Protective effect of treatment with low-dose gliclazide in a model of middle cerebral artery occlusion and reperfusion in rats

Tan, Fang; Li, Hua; Ma, Mengyuan; Yu, Yerong

doi:10.1016/j.brainres.2014.02.044

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…In several different models of moderate-severity ischemic stroke, sulfonylurea therapy favorably modulates CNS injury, neurogenesis, and long-term neurological function. In non-lethal stroke models, glibenclamide or gliclazide reduce lesion volume and cortical damage and improves functional neurological scores [ 17 , 19 , 23 , 24 ]. Glibenclamide treatment after focal ischemia also increases BrdU and NeuN labeling in and around areas of infarction, suggesting enhanced cortical neurogenesis [ 17 ].…”

Section: Ischemic Strokementioning

confidence: 99%

“…In the CNS, glibenclamide primarily inhibits the recently characterized sulfonylurea receptor 1–transient receptor potential melastatin 4 (Sur1–Trpm4) channel [ 15 ] and, in some cases, microglial Sur1–Kir6.2 (K ATP ) channels [ 16 , 17 ]. Several preclinical studies have found glibenclamide to be an effective treatment in rodent models of ischemic stroke [ 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 ], and retrospective studies suggest that being on a sulfonylurea drug and staying on it following ischemic CNS insults significantly improves outcomes [ 25 , 26 ]. The successes of these preclinical experiments [ 27 ] have set the stage for clinical trials examining glibenclamide’s protective effects following ischemic strokes [ 28 , 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

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Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Caffes

Kurland

Gerzanich

et al. 2015

IJMS

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Ischemic and hemorrhagic strokes are associated with severe functional disability and high mortality. Except for recombinant tissue plasminogen activator, therapies targeting the underlying pathophysiology of central nervous system (CNS) ischemia and hemorrhage are strikingly lacking. Sur1-regulated channels play essential roles in necrotic cell death and cerebral edema following ischemic insults, and in neuroinflammation after hemorrhagic injuries. Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1–transient receptor potential melastatin 4 (Sur1–Trpm4) channels and, in some cases, microglial KATP (Sur1–Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Robust preclinical studies have shown that glibenclamide and other sulfonylurea agents reduce infarct volumes, edema and hemorrhagic conversion, and improve outcomes in rodent models of ischemic stroke. Retrospective studies suggest that diabetic patients on sulfonylurea drugs at stroke presentation fare better if they continue on drug. Additional laboratory investigations have implicated Sur1 in the pathophysiology of hemorrhagic CNS insults. In clinically relevant models of subarachnoid hemorrhage, glibenclamide reduces adverse neuroinflammatory and behavioral outcomes. Here, we provide an overview of the preclinical studies of glibenclamide therapy for CNS ischemia and hemorrhage, discuss the available data from clinical investigations, and conclude with promising preclinical results that suggest glibenclamide may be an effective therapeutic option for ischemic and hemorrhagic stroke.

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Section: Ischemic Strokementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Caffes

Kurland

Gerzanich

et al. 2015

IJMS

View full text Add to dashboard Cite

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“…The Biopharmaceutical Classification System (BCS) recognizes gliclazide as a class II therapeutic agent characterized by high permeability and low solubility, and the significant inter-subject variation is attributed to gliclazide erratic absorption, where the gliclazide maximum plasma concentration is achieved within a rather wide range (2–8 h) following oral administration [ 35 , 36 , 37 ]. Beyond its glycaemic effects, gliclazide also has antioxidant, vascular benefits and neuroprotective effects in diabetic peripheral neuropathy [ 36 , 42 , 43 , 44 , 45 ]. Microparticles (microcapsules) are designed to control or target the drug release of their payload to a certain tissue or organ in a preprogramed fashion [ 46 , 47 ].…”

Section: Introductionmentioning

confidence: 99%

Novel Silicone-Grafted Alginate as a Drug Delivery Scaffold: Pharmaceutical Characterization of Gliclazide-Loaded Silicone-Based Composite Microcapsules

et al. 2023

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A novel gliclazide-loaded elastomeric carbohydrate pharmaceutical vehicle was successfully developed. This new siliconized alginate platform showed pseudoplastic rheology with a zeta potential ranging from (−43.8 mV to −75.5 mV). A Buchi-B390 encapsulator was employed to formulate different types of silicone-grafted alginate microcapsules loaded with gliclazide relying on the vibrational ionic gelation technology. The use of tetraethyl orthosilicate (TEOS) to crosslink the silicone elastomer (hydroxy terminated polydimethylsiloxane) of this new platform had improved the gliclazide encapsulation (>92.13% ± 0.76) of the free-flowing composite microcapsules, which showed good mechanical durability (up to 12 h in PBS pH 6.8) and promising results to sustain the drug release.

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Effect of Intermittent Hypoxia on Neuro-functional Recovery Post Brain Ischemia in Mice

et al. 2014

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Intermittent hypoxia was a simulation of a high-altitude environment. Neuro-inflammation post brain ischemia was considered as a vital impact which contributed to cognitive-functional deficit. The isoform of nitric oxide synthase (iNOS) was an inflammation factor secreted by microglias in neuro-inflammation. In this study, we established a high-altitude environment as the hypoxic condition. Twenty mice were selected and randomized into a hypoxia group (n = 10) or a normoxia group (n = 10) post three vessel occlusion-induced brain ischemia. An enhancement of cognitive-functional recovery was presented in the hypoxia group by survival neuron counting and revealed by the Morris water maze test. Meanwhile, a high level of hypoxia-inducable factor 1 (HIF-1) expression associated with a lower expression of iNOS was observed in the border between infarcts and normal tissue of the hippocampus in the hypoxia group. However, these phenomenons were blocked by HIF-1 inhibition. This suggested that the acceleration of cognitive-functional recovery induced by intermittent hypoxia may depend on HIF-1 activating. An imitation of the hypoxic condition with or without HIF-1 inhibition was operated on the BV-2 cell. A high level of HIF-1 expression associated with a lower-level expression of iNOS was performed in the hypoxic condition. These data suggested that intermittent hypoxia can accelerate cognitive function recovery through attenuating neuro-inflammation.

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Protective effect of treatment with low-dose gliclazide in a model of middle cerebral artery occlusion and reperfusion in rats

Cited by 10 publications

References 15 publications

Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Novel Silicone-Grafted Alginate as a Drug Delivery Scaffold: Pharmaceutical Characterization of Gliclazide-Loaded Silicone-Based Composite Microcapsules

Effect of Intermittent Hypoxia on Neuro-functional Recovery Post Brain Ischemia in Mice

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