PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20567501-8 2010 High glucose disturbed BK-induced NO generation by MNC-derived cultured angiogenic cells. Glucose 5-12 kininogen 1 Homo sapiens 23-25 20128797-9 2010 The effect of oligonol on BK dephosphorylation under high glucose was mimicked by protein kinase C (PKC) epsilon-neutralizing peptides. Glucose 58-65 kininogen 1 Homo sapiens 26-28 19923143-2 2010 METHODS AND RESULTS: High-glucose (HG) super-induced interleukin (IL)-6, CCL-2, transforming growth factor (TGF)-beta, vascular endothelial growth factor (VEGF) and B(2)K receptor (B(2)KR) mRNA in cultured proximal tubular epithelial cells (PTEC), whereas bradykinin (BK) upregulated IL-6, CCL-2 and TGF-beta mRNA. Glucose 26-33 kininogen 1 Homo sapiens 256-266 19923143-2 2010 METHODS AND RESULTS: High-glucose (HG) super-induced interleukin (IL)-6, CCL-2, transforming growth factor (TGF)-beta, vascular endothelial growth factor (VEGF) and B(2)K receptor (B(2)KR) mRNA in cultured proximal tubular epithelial cells (PTEC), whereas bradykinin (BK) upregulated IL-6, CCL-2 and TGF-beta mRNA. Glucose 26-33 kininogen 1 Homo sapiens 268-270 20128797-11 2010 Oligonol also prevented high glucose-induced attenuation of BK-stimulated NO production. Glucose 29-36 kininogen 1 Homo sapiens 60-62 19841473-10 2010 Bradykinin increased net glucose extraction (from -80 +/- 23 to -320 +/- 97 microg/min/100 ml at 200 ng/min bradykinin, P = 0.02), and L-NMMA (-143 +/- 50 microg/min/100 ml at 200 ng/min, P = 0.045) attenuated this effect. Glucose 25-32 kininogen 1 Homo sapiens 0-10 20128797-4 2010 KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells. Glucose 30-37 kininogen 1 Homo sapiens 141-151 20128797-4 2010 KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells. Glucose 30-37 kininogen 1 Homo sapiens 153-155 19841473-0 2010 Endogenous nitric oxide contributes to bradykinin-stimulated glucose uptake but attenuates vascular tissue-type plasminogen activator release. Glucose 61-68 kininogen 1 Homo sapiens 39-49 19841473-1 2010 Bradykinin causes vasodilation, stimulates tissue-type plasminogen activator (t-PA) release and, in rodents, increases muscle glucose uptake. Glucose 126-133 kininogen 1 Homo sapiens 0-10 18037911-6 2008 A 2-h incubation of high glucose impaired bradykinin-induced relaxation of subcutaneous vessels whilst, in contrast, the relaxation generated by bradykinin in mesenteric vessels was enhanced at the same time point. Glucose 25-32 kininogen 1 Homo sapiens 42-52 18037911-6 2008 A 2-h incubation of high glucose impaired bradykinin-induced relaxation of subcutaneous vessels whilst, in contrast, the relaxation generated by bradykinin in mesenteric vessels was enhanced at the same time point. Glucose 25-32 kininogen 1 Homo sapiens 145-155 16313901-7 2006 Thus, dihydropyridines and angiotensin converting enzyme inhibitors limit high glucose-induced superoxide formation and improve NO bioavailability in human endothelial cells, in part via bradykinin and p38MAPK. Glucose 79-86 kininogen 1 Homo sapiens 187-197 10973143-0 2000 Bradykinin enhances membrane electrical activity of pancreatic beta cells in the presence of low glucose concentrations. Glucose 97-104 kininogen 1 Homo sapiens 0-10 16340662-5 2006 For example, its potential for endothelium-dependent vasodilation, and for improvement of glucose transport and utilization, make bradykinin an important mediator for reducing the consequences of diabetes-related oxidative stress on both the myocardium and vessels. Glucose 90-97 kininogen 1 Homo sapiens 130-140 14871030-8 2003 These findings suggest that high glucose inhibits human aortic endothelial cell proliferation and that the