenuate the cardioprotective effects of metformin by its adverse influence on serum omentin-1 levels. Gliclazide 23-33 intelectin 1 Homo sapiens 307-314 27042415-0 2016 Effects of gliclazide add on metformin on serum omentin-1 levels in patients with type 2 diabetes mellitus. Gliclazide 11-21 intelectin 1 Homo sapiens 48-55 26653612-14 2016 CONCLUSIONS: In this large, real world study, progressive uptitration with gliclazide MR 60 mg once daily appears to be efficacious and safe in individuals with suboptimal glycemic control at various stages of the diabetes continuum. Gliclazide 75-85 lectin, mannose binding 1 Homo sapiens 86-91 28017142-5 2016 Switching antidiabetic therapy from gliclazide to acarbose and metformin, the patient"s serum insulin level and IAA decreased gradually. Gliclazide 36-46 insulin Homo sapiens 94-101 26361859-10 2015 CONCLUSION: Compared with other oral insulinotropic agents, gliclazide significantly reduced HbA1c with no difference regarding hypoglycemia risk. Gliclazide 60-70 hemoglobin subunit alpha 1 Homo sapiens 93-97 24602692-9 2014 These results suggest that the SUR1-regulated NCCa-ATP channel may be associated with MCAO/reperfusion injury and the infarct-reducing effects of intravenous treatment with gliclazide may be due, in part, to the blocked upregulation of SUR1 expression, the decreased infarct size and the reduced apoptosis in the ischemia-reperfusion brain. Gliclazide 173-183 ATP binding cassette subfamily C member 8 Rattus norvegicus 31-35 26161595-11 2015 The enzymatic activity of the liver enzymes hexokinase, glucose-6 phosphate dehydrogenase, fructose 1,6-biphosphatase, pyruvate kinase and glucose-6 phosphatase were enhanced by resveratrol and gliclazide, while losartan treatment was not associated with significant changes in liver carbohydrate metabolism. Gliclazide 194-204 glucose-6-phosphate dehydrogenase Rattus norvegicus 56-89 26161595-11 2015 The enzymatic activity of the liver enzymes hexokinase, glucose-6 phosphate dehydrogenase, fructose 1,6-biphosphatase, pyruvate kinase and glucose-6 phosphatase were enhanced by resveratrol and gliclazide, while losartan treatment was not associated with significant changes in liver carbohydrate metabolism. Gliclazide 194-204 fructose-bisphosphatase 1 Rattus norvegicus 91-117 26161595-11 2015 The enzymatic activity of the liver enzymes hexokinase, glucose-6 phosphate dehydrogenase, fructose 1,6-biphosphatase, pyruvate kinase and glucose-6 phosphatase were enhanced by resveratrol and gliclazide, while losartan treatment was not associated with significant changes in liver carbohydrate metabolism. Gliclazide 194-204 glucose-6-phosphatase catalytic subunit 1 Rattus norvegicus 139-160 25348414-7 2014 We found that both MgATP and MgADP increased gliclazide inhibition of Kir6.2/SUR1 channels and reduced inhibition of Kir6.2/SUR2A-Y1206S. Gliclazide 45-55 ATP-binding cassette sub-family C member 8 Xenopus laevis 77-81 25348414-11 2014 Mutation of one (or both) of the Walker A lysines in the catalytic site of the nucleotide-binding domains of SUR1 may have a similar effect to gliclazide on MgADP binding and transduction, but it does not appear to impair MgATP binding. Gliclazide 143-153 ATP-binding cassette sub-family C member 8 Xenopus laevis 109-113 25490375-2 2015 In this report, the interaction between the protein Human Serum Albumin (HSA) and two antidiabetics (Andb), Gliclazide (Gli) and Glipizide (Glip) was studied through fluorescence and docking assays, in order to characterize these systems. Gliclazide 108-118 albumin Homo sapiens 58-71 25490375-2 2015 In this report, the interaction between the protein Human Serum Albumin (HSA) and two antidiabetics (Andb), Gliclazide (Gli) and Glipizide (Glip) was studied through fluorescence and docking assays, in order to characterize these systems. Gliclazide 108-111 albumin Homo sapiens 58-71 25059539-4 2015 OBJECTIVE: Present study has been structured to investigate the role of insulin and pharmacological modulator of KATP channel (gliclazide) in experimental morphine withdrawal syndrome, both invivo and invitro. Gliclazide 127-137 