论文部分内容阅读
目的:研究芹菜素(apigenin,API)是否通过耗竭谷胱甘肽(glutathione,GSH)诱导人肝癌Hep G2细胞活性抑制和凋亡。方法:体外培养Hep G2细胞。分光光度法测定细胞GSH水平。MTS比色法测定细胞活力。PI染色FCM分析细胞凋亡率。结果:API降低Hep G2细胞GSH水平(P<0.05),呈浓度依赖性。API以浓度依赖方式抑制Hep G2细胞活性(P<0.05),同时,诱导Hep G2细胞Sub G1百分率增高(P<0.05);500μM GSH预孵育30min,能有效阻断API降低细胞GSH水平、抑制细胞活性和诱导细胞凋亡作用(P<0.05)。结论:API通过耗竭细胞GSH抑制Hep G2细胞活性和诱导细胞凋亡。
OBJECTIVE: To investigate whether apigenin (API) can inhibit the activity and apoptosis of Hep G2 cells induced by glutathione (GSH). Methods: Hep G2 cells were cultured in vitro. Spectrophotometric determination of cellular GSH levels. MTS colorimetric assay for cell viability. PI staining FCM analysis of apoptosis rate. Results: API reduced the level of GSH in Hep G2 cells (P <0.05) in a concentration-dependent manner. API inhibited Hep G2 cell activity in a concentration-dependent manner (P <0.05), while the percentage of Sub G1 induced Hep G2 cells increased (P <0.05). Preincubation with 500 μM GSH for 30 min could effectively block the decrease of GSH level in cells, Activity and induction of apoptosis (P <0.05). Conclusion: API inhibits Hep G2 cell activity and induces apoptosis by depleting cell GSH.