angiotensin-converting enzyme inhibitor temocaprilat inhibits high glucose-mediated suppression of human aortic endothelial cell proliferation, possibly through suppression of protein kinase C, bradykinin B2 receptors and oxidative stress. Glucose 174-181 kininogen 1 Homo sapiens 301-311 12767053-6 2003 One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport. Glucose 155-162 kininogen 1 Homo sapiens 37-47 12767053-6 2003 One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport. Glucose 155-162 kininogen 1 Homo sapiens 64-74 12767053-10 2003 These data support the concept that ACE inhibitors can beneficially modulate glucose control in insulin-resistant states, possibly through a NO-dependent effect of bradykinin and/or antagonism of ATII action on skeletal muscle. Glucose 77-84 kininogen 1 Homo sapiens 164-174 11181410-3 2001 Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187. Glucose 70-77 kininogen 1 Homo sapiens 234-244 10973143-9 2000 Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion. Glucose 103-110 kininogen 1 Homo sapiens 146-148 10973143-9 2000 Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion. Glucose 178-185 kininogen 1 Homo sapiens 58-60 10973143-9 2000 Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion. Glucose 178-185 kininogen 1 Homo sapiens 146-148 10893317-6 2000 Incubation with a high-glucose concentration for 7 days significantly downregulated, whereas insulin significantly upregulated, basal and bradykinin-stimulated NO production and eNOS expression in cultured endothelial cells. Glucose 23-30 kininogen 1 Homo sapiens 138-148 10948084-1 2000 We investigated the effect of angiotensin-converting enzyme inhibitors on glucose uptake regulation as well as the effect of bradykinin (BK) on glucose uptake and its regulation by using inhibitors of phospholipase C, BK B2 receptor, protein kinase C, phosphatidylinositol 3-kinase, tyrosine kinase, and intracellular Ca(2+). Glucose 144-151 kininogen 1 Homo sapiens 125-135 10948084-1 2000 We investigated the effect of angiotensin-converting enzyme inhibitors on glucose uptake regulation as well as the effect of bradykinin (BK) on glucose uptake and its regulation by using inhibitors of phospholipase C, BK B2 receptor, protein kinase C, phosphatidylinositol 3-kinase, tyrosine kinase, and intracellular Ca(2+). Glucose 144-151 kininogen 1 Homo sapiens 137-139 10948084-6 2000 In the presence of 1 nmol/L of insulin, exposure to 10 micromol/L BK stimulated glucose uptake from 89.2+/-8.1 to 171.6+/-10.1 pmol/h per mg protein. Glucose 80-87 kininogen 1 Homo sapiens 66-68 10948084-8 2000 One hundred nanomoles per liter of tyrphostin A-23 and genistein, which are tyrosine kinase inhibitors, significantly decreased the BK-induced glucose uptake from 142.0+/-8.4 to 87.6+/-6. Glucose 143-150 kininogen 1 Homo sapiens 132-134 10948084-10 2000 BK-induced glucose uptake was inhibited significantly by 10 micromol/L U73122 (a phospholipase C antagonist) from 142.0+/-8.4 to 95.7+/-9.5 pmol/h per mg protein. Glucose 11-18 kininogen 1 Homo sapiens 0-2 10948084-11 2000 One and 20 micromol/L of TMB-8 (an intracellular calcium antagonist) significantly decreased BK-induced glucose uptake from 142.0+/-8.4 to 108.0+/-9.6 and 100.8+/-11.4 pmol/h per mg protein. Glucose 104-111 kininogen 1 Homo sapiens 93-95 10948084-13 2000 BK-stimulated glucose uptake is related to phospholipase C, tyrosine kinase, and an increase in intracellular calcium. Glucose 14-21 kininogen 1 Homo sapiens 0-2 8826976-4 1996 Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%). Glucose 47-56 kininogen 1 Homo sapiens 183-193 10910005-8 2000 Moreover, the exercise-induced increase in bradykinin may be involved