insulin Canis lupus familiaris 72-79 25115353-1 2014 The aim of the present study was to investigate the effect of the E23K variant of the potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) gene on gliclazide modified release (MR) treatment in newly diagnosed patients with type 2 diabetes mellitus (T2DM). Gliclazide 165-175 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 149-155 24710641-9 2014 At the end of the month 12, the decreases in insulin and HOMA-IR score were more pronounced with PIO compared to gliclazide. Gliclazide 113-123 insulin Homo sapiens 45-52 24602692-9 2014 These results suggest that the SUR1-regulated NCCa-ATP channel may be associated with MCAO/reperfusion injury and the infarct-reducing effects of intravenous treatment with gliclazide may be due, in part, to the blocked upregulation of SUR1 expression, the decreased infarct size and the reduced apoptosis in the ischemia-reperfusion brain. Gliclazide 173-183 ATP binding cassette subfamily C member 8 Rattus norvegicus 236-240 23071106-1 2013 Tolbutamide and gliclazide block the K(ATP) channel K(ir)6.2/Sur1, causing membrane depolarization and stimulating insulin secretion in pancreatic beta cells. Gliclazide 16-26 ATP binding cassette subfamily C member 8 Rattus norvegicus 61-65 23700263-9 2013 The primary outcome measure of this study was dose of glimepiride, glibenclamide or gliclazide prescribed for DPP-4 and non-DPP-4 patients. Gliclazide 84-94 dipeptidyl peptidase 4 Homo sapiens 110-115 23509454-0 2013 Association between TCF7L2 Genotype and Glycemic Control in Diabetic Patients Treated with Gliclazide. Gliclazide 91-101 transcription factor 7 like 2 Homo sapiens 20-26 23509454-3 2013 The aim of the present study was to compare TCF7L2 genotype specific effect of gliclazide binding to KATP channel A-site (Group 1) with sulfonylureas binding to AB-site (Group 2). Gliclazide 79-89 transcription factor 7 like 2 Homo sapiens 44-50 23509454-10 2013 The results indicate significantly higher difference in DeltaHbA1c among the TCF7L2 genotypes in patients treated with gliclazide than in patients treated with glimepiride, glibenclamide, or glipizide. Gliclazide 119-129 transcription factor 7 like 2 Homo sapiens 77-83 22787179-4 2012 Following a genetic diagnosis of HNF1A-MODY in the proband and her father, both patients were treated with gliclazide, with improvement in HbA1c. Gliclazide 107-117 HNF1 homeobox A Homo sapiens 33-43 22732450-0 2012 Protective effect of gliclazide on diabetic peripheral neuropathy through Drp-1 mediated-oxidative stress and apoptosis. Gliclazide 21-31 dynamin 1-like Rattus norvegicus 74-79 22732450-8 2012 CONCLUSION: Gliclazide showed protective effect on DPN through modulating Drp-1-mediated oxidative stress and apoptosis. Gliclazide 12-22 dynamin 1-like Rattus norvegicus 74-79 22766067-2 2012 We evaluated the effects of a selective SUR1 blocker gliclazide on cardiac function and arrhythmia after isoprenaline-induced myocardial injury in obese rats. Gliclazide 53-63 ATP binding cassette subfamily C member 8 Rattus norvegicus 40-44 21691805-8 2011 However, only in the gliclazide group a significant association between CYP2C9 genotype and hypoglycaemic attacks was observed (P = 0.035). Gliclazide 21-31 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 72-78 21923736-10 2012 The C(SS) for gliclazide, glipizide, mitiglinide and nateglinide lie between IC(50) values for SUR1 and SUR2A/SUR2B, suggesting that these drugs bind selectively to pancreatic receptors. Gliclazide 14-24 ATP binding cassette subfamily C member 8 Homo sapiens 95-99 22385882-10 2012 The relationship of treatment response with KCNJ11 genotype was also significant in the biggest subgroup of patients treated with gliclazide (n=55). Gliclazide 130-140 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 44-50 22385882-11 2012 CONCLUSIONS: Carriers of the KCNJ11 K-allele have better therapeutic response to gliclazide. Gliclazide 81-91 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 29-35 21691805-10 2011 CONCLUSIONS: CYP2C9 polymorphisms leading to decreased enzyme activity show