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目的:研究紫花牡荆素诱导人结肠癌细胞凋亡作用及其作用机制。方法:体外培养人结肠癌HT-29细胞。碘化丙啶(P)I染色流式细胞术(FCM)和细胞凋亡ELISA试剂盒检测细胞凋亡。荧光探针二氯荧光素(DCFH-DA)标记FCM测定细胞内活性氧的含量。Western blot和小干扰RNA转染用于探索其分子机制。结果:紫花牡荆素以浓度依赖性的方式诱导结肠癌HT-29细胞系细胞凋亡。紫花牡荆素引起活性氧(ROS)的产生,并激活HT-29细胞的凋亡信号调节激酶1(ASK1)。N-乙酰半胱氨酸(NAC)预处理HT-29细胞有效地抑制ASK1活性,减弱紫花牡荆素处理引起的细胞凋亡。ASK1特异小干扰RNA能显著减弱紫花牡荆素诱导HT-29细胞凋亡作用。结论:紫花牡荆素通过刺激活性氧形成活化ASK1诱导结肠癌HT-29细胞凋亡。
Objective: To study the apoptosis of human colon cancer cells induced by Vitexin and its mechanism. Methods: Human colon cancer HT-29 cells were cultured in vitro. Propidium iodide (P) I staining flow cytometry (FCM) and apoptosis ELISA kit detection of apoptosis. Fluorescence probe dichlorofluorescein (DCFH-DA) labeled FCM determination of intracellular reactive oxygen species. Western blot and small interfering RNA transfection were used to explore the molecular mechanism. Results: Vitexin induced cell apoptosis of HT-29 colon cancer cells in a concentration-dependent manner. Vitexin causes the production of reactive oxygen species (ROS) and activates apoptotic signal-regulated kinase 1 (ASK1) in HT-29 cells. N-acetylcysteine (NAC) pretreatment of HT-29 cells effectively inhibited the activity of ASK1 and attenuated the apoptosis induced by Vitexin. ASK1 specific small interfering RNA can significantly reduce the apoptosis of HT-29 cells induced by Vitexin. Conclusion: Vitexin can induce the apoptosis of colon cancer HT-29 cells by activating activated oxygen to form activated ASK1.