The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
S. J. Walter - One of the best experts on this subject based on the ideXlab platform.
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The natriuretic effect of Glibenclamide: evidence for a non-luminal site of action.
Pflugers Archiv : European journal of physiology, 2002Co-Authors: Matthew A. Bailey, David G. Shirley, Christopher J. Stocking, Jonathan M. Slater, S. J. WalterAbstract:Inhibition of sodium reabsorption in the loop of Henle (LOH) contributes to the natriuretic effect of systemically administered Glibenclamide. Although it has been suggested that the underlying mechanism involves inhibition of low-conductance potassium channels in the apical membrane of the thick ascending limb, these channels are relatively insensitive to Glibenclamide (Ki ~200 µM). In the present study we used capillary electrophoresis techniques to determine plasma and tubular fluid concentrations of Glibenclamide in anaesthetised, Glibenclamide-infused rats during maximal natriuresis. The plasma Glibenclamide concentration was 158±29 µM, whereas that in the tubular fluid entering the LOH was below detectable limits (10 µM). In additional experiments, rats were infused intravenously with either Glibenclamide or vehicle alone, while the LOH was perfused with a standard, Glibenclamide-free solution. Loop sodium reabsorption (JNa) was significantly reduced in the rats receiving the drug (vehicle: JNa 1.65±0.05 nmol/min, n=23; Glibenclamide: JNa 1.34±0.07 nmol/min, n=36; P
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Renal effects of Glibenclamide: a micropuncture study.
The Journal of pharmacology and experimental therapeutics, 1998Co-Authors: Matthew A. Bailey, S. J. WalterAbstract:The renal effects of Glibenclamide were investigated using free flow micropuncture techniques in anesthetized Sprague-Dawley rats. Intravenous infusion of the drug (3 mg/hr) evoked a natriuresis and diuresis; potassium excretion remained unchanged. Fractional reabsorption in the proximal convoluted tubule in Glibenclamide-infused rats did not differ significantly from that in control animals, although the late proximal tubular fluid to plasma concentration ratio for potassium was reduced. Fractional sodium delivery to the early distal tubule was elevated, while the fractional deliveries of water and potassium to this nephron site were unaffected. We conclude that Glibenclamide impairs sodium reabsorption in one or more of the nephron segments that comprise the loop of Henle. These results are consistent with the hypothesis that the natriuresis resulting from Glibenclamide administration is a consequence of blockade of potassium channels in the apical membrane of the thick ascending limb of Henle’s loop. The data suggest that Glibenclamide may additionally inhibit a small secretory potassium flux in the proximal tubule.
Sunil Gurtu - One of the best experts on this subject based on the ideXlab platform.
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Glibenclamide or metformin combined with honey improves glycemic control in streptozotocin induced diabetic rats
International Journal of Biological Sciences, 2011Co-Authors: Omotayo O Erejuwa, Siti Amrah Sulaiman, Mohd Ab S Wahab, K N S Sirajudeen, Salzihan Md Salleh, Sunil GurtuAbstract:Diabetes mellitus is associated with deterioration of glycemic control and progressive metabolic derangements. This study investigated the effect of honey as an adjunct to Glibenclamide or metformin on glycemic control in streptozotocin-induced diabetic rats. Diabetes was induced in rats by streptozotocin. The diabetic rats were randomized into six groups and administered distilled water, honey, Glibenclamide, Glibenclamide and honey, metformin or metformin and honey. The animals were treated orally once daily for four weeks. The diabetic control rats showed hypoinsulinemia (0.27 ± 0.01 ng/ml), hyperglycemia (22.4 ± 1.0 mmol/L) and increased fructosamine (360.0 ± 15.6 µmol/L). Honey significantly increased insulin (0.41 ± 0.06 ng/ml), decreased hyperglycemia (12.3 ± 3.1 mmol/L) and fructosamine (304.5 ± 10.1 µmol/L). Although Glibenclamide or metformin alone significantly (p < 0.05) reduced hyperglycemia, Glibenclamide or metformin combined with honey produced significantly much lower blood glucose (8.8 ± 2.9 or 9.9 ± 3.3 mmol/L, respectively) compared to Glibenclamide or metformin alone (13.9 ± 3.4 or 13.2 ± 2.9 mmol/L, respectively). Similarly, Glibenclamide or metformin combined with honey produced significantly (p < 0.05) lower fructosamine levels (301.3 ± 19.5 or 285.8 ± 22.6 µmol/L, respectively) whereas Glibenclamide or metformin alone did not decrease fructosamine (330.0 ± 29.9 or 314.6 ± 17.9 µmol/L, respectively). Besides, these drugs or their combination with honey increased insulin levels. Glibenclamide or metformin combined with honey also significantly reduced the elevated levels of creatinine, bilirubin, triglycerides, and VLDL cholesterol. These results indicate that combination of Glibenclamide or metformin with honey improves glycemic control, and provides additional metabolic benefits, not achieved with either Glibenclamide or metformin alone.