a modest impact on the risk of mild hypoglycaemia attacks during oral antidiabetic treatment, with a significant association in patients treated with gliclazide. Gliclazide 226-236 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 13-19 21142918-3 2010 The Ser1369Ala variant in the sulfonylurea receptor gene ABCC8 which encodes a subunit of the K(ATP) channel complex has been demonstrated to be associated with the hypoglycemic effect of gliclazide, which binds to the A site. Gliclazide 188-198 ATP binding cassette subfamily C member 8 Homo sapiens 57-62 21922305-0 2011 High-performance affinity chromatography and the analysis of drug interactions with modified proteins: binding of gliclazide with glycated human serum albumin. Gliclazide 114-124 albumin Homo sapiens 145-158 21922305-1 2011 This study used high-performance affinity chromatography (HPAC) to examine the binding of gliclazide (i.e., a sulfonylurea drug used to treat diabetes) with the protein human serum albumin (HSA) at various stages of modification due to glycation. Gliclazide 90-100 albumin Homo sapiens 175-188 21922305-1 2011 This study used high-performance affinity chromatography (HPAC) to examine the binding of gliclazide (i.e., a sulfonylurea drug used to treat diabetes) with the protein human serum albumin (HSA) at various stages of modification due to glycation. Gliclazide 90-100 albumin Homo sapiens 190-193 21922305-2 2011 Frontal analysis conducted with small HPAC columns was first used to estimate the number of binding sites and association equilibrium constants (K(a)) for gliclazide with normal HSA and glycated HSA. Gliclazide 155-165 albumin Homo sapiens 178-181 21922305-2 2011 Frontal analysis conducted with small HPAC columns was first used to estimate the number of binding sites and association equilibrium constants (K(a)) for gliclazide with normal HSA and glycated HSA. Gliclazide 155-165 albumin Homo sapiens 195-198 21922305-4 2011 Two samples of glycated HSA had similar affinities to normal HSA for gliclazide at Sudlow site I, but one sample had a 1.9-fold increase in affinity at this site. Gliclazide 69-79 albumin Homo sapiens 24-27 21922305-4 2011 Two samples of glycated HSA had similar affinities to normal HSA for gliclazide at Sudlow site I, but one sample had a 1.9-fold increase in affinity at this site. Gliclazide 69-79 albumin Homo sapiens 61-64 21922305-5 2011 All three glycated HSA samples differed from normal HSA in their affinity for gliclazide at Sudlow site II. Gliclazide 78-88 albumin Homo sapiens 19-22 21922305-5 2011 All three glycated HSA samples differed from normal HSA in their affinity for gliclazide at Sudlow site II. Gliclazide 78-88 albumin Homo sapiens 52-55 21518407-6 2011 One PAN was heterozygous for P112L mutation in HNF1A and transferred from insulin to oral gliclazide. Gliclazide 90-100 HNF1 homeobox A Homo sapiens 47-52 21863614-5 2011 KCNJ11 gene Glu23Lys polymorphism was associated with an increased risk of SU secondary failure, while Ser1369Ala polymorphism of ABCC8 gene had influence antidiabetic efficacy of SU drug gliclazide. Gliclazide 188-198 ATP binding cassette subfamily C member 8 Homo sapiens 130-135 21362360-1 2011 BACKGROUND: Both repaglinide and gliclazide are insulin secretagogues widely used in the treatment of type 2 diabetes. Gliclazide 33-43 insulin Homo sapiens 48-55 21455728-12 2011 Adipose AMPK activity was increased following metformin compared with gliclazide therapy (0.057 +- 0.007 vs 0.030 +- 0.005 [mean +- SEM] nmol min(-1) [mg lysate](-1); p < 0.005), independent of AMPK level, glycaemia or plasma adiponectin concentrations. Gliclazide 70-80 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 8-12 21356265-0 2011 Reduced catalytic activity of human CYP2C9 natural alleles for gliclazide: molecular dynamics simulation and docking studies. Gliclazide 63-73 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 36-42 21356265-1 2011 Amongst sulfonylureas, gliclazide is one of the mostly prescribed drugs to diabetic patients and is metabolized extensively by P450 CYP2C9. Gliclazide 23-33 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 