The Effect and Mechanism of Salvianolic Acid A on OGD/R-Induced Apoptosis and Oxidative Stress Dam-age in Cerebral Microvascular Endothelial Cells
OBJECTIVE To investigate the protective effect and mechanism of salvianolic acid A(SAL-A)on mouse brain mi-crovascular endothelial(b.End.3)cell apoptosis and oxidative stress injury after oxygen-glucose deprivation/reoxygenation(OGD/R).METHODS OGD/R injury was established with b.End.3 cells for injury model.Cell apoptosis was detected by Annexin Ⅴ-fluorescein isothiocyanate(Annexin Ⅴ-FITC)probe and propidium iodide(PI)staining;Reactive oxygen species(ROS)generation was detected by 2,7-dichlorofluorescein diacetate(DCFH-DA)probe;Mitochondrial membrane potential was detected by JC-1 staining.The expression of proteins related to apoptosis,oxidative stress,and Akt/GSK3β/Nrf2 pathway was detected by Western Blot.RESULTS Compared with the control group,the expression of anti-apoptotic proteins,mitochondrial membrane potential,expression of related antioxidant proteins and Akt/GSK3β/Nrf2 pathway were significantly decreased in the OGD/R group(P＜0.05).In addition,the number of apoptotic cells,the expression of apoptosis-inducing proteins,and the production of intracellular ROS were significantly increased in the OGD/R group(P＜0.05).Whereas,the SAL-A treatment can improve OGD/R-induced cell apoptosis and oxidative stress,the expression of Akt/GSK3β/Nrf2 pathway were significantly increased in the SAL-A-10 group.CONCLUSION SAL-A inhibited OGD/R-induced apoptosis and oxidative stress injury in b.End.3 cells,and the mechanism may be related with affecting the Akt/GSK3β/Nrf2 pathway.
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