Purpose: To investigate the effect of remimazolam (Re) on oxygen glucose deprivation/reoxygenation (OGD/R) model, and to elucidate the mechanism of action. Methods: The neuron cells were treated with OGD/R. MTT assays were performed to confirm The effect of Re on cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while flow cytometry (FCM) assay was conducted to determine the apoptosis of OGD/R cells. Immunostaining assay and enzyme-linked immunosorbent assay (ELISA) were used to evaluate the effects of Re on mitochondria damage, while immunoblot assay was used unravel its mechanism of action. Results: Remimazolam (Re) significantly enhanced OGD/R-induced neuronal survival (p < 0.05). In addition, it significantly inhibited OGD/R-induced neuronal apoptosis, and OGD/R-induced neuron mitochondrial damage. Furthermore, it suppressed MAPK pathway in OGD/R-induced neuron, thus protecting the neuronal cells from OGD/R-induced damage (p < 0.05). Conclusion: Remimazolam protects neuronal cells from OGD/R-induced damage by mediating MAPK pathway. Therefore, it is a potential drug for the management of Ischemia-reperfusion injury (IRI). However, in vivo studies are required to buttress this.
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Wan et al. (2024) studied this question.
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