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目的探讨雷公藤红素(CSL)对人结肠癌细胞株HCT-116生长的影响及可能的作用机制。方法采用不同浓度的CSL处理HCT-116细胞,MTT法检测细胞生长的抑制率;流式细胞术(FCM)检测细胞周期;透射电镜观察细胞凋亡形态变化;荧光底物法检测细胞蛋白酶体活性;Westernblot检测p27、Bax的表达变化。结果CSL明显抑制HCT-116细胞生长,呈现时间、剂量依赖性;流式细胞术显示CSL可阻止细胞周期于G0/G1期;电镜下观察部分细胞具有典型的凋亡细胞形态特征;CSL对HCT-116细胞糜蛋白酶活性具有明显的抑制作用,其效应呈现浓度依赖性;CSL干预后细胞内p27、Bax蛋白表达明显增加。结论CSL具有抑制结肠癌HCT-116细胞的生长、阻滞细胞周期、诱导凋亡的作用,其分子机制可能与其抑制细胞内蛋白酶体活性,导致p27、Bax蛋白降解受阻有关。
Objective To investigate the effects of tripterine (CSL) on the growth of human colon carcinoma cell line HCT-116 and its possible mechanism. Methods HCT-116 cells were treated with different concentrations of CSL, the inhibition rate of cell growth was detected by MTT assay, the cell cycle was detected by flow cytometry (FCM), the morphological changes of apoptotic cells were observed by transmission electron microscopy, the proteasome activity ; Western blot analysis of p27, Bax expression changes. Results CSL significantly inhibited the growth of HCT-116 cells in a time-and dose-dependent manner. Flow cytometry showed that CSL prevented the cell cycle at G0 / G1 phase. The morphological features of apoptotic cells were observed under electron microscope. -116 chymotrypsin had a significant inhibitory effect, the effect of a concentration-dependent manner; CSL intervention intracellular p27, Bax protein expression increased significantly. Conclusion CSL can inhibit the growth of human colon cancer HCT-116 cells, arrest cell cycle and induce apoptosis. Its molecular mechanism may be related to the inhibition of intracellular proteasome activity and the impaired p27 and Bax protein degradation.