铁皮石斛多糖通过激活Akt/mTOR信号轴减轻OGD/R诱导的HT22细胞凋亡

Objective To investigate the protective effect of Dendrobium officinale polysaccharides(DOP) against oxygen-glucose deprivation/reperfusion(OGD/R)-induced injury in mouse hippocampal neuronal(HT22) cells and its underlying mechanism involving the protein kinase B/Mammalian target of rapamycin(Akt/mTOR) signaling axis. Methods An in vitro cerebral ischemia-reperfusion model was established by subjecting HT22 cells to OGD for 3h followed by 24h of reperfusion. Cells were randomly divided into Control, OGD/R, and DOP-low,-medium, and-high dose(20, 40, and 80 μg/mL) groups. Cell viability was assessed by CCK-8 assay. Hoechst 33258 staining was employed to observe apoptotic morphology. Western blotting(WB) experiments were performed to evaluate the expression of apoptosis-related proteins(Bax, Bcl-2, and Caspase-3) and the activity of the Akt/mTOR pathway. Results Compared with the Control group, OGD/R significantly reduced cell viability, upregulated Bax and Caspase-3 expression, downregulated Bcl-2 expression, and induced prominent nuclear condensation(P<0.05). DOP treatment markedly reversed these alterations, with significant elevation in the p-Akt/Akt and p-mTOR/mTOR ratios(P<0.05). Conclusion DOP exerts neuroprotective effects by activating the Akt/mTOR signaling axis to suppress OGD/R-induced mitochondrial apoptotic pathway.