Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== Calenduloside E ====== [[Calenduloside E]] (CE) isolated from Aralia elata (Miq.) Seem. is a natural [[triterpenoid saponin]] that can reportedly ameliorate [[myocardial ischemia]]/[[reperfusion injury]]. However, its potential roles and mechanism in [[Cerebral ischemia-reperfusion injury]] are barely understood. Li et al. established an oxygen-glucose deprivation/reoxygenation (OGD/R) model in [[HT22]] cells. They found that CE significantly attenuated the OGD/R-induced inhibition of cell viability and apoptotic [[cell death]] in HT22 cells. Moreover, CE treatment significantly ameliorated OGD/R-induced mitochondrial fission by inhibiting mitochondrial dynamin-related protein 1 (Drp1) recruitment and increasing Drp1 phosphorylation at Ser637. CE treatment significantly ameliorated OGD/R-induced mitochondrial dysfunction by increasing the mitochondrial membrane potential and reducing the mitochondrial ROS and cellular calcium accumulation. Moreover, CE treatment significantly inhibited the OGD/R-induced release of mitochondrial Cytochrome C and increase Bax, Cleaved-caspase3, and Cleaved-caspase9 protein levels, whereas CE treatment significantly reversed the OGD/R-induced decrease in Bcl-2 and full length of caspase3 and caspase9 protein levels. In vivo, we found that CE treatment significantly ameliorated ischemic/hypoxia-induced brain infarct volume, neurological deficits, and neuronal apoptosis in mice after middle cerebral artery occlusion and reperfusion. CE treatment also significantly ameliorated the mitochondrial transmembrane potential, decreased Cytochrome C release, and reversed the increase in Bax, Cleaved-caspase3, and Cleaved-caspase9 protein levels and the decrease in Bcl-2 and full length of caspase3 and caspase9 protein levels induced by cerebral ischemia/reperfusion (I/R). All these results indicated that CE treatment exerted a neuroprotective effect by ameliorating [[mitochondrial dysfunction]] during cerebral I/R injury ((Li J, Bu Y, Li B, Zhang H, Guo J, Hu J, Zhang Y. Calenduloside E alleviates cerebral ischemia/reperfusion injury by preserving mitochondrial function. J Mol Histol. 2022 Jul 12. doi: 10.1007/s10735-022-10087-5. Epub ahead of print. PMID: 35819738.)). calenduloside_e.txt Last modified: 2024/06/07 02:57by 127.0.0.1