132-138 21356265-2 2011 Among 24-CYP2C9 alleles, the *2/*2 and *3/*3 genotypes showed significantly lower gliclazide clearances with reductions of 25 and 57%, respectively. Gliclazide 82-92 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 9-15 21356265-4 2011 In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants. Gliclazide 106-116 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 136-142 21356265-4 2011 In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants. Gliclazide 106-116 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 192-198 21356265-4 2011 In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants. Gliclazide 199-209 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 136-142 21356265-4 2011 In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants. Gliclazide 199-209 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 192-198 21242637-7 2011 Initial management with diet alone was not sufficient, but he responded well to 20 mg oral gliclazide once a day with an improvement of HbA 1C from 7.2% to 6.5% within 3 months of treatment. Gliclazide 91-101 hemoglobin subunit alpha 1 Homo sapiens 136-141 19805912-8 2009 Upregulation of antioxidant enzymes and reduced sensitivity of Sur1-/- cells to H2O2-induced apoptosis were mimicked by treatment with the sulfonylureas tolbutamide and gliclazide. Gliclazide 169-179 ATP-binding cassette, sub-family C (CFTR/MRP), member 8 Mus musculus 63-67 20070990-10 2010 Multiple regression analysis showed that percentage change of ADP-induced platelet aggregate formation (standardized beta = 0.540, P < .05) was independently associated with percentage change of plasma PAI-1 level in addition to percentage change of HbA(1c) (standardized beta = 0.657, P < .05) (R = 0.939, P < .05) after switching to gliclazide. Gliclazide 344-354 serpin family E member 1 Homo sapiens 205-210 20455956-7 2010 CONCLUSION: Male type 2 diabetic patients undertaking the Ramadan fast can safely maintain glycaemic control with evening administration of gliclazide MR 60 mg during the fast, and reverting to a morning schedule thereafter. Gliclazide 140-150 lectin, mannose binding 1 Homo sapiens 151-156 20831536-0 2010 Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers. Gliclazide 98-108 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 13-19 20831536-0 2010 Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers. Gliclazide 98-108 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 24-31 20831536-1 2010 BACKGROUND AND OBJECTIVE: CYP2C9 is the major contributor to gliclazide metabolic clearance in vitro, while the pharmacokinetics of gliclazide modified release are affected mainly by CYP2C19 genetic polymorphisms in vivo. Gliclazide 61-71 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 26-32 20831536-1 2010 BACKGROUND AND OBJECTIVE: CYP2C9 is the major contributor to gliclazide metabolic clearance in vitro, while the pharmacokinetics of gliclazide modified release are affected mainly by CYP2C19 genetic polymorphisms in vivo. Gliclazide 132-142 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 183-190 20831536-2 2010 This study aims to investigate the influence of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers. Gliclazide 137-147 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 48-54 20831536-2 2010 This study aims to investigate the influence of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers. Gliclazide 137-147 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 59-66 20831536-11 2010 CYP2C19 polymorphisms appear to exert the dominant influence on the pharmacokinetics of gliclazide in healthy Chinese Han subjects, and may also affect the observed pharmacodynamics of the drug as a result. Gliclazide 88-98 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 0-7 20132997-7 2010 Some of the novel HNF1A mutation carriers were successfully transferred from insulin to gliclazide, while some of the novel GCK mutation carriers had a good clinical response when switched from insulin or oral antidiabetic drugs to diet. Gliclazide 88-98 HNF1 homeobox A Homo sapiens 