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黄连素对A549细胞增殖和凋亡的影响 被引量:1

EEffect of Berberine on proliferation and apoptosis of A549 cells
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摘要 目的探讨黄连素(berberine)对人肺腺癌细胞株A549的作用及其机制。方法将对数生长期A549细胞分成对照组和黄连素组。对照组细胞常规培养,黄连素组细胞培养体系中分别加入黄连素100μmol/L。各组细胞培养24 h后,利用MTT检测细胞增殖;流式检测细胞凋亡,RT-PCR检测细胞JAK2和STAT3 m RNA水平;Western blot检测细胞中JAK2、STAT3、p-JAK2和p-STAT3蛋白的变化。结果与对照组相比,黄连素组A549细胞增殖率明显下降(P<0.05),凋亡率明显升高,A549细胞JAK2与STAT3 m RNA表达水平差异无统计学意义。Western blot检测显示,黄连素组A549细胞JAK2和STAT总蛋白无明显变化(P>0.05),但p-JAK2和p-STAT3总蛋白明显增加(P<0.05)。结论黄连素能抑制A549细胞增殖,促进A549细胞凋亡,其作用可能是通过激活JAK2/STAT3信号传导通路实现的。 【Objective】 To investigate the effect of Berberine on the human lung adenocarcinoma cell line A549 and its mechanisms. 【Methods】 The A549 cells at logarithmic growth phase were divided into control and Berberine groups. The cells in the control group were normally treated and the cells in the Berberine group were incubated with Berberine(100 μmol/L). MTT and flow cytometry were used to examine the proliferation and apoptotic changes of A549 cells respectively in both groups after incubation for 24 h. The m RNA levels of JAK2 and STAT3 were detected by RT-PCR. The changes of JAK2, STAT3, p-JAK2 and p-STAT3 proteins were detected by Western blot. 【Results】 Compared with the control group, the proliferation rate of A549 cells was significantly decreased(P〈0.05), but the apoptotic rate was significantly increased in the Berberine group(P〈0.05). There were no differences in the m RNA levels of JAK2 and STAT3 between both groups(P〉0.05). Western blot showed that there was no difference in the expression of total JAK2 or STAT3 protein between both groups(P〉0.05), but the Berberine group had higher expression levels of p-JAK2 and p-STAT3 proteins than the control group(P〈0.05). 【Conclusions】 Berberine could inhibit the proliferation and promote the apoptosis of A549 cells, and the effect may be achieved through activating JAK2/STAT3 signal transduction pathway.
作者 孙秀梅 郑祎
出处 《中国现代医学杂志》 CAS 北大核心 2015年第24期9-13,共5页 China Journal of Modern Medicine
关键词 黄连素 A549细胞 增殖 凋亡 JAK2/STAT3 Berberine A549 cell proliferation apoptosis JAK2/ STAT3
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