in modulating exercise-induced glucose transport through an increase of GLUT-4 translocation, as well as enhancement of the insulin signal pathway, during the postexercise period in skeletal muscle, resulting in a decrease of blood glucose. Glucose 101-108 kininogen 1 Homo sapiens 43-53 10714896-5 2000 During reverse microdialysis with bradykinin and enalaprilate a significant decrease in arterial-interstitial-gradient for glucose (AIG(glu)) was observed (from 1.49 +/- 0.08 mM to 0.12 +/- 0.63 mM (p = 0.018) for bradykinin and from 1.5 +/- 0.07 mM to 0.24 +/- 0.67 mM (p = 0.043) for enalaprilate). Glucose 123-130 kininogen 1 Homo sapiens 34-44 10714896-7 2000 The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018). Glucose 30-37 kininogen 1 Homo sapiens 55-65 10714896-7 2000 The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018). Glucose 30-37 kininogen 1 Homo sapiens 201-211 10910005-2 2000 In this study, we evaluated the involvement of bradykinin in exercise-induced glucose uptake in humans and rats. Glucose 78-85 kininogen 1 Homo sapiens 47-57 8826976-1 1996 Pretreatment of porcine aortic endothelial cells with high D-glucose results in enhanced endothelium-derived relaxing factor (EDRF) formation (39%) due to increased endothelial Ca2+ release (57%) and Ca2+ entry (97%) to bradykinin. Glucose 59-68 kininogen 1 Homo sapiens 220-230 8826976-4 1996 Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%). Glucose 126-135 kininogen 1 Homo sapiens 183-193 8826976-8 1996 Like high D-glucose, pretreatment with the O2(-)-generating system, xanthine oxidase/hypoxanthine, elevated bradykinin-stimulated Ca2+ release (+10%), Ca2+ entry (+75%), and EDRF (+73%). Glucose 10-19 kininogen 1 Homo sapiens 108-118 8039606-3 1994 Pretreatment with high D-glucose (44 vs. 5 mM) enhanced release of intracellular Ca2+ by bradykinin as a result of a 2.0-fold increased formation of inositol 1,4,5-trisphosphate. Glucose 23-32 kininogen 1 Homo sapiens 89-99 8601640-8 1996 Glucose extraction by skeletal muscle was 44% higher in the control (2.6+/-0.2 mmol/liter) than the bradykinin-infused leg (1.8+/-0.2 mmol/liter, P<0.01). Glucose 0-7 kininogen 1 Homo sapiens 100-110 8601640-9 1996 When bradykinin was infused in the basal state, flow was 98% higher in the bradykinin-infused (58+/-12 ml/kg muscle x min) than the control leg (28+/-6 ml/kg muscle x min, P<0.01) but rates of muscle glucose uptake were identical in both legs (10.1+/-0.9 vs. 10.6+/-0.8 micromol/kg x min). Glucose 203-210 kininogen 1 Homo sapiens 5-15 8601640-9 1996 When bradykinin was infused in the basal state, flow was 98% higher in the bradykinin-infused (58+/-12 ml/kg muscle x min) than the control leg (28+/-6 ml/kg muscle x min, P<0.01) but rates of muscle glucose uptake were identical in both legs (10.1+/-0.9 vs. 10.6+/-0.8 micromol/kg x min). Glucose 203-210 kininogen 1 Homo sapiens 75-85 7626667-4 1995 Among the factors of the second group that were tested (heparin, ADP, histamine, bradykinin), histamine was found to stimulate glucose transport in CEC by 10-50%. Glucose 127-134 kininogen 1 Homo sapiens 81-91 8039606-5 1994 In high D-glucose preincubated cells, stimulation with bradykinin significantly increased transplasmalemmal 45Ca2+ flux (3.2-fold) and caused a 2.0-fold increase in permeability to Mn2+, a surrogate for endothelial plasma membrane Ca2+ channels. Glucose 8-17 kininogen 1 Homo sapiens 55-65 34557552-0 2021 Bradykinin Protects Human Endothelial Progenitor Cells from High-Glucose-Induced Senescence through B2 Receptor-Mediated Activation of the Akt/eNOS Signalling Pathway. Glucose 65-72 kininogen 1 Homo sapiens 0-10 8177372-5 1994 Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose. Glucose 