18-23 18394931-0 2009 Normal insulin response to short-term intense exercise is abolished in Type 2 diabetic patients treated with gliclazide. Gliclazide 109-119 insulin Homo sapiens 7-14 18394931-2 2009 The aim of the study was to analyze insulin response to the short-term intense exercise in middle-aged Type 2 diabetic patients treated with gliclazide. Gliclazide 141-151 insulin Homo sapiens 36-43 18394931-11 2009 Normal insulin response to the exercise was abolished in Type 2 diabetic patients treated with gliclazide. Gliclazide 95-105 insulin Homo sapiens 7-14 19502091-6 2009 Compared with NG, insulin expression decreased significantly with HG, and increased similarly with gliclazide as with glibenclamide. Gliclazide 99-109 insulin Homo sapiens 18-25 19891554-3 2009 In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide. Gliclazide 208-218 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 56-62 19502091-7 2009 However, exposure to gliclazide, but not glibenclamide, significantly induced expression (at both gene and protein levels) of PDX-1, a fundamental beta-cell differentiation transcription factor, and Ki67, a marker of proliferation. Gliclazide 21-31 pancreatic and duodenal homeobox 1 Homo sapiens 126-131 19375767-4 2009 Compared with normal rats, untreated diabetic rats had a 30% and 61% increase in lipoprotein lipase protein expression and activity, which were decreased by insulin and gliclazide (P < .05). Gliclazide 169-179 lipoprotein lipase Rattus norvegicus 81-99 19799532-5 2009 CYP2C19 genotype is more influential for gliclazide pharmacokinetics when compared to CYP2C9. Gliclazide 41-51 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 0-7 19799532-8 2009 Diabetics with the SUR1 exon 33 G allele are more sensitive to gliclazide and the rs5210 variant of the KCNJ11 gene was associated with improved clinical efficacy of gliclazide. Gliclazide 63-73 ATP binding cassette subfamily C member 8 Homo sapiens 19-23 19799532-8 2009 Diabetics with the SUR1 exon 33 G allele are more sensitive to gliclazide and the rs5210 variant of the KCNJ11 gene was associated with improved clinical efficacy of gliclazide. Gliclazide 166-176 ATP binding cassette subfamily C member 8 Homo sapiens 19-23 19799532-8 2009 Diabetics with the SUR1 exon 33 G allele are more sensitive to gliclazide and the rs5210 variant of the KCNJ11 gene was associated with improved clinical efficacy of gliclazide. Gliclazide 166-176 potassium inwardly rectifying channel subfamily J member 11 Homo sapiens 104-110 19799532-10 2009 On the other hand, patients with HNF-1alpha mutations had a significant greater response to gliclazide when compared to those with type 2 diabetes. Gliclazide 92-102 HNF1 homeobox A Homo sapiens 33-43 19375767-5 2009 Fatty acid translocase protein was down-regulated by 45% in untreated diabetic rats, which was up-regulated by 31% and 26% with insulin and gliclazide, respectively (P < .05). Gliclazide 140-150 CD36 molecule Rattus norvegicus 0-22 18801483-0 2009 The oral anti-diabetic agent, gliclazide, inhibits oxidized LDL-mediated LOX-1 expression, metalloproteinase-9 secretion and apoptosis in human aortic endothelial cells. Gliclazide 30-40 oxidized low density lipoprotein receptor 1 Homo sapiens 73-78 18801483-3 2009 In the present study, we examined the effect of gliclazide, a second generation sulfonylurea with antioxidant properties, on LOX-1 expression and LOX-1-mediated MMP-9 expression and apoptosis in oxLDL-treated human aortic endothelial cells (HAECs). Gliclazide 48-58 oxidized low density lipoprotein receptor 1 Homo sapiens 125-130 18801483-3 2009 In the present study, we examined the effect of gliclazide, a second generation sulfonylurea with antioxidant properties, on LOX-1 expression and LOX-1-mediated MMP-9 expression and apoptosis in oxLDL-treated human aortic endothelial cells (HAECs). Gliclazide 48-58 oxidized low density lipoprotein receptor 1 Homo sapiens 146-151 18801483-5 2009 Treatment with an anti-LOX-1 antibody or with antioxidants, including gliclazide, inhibited these effects. Gliclazide 70-80 oxidized low density lipoprotein