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目的:探讨峨参内酯对4种肿瘤细胞凋亡的影响及其相关机制研究。方法:采用流式细胞仪检测峨参内酯对肿瘤细胞周期进程的影响及对细胞凋亡的观察;阳性对照组采用紫杉醇处理、峨参内酯组采用峨参内酯处理,空白对照组采用0.1%DMSO处理;采用ELISA试剂盒检测峨参内酯对4种肿瘤细胞Bcl-2、Bax影响;采用western blot法检测峨参内酯对STAT3、P53、NF-κB蛋白表达。结果:峨参内酯对4种肿瘤细胞周期进程及凋亡,随着作用时间的增加,G0/G1期细胞百分数逐渐降低,G2/M期细胞百分数变化不大,而S期细胞百分数逐渐上升;阳性对照组、峨参内酯组与空白对照组比较,Bcl-2/Bax比值明显降低,且有显著性差异(P<0.05),峨参内酯组比值显著低于阳性对照组,且有显著性差异(P<0.05);阳性对照组和峨参内酯组与空白对照组比较,STAT3和NF-κBP65表达明显降低,而P53表达明显上升。结论:峨参内酯阻滞4种肿瘤细胞于S期且具有诱导肿瘤细胞凋亡的作用,其机制是通过上调Bax、P53表达,下调Bcl-2、STAT3、NF-κBP65表达而实现的。
Objective: To investigate the effects of anthracnose on the apoptosis of four kinds of tumor cells and its related mechanisms. Methods: Flow cytometry (FCM) was used to detect the cell cycle progression of the tumor cells and the observation of cell apoptosis. The positive control group was treated with paclitaxel, and the cells treated with anthraquinone lactone in the base group. The blank control group was treated with 0.1% DMSO The Bcl-2 and Bax expression of four tumor cells was detected by ELISA kit. The expression of STAT3, P53 and NF-κB was determined by western blot. Results: The cell cycle progression and apoptosis of four tumor cell lines were studied. The percentage of cells in G0 / G1 phase decreased gradually while the cell percentage in G2 / M phase changed little while the percentage of cells in S phase increased gradually with the increase of time. The ratio of Bcl-2 / Bax was significantly lower in the positive control group and the Emethyong lactone group compared with the blank control group (P <0.05), and the ratio of the Emethyong lactone group was significantly lower than that in the positive control group (P <0.05). Compared with the blank control group, the expression of STAT3 and NF-κB p65 in the positive control group and the anthidol lactone group were significantly decreased, while the expression of P53 was significantly increased. CONCLUSION: Anthracene lactone blocks four kinds of tumor cells in the S phase and induces the apoptosis of tumor cells. Its mechanism is through up-regulating the expression of Bax and P53 and down-regulating the expression of Bcl-2, STAT3 and NF-κBP65.