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comparison of antioxidant effects of honey Glibenclamide metformin and their combinations in the kidneys of streptozotocin induced diabetic rats
International Journal of Molecular Sciences, 2011Co-Authors: Omotayo O Erejuwa, Siti Amrah Sulaiman, Mohd Ab S Wahab, Salzihan Md Salleh, Sirajudeen Kuttulebbai Nainamohammed Salam, Sunil GurtuAbstract:Hyperglycemia-induced increase in oxidative stress is implicated in diabetic complications. This study investigated the effect of metformin and/or Glibenclamide in combination with honey on antioxidant enzymes and oxidative stress markers in the kidneys of streptozotocin (60 mg/kg; intraperitoneal)-induced diabetic rats. Diabetic rats were randomized into eight groups of five to seven rats and received distilled water (0.5 mL); honey (1.0 g/kg); metformin (100 mg/kg); metformin (100 mg/kg) and honey (1.0 g/kg); Glibenclamide (0.6 mg/kg); Glibenclamide (0.6 mg/kg) and honey (1.0 g/kg); metformin (100 mg/kg) and Glibenclamide (0.6 mg/kg); or metformin (100 mg/kg), Glibenclamide (0.6 mg/kg) and honey (1.0 g/kg) orally once daily for four weeks. Malondialdehyde (MDA) levels, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were significantly elevated while catalase (CAT) activity, total antioxidant status (TAS), reduced glutathione (GSH), and GSH:oxidized glutathione (GSSG) ratio was significantly reduced in the diabetic kidneys. CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or Glibenclamide. In contrast, metformin or Glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH. These results suggest that combination of honey with metformin or Glibenclamide might offer additional antioxidant effect to these drugs. This might reduce oxidative stress-mediated damage in diabetic kidneys.
Oliver W Sakowitz - One of the best experts on this subject based on the ideXlab platform.
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Glibenclamide reduces secondary brain damage after experimental traumatic brain injury
Neuroscience, 2014Co-Authors: Klaus Zweckberger, Katharina A M Hackenberg, Carla S Jung, Daniel N Hertle, Karl L Kiening, Andreas Unterberg, Oliver W SakowitzAbstract:Following traumatic brain injury (TBI) SUR1-regulated NCCa-ATP (SUR1/TRPM4) channels are transcriptionally up-regulated in ischemic astrocytes, neurons, and capillaries. ATP depletion results in depolarization and opening of the channel leading to cytotoxic edema. Glibenclamide is an inhibitor of SUR-1 and, thus, might prevent cytotoxic edema and secondary brain damage following TBI. Anesthetized adult Sprague-Dawley rats underwent parietal craniotomy and were subjected to controlled cortical impact injury (CCI). Glibenclamide was administered as a bolus injection 15min after CCI injury and continuously via osmotic pumps throughout 7days. In an acute trial (180min) mean arterial blood pressure, heart rate, intracranial pressure, encephalographic activity, and cerebral metabolism were monitored. Brain water content was assessed gravimetrically 24h after CCI injury and contusion volumes were measured by MRI scanning technique at 8h, 24h, 72h, and 7d post injury. Throughout the entire time of observation neurological function was quantified using the "beam-walking" test. Glibenclamide-treated animals showed a significant reduction in the development of brain tissue water content(80.47%±0.37% (Glibenclamide) vs. 80.83%±0.44% (control); p<0.05; n=14). Contusion sizes increased continuously within 72h following CCI injury, but Glibenclamide-treated animals had significantly smaller volumes at any time-points, like 172.53±38.74mm(3) (Glibenclamide) vs. 299.20±64.02mm(3) (control) (p<0.01; n=10; 24h) or 211.10±41.03mm(3) (Glibenclamide) vs. 309.76±19.45mm(3) (control) (p<0.05; n=10; 72h), respectively. An effect on acute parameters, however, could not be detected, most likely because of the up-regulation of the channel within 3-6h after injury. Furthermore, there was no significant effect on motor function assessed by the beam-walking test throughout 7days. In accordance to these results and the available literature, Glibenclamide seems to have promising potency in the treatment of TBI.