receptor 1 Homo sapiens 23-28 18801483-10 2009 The anti-apoptotic effect of gliclazide was associated with an increase in PKB activity and a decrease in caspase-3 and -9 activities. Gliclazide 29-39 caspase 3 Homo sapiens 106-122 18801483-11 2009 These results demonstrate that gliclazide inhibits endothelial LOX-1 expression and prevents LOX-1-mediated proatherogenic effects associated with endothelial dysfunction and plaque rupture. Gliclazide 31-41 oxidized low density lipoprotein receptor 1 Homo sapiens 63-68 18801483-11 2009 These results demonstrate that gliclazide inhibits endothelial LOX-1 expression and prevents LOX-1-mediated proatherogenic effects associated with endothelial dysfunction and plaque rupture. Gliclazide 31-41 oxidized low density lipoprotein receptor 1 Homo sapiens 93-98 19304558-1 2009 The objective of the present investigation was to study the effect of polyethylene glycol 4000 (PEG 4000) on in vitro dissolution of gliclazide from solid dispersions. Gliclazide 133-143 progestagen associated endometrial protein Homo sapiens 96-99 19298459-11 2009 Insulin sensitivity of FFA rose when pioglitazone was added to sulfonylurea (P<0.05), but decreased for gliclazide + metformin (P<0.05). Gliclazide 107-117 insulin Homo sapiens 0-7 19304558-4 2009 PEG was found to be effective in increasing the dissolution of gliclazide in solid dispersions when compared to pure drug. Gliclazide 63-73 progestagen associated endometrial protein Homo sapiens 0-3 18541345-0 2009 The metabolism of CYP2C9 and CYP2C19 for gliclazide by homology modeling and docking study. Gliclazide 41-51 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 18-24 18541345-0 2009 The metabolism of CYP2C9 and CYP2C19 for gliclazide by homology modeling and docking study. Gliclazide 41-51 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 29-36 18541345-5 2009 Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway. Gliclazide 105-115 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 32-39 18541345-5 2009 Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway. Gliclazide 105-115 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 69-75 18541345-5 2009 Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway. Gliclazide 272-282 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 32-39 18541345-5 2009 Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway. Gliclazide 272-282 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 69-75 18541345-6 2009 It is exciting that substrate inhibition phenomenon can be found in metabolisms of CYP2C9 and CYP2C19 for gliclazide in two metabolic pathways. Gliclazide 106-116 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 83-89 18541345-6 2009 It is exciting that substrate inhibition phenomenon can be found in metabolisms of CYP2C9 and CYP2C19 for gliclazide in two metabolic pathways. Gliclazide 106-116 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 94-101 18541345-7 2009 Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19. Gliclazide 0-10 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 195-201 18541345-7 2009 Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19. Gliclazide 0-10 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 206-213 18541345-7 2009 Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19. Gliclazide 105-115 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 195-201 18541345-7 2009 Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19. Gliclazide 105-115 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 206-213 19484971-4 2009 Early insulin and gliclazide treatment normalized PEPCK protein level. Gliclazide 18-28 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 50-55 19484971-7 2009 mRNAs encoding IL-1beta and TNFalpha were increased, which were reduced to normal levels after insulin and gliclazide treatment. Gliclazide 107-117 interleukin 1 beta Rattus norvegicus 15-23 19484971-7 2009 mRNAs encoding IL-1beta and TNFalpha were increased, which were reduced to normal levels after insulin and gliclazide treatment. Gliclazide 107-117 tumor necrosis factor Rattus norvegicus 28-36