Glimepiride and glibenclamide have comparable efficacy in treating acute ischemic stroke in mice

Wu, Xiaoqiang; Chang, Yuan; He, Yihua; Lyu, Chenfei; Li, Hua; Zhu, Jing; Liu, Kewei; Y, Hu; Huang, Kaibin; Pan, Suyue

doi:10.1016/j.neuropharm.2019.107845

Cited by 23 publications

(25 citation statements)

References 33 publications

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“…In cerebral ischemia, glibenclamide reduced brain edema, was neuroprotectant [14], and decreased the risk of haemorrhagic transformation after severe ischemia [13]. Recently, in a model oftemporary middle cerebral artery occlusion, low doses of oral glimepiride improved neurological functions, reduced infarct volume and brain edema, restored tight junction protein expression and suppressed inflammatory cytokines [15]. Large meta analysis have recapitulated results on the protective effect of oral sulfonylurea drugs and tried to define their therapeutic potential in stroke [16].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

et al. 2021

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Diabetic retinopathy (DR) remains a major cause of vision loss, due to macular edema, retinal ischemia and death of retinal neurons. We previously demonstrated that acute administration of glibenclamide into the vitreous, or given orally at a non-hypoglycemic dose, protected the structure and the function of the retina in three animal models that each mimic aspects of diabetic retinopathy in humans. In this pilot study, we investigated whether one year of chronic oral glibenclamide, in a non-hypoglycemic regimen (Amglidia®, 0.4 mg/kg, Ammtek/Nordic Pharma, 5 d/week), could alleviate the retinopathy that develops in the Goto-Kakizaki (GK) rat. In vivo, retinal function was assessed by electroretinography (ERG), retinal thickness by optical coherence tomography (OCT) and retinal perfusion by fluorescein and indocyanin green angiographies. The integrity of the retinal pigment epithelium (RPE) that constitutes the outer retinal barrier was evaluated by quantitative analysis of the RPE morphology on flat-mounted fundus ex vivo. Oral glibenclamide did not significantly reduce the Hb1Ac levels but still improved retinal function, as witnessed by the reduction in scotopic implicit times, limited diabetes-induced neuroretinal thickening and the extension of ischemic areas, and it improved the capillary coverage. These results indicate that low doses of oral glibenclamide could still be beneficial for the prevention of type 2 diabetic retinopathy. Whether the retinas ofpatients treated specifically with glibenclamideare less at risk of developing diabetic complications remains to be demonstrated.

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Section: Introductionmentioning

confidence: 99%

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

et al. 2021

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“…To explore the influence of cerebral edema on glymphatic system function, we used genetic deletion of Trpm4 and glibenclamide treatment to reduce cerebral edema ( 5 , 28 ). As expected, glymphatic system function recovered earlier, at 5 post-SE days, after intervention for cerebral edema, which further supports the assumption that a special connection exists between cerebral edema and glymphatic system dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Glibenclamide (Sigma-Aldrich) was dissolved in dimethyl sulfoxide (DMSO) and then diluted in saline, with a final DMSO concentration of 0.05%. Mice in the glibenclamide group received intraperitoneal administration of glibenclamide at a loading dose of 10 mg/kg followed by 1.2 mg/6 hours for 3 days, while mice in the vehicle group received an equal volume of DMSO and saline ( 28 ).…”

Section: Methodsmentioning

confidence: 99%

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Attenuation of cerebral edema facilitates recovery of glymphatic system function after status epilepticus

Liu¹,

Zhu²,

Chang³

et al. 2021

JCI Insight

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Status epilepticus (SE) is a neurological emergency usually accompanied by acute cerebral edema and long-term cognitive impairment, and is characterized by neurodegeneration and aberrant hyperphosphorylated tau protein (p-tau) aggregation. The glia-lymphatic (glymphatic) system plays a central role in facilitating the clearance of metabolic waste from the brain, but its relationship with cerebral edema and cognitive dysfunction after SE is unclear. We hypothesized that cerebral edema after SE might impair glymphatic system function through compression, thus leading to impaired removal of metabolic waste, and ultimately affecting long-term cognitive function. Our results showed that glymphatic system function was temporarily impaired, as evidenced by 2-photon imaging, MRI enhancement, imaging of brain sections, and astrocytic water channel aquaporin 4 (AQP4) protein polarization. The severity of cerebral edema on MRI correlated well with glymphatic system dysfunction within 8 days following SE. Moreover, when cerebral edema was alleviated by glibenclamide treatment or genetic deletion of Trpm4 , post-SE glymphatic system function recovered earlier, along with fewer p-tau–deposited neurons and neuronal degeneration and better cognitive function. These findings suggest that SE-induced cerebral edema may cause glymphatic system dysfunction and render the post-SE brain vulnerable to p-tau aggregation and neurocognitive impairment.

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“…Recent studies demonstrated that sulfonylurea receptor 1 (SUR1) is involved in brain injury in rodent models of stroke (Hussien et al, 2018). The SUR drugs glibenclamide and glimepiride have neuroprotective effects (Ortega et al, 2013;Wang et al, 2019) and ameliorate cerebral stroke, spinal cord injury, premature encephalopathy, and TBI (Tosun et al, 2013). The neuroprotective effect of SUR agents is not fully understood but glibenclamide blocks SUR1, a regulatory subunit of the microglial K ATP channel.…”

Section: Sulfonylureamentioning

confidence: 99%

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

Poupon-Bejuit

Rocha‐Ferreira

Thornton

et al. 2020

Front. Cell. Neurosci.

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Glimepiride and glibenclamide have comparable efficacy in treating acute ischemic stroke in mice

Cited by 23 publications

References 33 publications

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

Attenuation of cerebral edema facilitates recovery of glymphatic system function after status epilepticus

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

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