66-73 kininogen 1 Homo sapiens 196-206 8177372-8 1994 myo-Inositol metabolism and content and bradykinin-stimulated phosphatidylinositol synthesis were also maintained when media containing 30 mM glucose, galactose, or mannose was supplemented with 250 microM myo-inositol. Glucose 142-149 kininogen 1 Homo sapiens 40-50 8499491-1 1993 Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3. Glucose 103-110 kininogen 1 Homo sapiens 138-148 34580391-9 2021 Four proteins with vascular effects were identified (angiotensinogen, kininogen-1, alpha-2-HS-glycoprotein and hemoglobin subunit beta), all upregulated after glucose provocation compared to baseline in all three compartments. Glucose 159-166 kininogen 1 Homo sapiens 70-81 34580391-10 2021 Glucose provocation is known to cause insulin-induced vasodilation through the nitric oxide pathway, and this study indicates that this is facilitated through the interactions of the RAS (angiotensinogen) and kallikrein-kinin (kininogen-1) systems. Glucose 0-7 kininogen 1 Homo sapiens 227-238 8167144-1 1994 Bradykinin (BK), a peptide released during inflammatory response, has been investigated for its ability to regulate glucose metabolism in human fibroblasts. Glucose 116-123 kininogen 1 Homo sapiens 0-10 8167144-1 1994 Bradykinin (BK), a peptide released during inflammatory response, has been investigated for its ability to regulate glucose metabolism in human fibroblasts. Glucose 116-123 kininogen 1 Homo sapiens 12-14 8167144-3 1994 The strict relationship between the glycolytic rate and the levels of fructose 2,6-bisphosphate (Fru-2,6-P2) strongly suggests that the metabolite plays a key role in the regulation of glucose metabolism by bradykinin. Glucose 185-192 kininogen 1 Homo sapiens 207-217 1845801-1 1991 The possible role of cAMP and/or arachidonic acid (and metabolites) in the stimulation of glucose transport elicited by bradykinin in Swiss 3T3 fibroblasts was investigated with particular attention to the part of this effect inhibitable by pertussis toxin. Glucose 90-97 kininogen 1 Homo sapiens 120-130 1845801-3 1991 In contrast, arachidonic acid, which is released by the cells exposed to bradykinin, was able to markedly stimulate glucose transport, however, only at relatively high concentrations (EC50 approximately 30 microM). Glucose 116-123 kininogen 1 Homo sapiens 73-83 1845801-5 1991 Neither of the last treatments affected the glucose transport activated by bradykinin to a great extent. Glucose 44-51 kininogen 1 Homo sapiens 75-85 1845801-6 1991 Moreover, the bradykinin-induced arachidonic acid release was unaffected by pertussis toxin and markedly inhibited by two treatments ineffective on glucose transport, the blockade of [Ca2+]i increases elicited by the peptide and the administration of the phospholipase A2 blocker, quinacrine. Glucose 148-155 kininogen 1 Homo sapiens 14-24 1845801-7 1991 These results exclude that glucose transport stimulation by bradykinin is mediated intracellularly via arachidonic acid release. Glucose 27-34 kininogen 1 Homo sapiens 60-70 1967418-0 1990 Effect of low-dose bradykinin on glucose metabolism and nitrogen balance in surgical patients. Glucose 33-40 kininogen 1 Homo sapiens 19-29 2570343-1 1989 The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers. Glucose 93-100 kininogen 1 Homo sapiens 25-35 2570343-1 1989 The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers. Glucose 93-100 kininogen 1 Homo sapiens 37-39 3143746-6 1988 Increased release of 15-HETE in the presence of elevated glucose in response to A23187, bradykinin, and thrombin was confirmed by RIA. Glucose 57-64 kininogen 1 Homo sapiens 88-98 3123876-0 1988 Low-dose