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目的:研究桃叶珊瑚苷通过ROS/P38通路抑制UVA诱导HSF细胞凋亡的机制。方法:HSF细胞随机分为正常对照组、模型组及桃叶珊瑚苷高、中、低剂量组。检测ROS相对含量及LDH活性,流式细胞术检测细胞凋亡率,Western blot检测p-P38蛋白的表达量,RT-PCR检测Caspase-9、Caspase-3 mRNA的表达,试剂盒检测Caspase-9、Caspase-3的活性。结果:不同浓度桃叶珊瑚苷干预的光损伤HSF细胞ROS含量及LDH、Casepase-9、Caspase-3活性降低,p-P38蛋白表达量减少,细胞凋亡率下降,其作用呈现浓度依赖性;中、高浓度组与模型组比较,差异具有统计学意义(P<0.05或P<0.01)。结论:桃叶珊瑚苷通过清除ROS减轻细胞的氧化损伤,通过下调p-P38、Casepase-9、Caspase-3表达,抑制细胞凋亡,保护受损的HSF细胞。
Objective: To study the mechanism of aucubin inhibiting UVA-induced HSF apoptosis through ROS / P38 pathway. Methods: HSF cells were randomly divided into normal control group, model group and aucubin high, medium and low dose groups. The relative content of ROS and the activity of LDH were detected. The apoptosis rate was detected by flow cytometry. The expression of p-P38 protein was detected by Western blot. The expressions of Caspase-9 and Caspase-3 mRNA were detected by RT- , Caspase-3 activity. Results: The ROS content and the activities of LDH, Casepase-9 and Caspase-3 in photic injury HSV cells were decreased and the expression of p-P38 protein was decreased and the apoptosis rate was decreased in a concentration-dependent manner. Compared with model group, the difference was statistically significant (P <0.05 or P <0.01). CONCLUSION: Aucubin can reduce the oxidative damage of cells by scavenging ROS, and can protect the damaged HSF cells by down-regulating the expression of p-P38, Casepase-9 and Caspase-3 and inhibiting apoptosis.