Hengli Tian - One of the best experts on this subject based on the ideXlab platform.
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Glibenclamide attenuates blood brain barrier disruption in adult mice after traumatic brain injury
Journal of Neurotrauma, 2017Co-Authors: Fang Yuan, Yingliang Liu, Jun Ding, Hengli TianAbstract:Abstract Glibenclamide is a hypoglycemic drug that is widely used for the treatment of diabetes mellitus type 2 (DM II), but it also plays a protective role following injury to the central nervous system (CNS). However, the precise mechanisms underlying its neuroprotective actions remain to be elucidated. Therefore, the present study evaluated the effects of Glibenclamide on the blood–brain barrier (BBB) in a mouse model of traumatic brain injury (TBI). In the present study, 86 adult male C57BL/6 mice were exposed to a controlled cortical impact (CCI) injury and then received Glibenclamide (10 μg) for 3 days. Tight junction (TJ) protein levels, BBB permeability, and tissue hemoglobin levels were evaluated following the CCI injury. Additionally, a biaxial stretch injury was applied to cell cultures of bEnd.3 cells using the Cell Injury Controller II system to explore the mechanisms by which Glibenclamide inhibits apoptosis-signaling pathways. Compared with the control group, Glibenclamide-treated mice exhi...
Matthew A. Bailey - One of the best experts on this subject based on the ideXlab platform.
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The natriuretic effect of Glibenclamide: evidence for a non-luminal site of action.
Pflugers Archiv : European journal of physiology, 2002Co-Authors: Matthew A. Bailey, David G. Shirley, Christopher J. Stocking, Jonathan M. Slater, S. J. WalterAbstract:Inhibition of sodium reabsorption in the loop of Henle (LOH) contributes to the natriuretic effect of systemically administered Glibenclamide. Although it has been suggested that the underlying mechanism involves inhibition of low-conductance potassium channels in the apical membrane of the thick ascending limb, these channels are relatively insensitive to Glibenclamide (Ki ~200 µM). In the present study we used capillary electrophoresis techniques to determine plasma and tubular fluid concentrations of Glibenclamide in anaesthetised, Glibenclamide-infused rats during maximal natriuresis. The plasma Glibenclamide concentration was 158±29 µM, whereas that in the tubular fluid entering the LOH was below detectable limits (10 µM). In additional experiments, rats were infused intravenously with either Glibenclamide or vehicle alone, while the LOH was perfused with a standard, Glibenclamide-free solution. Loop sodium reabsorption (JNa) was significantly reduced in the rats receiving the drug (vehicle: JNa 1.65±0.05 nmol/min, n=23; Glibenclamide: JNa 1.34±0.07 nmol/min, n=36; P
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Renal effects of Glibenclamide: a micropuncture study.
The Journal of pharmacology and experimental therapeutics, 1998Co-Authors: Matthew A. Bailey, S. J. WalterAbstract:The renal effects of Glibenclamide were investigated using free flow micropuncture techniques in anesthetized Sprague-Dawley rats. Intravenous infusion of the drug (3 mg/hr) evoked a natriuresis and diuresis; potassium excretion remained unchanged. Fractional reabsorption in the proximal convoluted tubule in Glibenclamide-infused rats did not differ significantly from that in control animals, although the late proximal tubular fluid to plasma concentration ratio for potassium was reduced. Fractional sodium delivery to the early distal tubule was elevated, while the fractional deliveries of water and potassium to this nephron site were unaffected. We conclude that Glibenclamide impairs sodium reabsorption in one or more of the nephron segments that comprise the loop of Henle. These results are consistent with the hypothesis that the natriuresis resulting from Glibenclamide administration is a consequence of blockade of potassium channels in the apical membrane of the thick ascending limb of Henle’s loop. The data suggest that Glibenclamide may additionally inhibit a small secretory potassium flux in the proximal tubule.