bradykinin infusion reduces endogenous glucose production in surgical patients. Glucose 48-55 kininogen 1 Homo sapiens 9-19 3123876-1 1988 The systemic effect of low-dose bradykinin infusion on total body glucose production and arterial substrate concentrations was examined during D5W infusion (1.0 mg/kg/min) in five normal-weight postsurgical subjects and compared to the response in four saline infused control patients, well matched for age, weight, and degree of postoperative stress. Glucose 66-73 kininogen 1 Homo sapiens 32-42 3123876-1 1988 The systemic effect of low-dose bradykinin infusion on total body glucose production and arterial substrate concentrations was examined during D5W infusion (1.0 mg/kg/min) in five normal-weight postsurgical subjects and compared to the response in four saline infused control patients, well matched for age, weight, and degree of postoperative stress. Glucose 143-146 kininogen 1 Homo sapiens 32-42 3123876-4 1988 After 75 minutes of bradykinin, endogenous glucose production was significantly reduced as compared to basal values (1.63 +/- 0.21 mg/kg/min, P less than .0125 v 2.20 +/- 0.35 basal). Glucose 43-50 kininogen 1 Homo sapiens 20-30 3123876-9 1988 These results demonstrate the inhibitory effect of low-dose bradykinin on glucose production in surgically stressed patients. Glucose 74-81 kininogen 1 Homo sapiens 60-70 3121350-1 1987 Bradykinin infusion has been shown to improve glucose metabolism in non-insulin-dependent diabetic subjects (NIDD). Glucose 46-53 kininogen 1 Homo sapiens 0-10 3322322-2 1987 Also, bradykinin, a vasoactive product of kallikrein"s action upon kininogen substrates, increases glucose uptake when infused into the human forearm. Glucose 99-106 kininogen 1 Homo sapiens 6-16 3322322-8 1987 These studies suggest that the previously observed in vivo effects of bradykinin on peripheral glucose uptake are probably mediated by changes in tissue perfusion rather than direct kinin effects on skeletal muscle, and that the putative membrane serine protease involved in the insulin-effector system is not tissue kallikrein. Glucose 95-102 kininogen 1 Homo sapiens 70-80 3121350-2 1987 Therefore, we tested the following hypothesis: inhibition of Kininase II, the bradykinin (BK) degrading enzyme, by captopril may also improve glucose metabolism in NIDD. Glucose 142-149 kininogen 1 Homo sapiens 78-88 3518739-1 1986 The effect of bradykinin on insulin-stimulated glucose metabolism was studied in 5 operated patients using the euglycemic insulin clamp technique and the forearm catheter technique. Glucose 47-54 kininogen 1 Homo sapiens 14-24 639619-2 1978 With bradykinin a normalization of the postoperative decreased assimilation of glucose was found. Glucose 79-86 kininogen 1 Homo sapiens 5-15 3022274-5 1986 In NIDD as well as in POP subjects, impaired peripheral insulin responsiveness, as evaluated by whole body glucose consumption, was improved up to 50% by application of BK (80 micrograms/h i.v.) Glucose 107-114 kininogen 1 Homo sapiens 169-171 6618444-0 1983 Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man. Glucose 63-70 kininogen 1 Homo sapiens 25-35 6618444-3 1983 At lower bradykinin concentrations (2.5-25 ng/min), muscular glucose uptake was raised parallel to the increased blood flow from basal 0.71 +/- 0.30 to 2.93 +/- 0.50 mumol/(100 g X min). Glucose 61-68 kininogen 1 Homo sapiens 9-19 495337-0 1979 Improvement of glucose assimilation and protein degradation by bradykinin in maturity onset diabetics and in surgical patients. Glucose 15-22 kininogen 1 Homo sapiens 63-73 713429-0 1978 [Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author"s transl)]. Glucose 29-36 kininogen 1 Homo