【摘要】 目的研究落新妇苷对H₂O₂诱导的氧化应激损伤的PC12细胞影响。方法将PC12细胞分为5组:对照组、H₂O₂组及不同浓度（1μmol/L、10μmol/L、20μmol/L）落新妇苷组。采用CCK8实验检测各组细胞的活力; Annexin V-FITC/PI细胞凋亡实验检测各组细胞凋亡率; Western blot检测PI3K、AKT、Caspase3和P38蛋白及其磷酸化激活蛋白的表达水平。结果与H₂O₂组相比,落新妇苷组细胞的活力显著提高,细胞凋亡率明显降低,活化的凋亡相关蛋白Cleaved Caspase3表达水平降低,PI3K/AKT途径相关蛋白p-PI3K和p-AKT的表达水平升高,P38 MAPK途径重要蛋白p-P38的表达水平降低。结论落新妇苷对H₂O₂诱导的氧化应激损伤的PC12细胞有明显保护作用;这种保护作用可能是通过激活PI3K/AKT信号通路及抑制P38MAPK信号通路实现的。更多还原

【Abstract】 Objective To investigate the effects of Astilbin on H₂O₂ induced PC12 cells oxidative damage. Methods PC12 cells were divided into control group,H₂O₂ group,Astilbin groups（ 1 μM,10 μM,20 μM）. Cell viability was detected by CCK8 assay. The proportion of apoptotic cells was tested by Annexin V-FITC/PI apoptosis assay. The activation and expression of Caspase3,PI3 K,Akt and P38 were detected by Western blot. Results Compared with H₂O₂ group,Astilbin significantly improved cell viability,reduced the proportion of apoptosis,inhibited the activation of Cleaved Caspase3,increased the expression of p-PI3 K and p-AKT,and decreased the expression of p-P38. Conclusion Astilbin can protect PC12 cells from oxidative stress induced by H₂O₂,which may be achieved by activating PI3 K/AKT signal pathway and suppressing P38 MAPK signal pathway.更多还原