sapiens 50-60 713429-4 1978 In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers. Glucose 39-46 kininogen 1 Homo sapiens 27-29 713429-6 1978 In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21). Glucose 48-55 kininogen 1 Homo sapiens 36-38 6341768-1 1983 It has recently been observed that administration of bradykinin to diabetic patients improves peripheral glucose utilization. Glucose 105-112 kininogen 1 Homo sapiens 53-63 6344581-0 1983 Effect of bradykinin upon impaired glucose assimilation in patients with chronic renal failure and in patients on regular haemodialysis. Glucose 35-42 kininogen 1 Homo sapiens 10-20 6449838-2 1980 It is most likely that the utilization of glucose is enhanced directly within the energy metabolizing cell itself but not indirectly by way of an insulin release in the pancreatic islets, since the in vitro studies on isolated islets of Langerhans did not reveal any effect of bradykinin on insulin secretion or insulin release. Glucose 42-49 kininogen 1 Homo sapiens 277-287 31119778-0 2019 Bradykinin protects cardiac c-kit positive cells from high-glucose-induced senescence through B2 receptor signaling pathway. Glucose 59-66 kininogen 1 Homo sapiens 0-10 870748-0 1977 [Effect of bradykinin on muscular glucose uptake in man (author"s transl)]. Glucose 34-41 kininogen 1 Homo sapiens 11-21 870748-1 1977 Glucose metabolism of the human forearm was studied in 4 healthy volunteers by monitoring arterial deepvenous glucose concentration differences and by the determination of muscle blood flow, using 133xenon as a tracer, during 25 min intra-brachial-arterial infusion of bradykinin (13.3 ng per min). Glucose 0-7 kininogen 1 Homo sapiens 269-279 31119778-4 2019 However, whether bradykinin prevents cardiac c-kit positive cells from high-glucose-induced senescence is unknown. Glucose 76-83 kininogen 1 Homo sapiens 17-27 31119778-6 2019 Bradykinin B2 receptor (B2R) expression was declined by glucose-induced senescence. Glucose 56-63 kininogen 1 Homo sapiens 0-10 31119778-11 2019 Western blot showed that bradykinin leads to AKT and mammalian target of rapamycin (mTOR) phosphorylation and decreased levels of P53 and P16 when compared with glucose treatment alone. Glucose 161-168 kininogen 1 Homo sapiens 25-35 31119778-14 2019 In conclusion, bradykinin prevents the glucose-induced premature senescence of cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways. Glucose 39-46 kininogen 1 Homo sapiens 15-25 31298304-12 2019 BK significantly inhibited the proliferation of hRECs cells, enhanced Caspase-3 activity, decreased the content of LDH and ROS, increased SOD activity, reduced the expressions of HMGB-1 and NF-kappaB protein, attenuated the expression of VEGF, and restrained the secretion of TNF-alpha and IL-1beta compared with high glucose group (p < 0.05). Glucose 318-325 kininogen 1 Homo sapiens 0-2 22652200-8 2012 In cultured ASM cells, incubation with high glucose concentrations significantly (P < 0.05) enhanced bradykinin-induced intracellular calcium flux and the levels of pMYPT1, which were inhibited by Y27632 (P < 0.05). Glucose 44-51 kininogen 1 Homo sapiens 104-114 22523335-0 2012 The interaction of blood flow, insulin, and bradykinin in regulating glucose uptake in lower-body adipose tissue in lean and obese subjects. Glucose 69-76 kininogen 1 Homo sapiens 44-54 22523335-2 2012 Insulin and bradykinin are meal-stimulated promoters of AT blood flow and glucose metabolism. Glucose 74-81 kininogen 1 Homo sapiens 12-22 22523335-9 2012 In the lean group, bradykinin increased insulin-mediated AT glucose uptake from 8.6 +- 1.6 to 12.3 +- 2.4 mumol/min kg (P = 0.038). Glucose 60-67 kininogen 1 Homo sapiens 19-29