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目的:探讨黄连素对人慢性髓系白血病细胞K562的作用及其机制。方法:将对数生长期的K562细胞随机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加入黄连素(40μmol/L)。各组细胞培养24h后,利用MTT检测细胞增殖;RT-PCR检测细胞Bax和Bcl-2基因表达水平;Western blotting检测细胞JAK2,STAT3,p-JAK2,p-STAT3,Bax和Bcl-2蛋白的变化。结果:与对照组比较,黄连素组K562细胞增殖率明显下降(P<0.05)。RT-PCR检测显示Bax mRNA表达水平明显增加,而Bcl-2mRNA表达水平明显减少。Western blotting检测显示,黄连素组与对照组比较,K562细胞JAK2、STAT3蛋白表达无明显变化(P>0.05),但p-JAK2、p-STAT3和Bcl-2蛋白表达水平明显降低,而Bax蛋白表达水平明显增加(P<0.05)。结论:黄连素能诱导K562细胞增殖抑制和凋亡,其机制可能是通过抑制JAK2/STAT3信号传导通路实现的。
Objective: To investigate the effect of berberine on human chronic myeloid leukemia cell line K562 and its mechanism. Methods: The logarithmic growth phase K562 cells were randomly divided into control group and berberine group. The control group cells routine culture, berberine group cell culture system by adding berberine (40μmol / L). Cell proliferation was detected by MTT assay. The expression of Bax and Bcl-2 was detected by RT-PCR. The protein expression of JAK2, STAT3, p-JAK2, p-STAT3, Bax and Bcl- Variety. Results: Compared with the control group, the proliferation rate of K562 cells in the berberine group was significantly decreased (P <0.05). RT-PCR showed that Bax mRNA expression increased significantly, while Bcl-2 mRNA expression decreased significantly. Western blotting showed that the expression of JAK2 and STAT3 protein in K562 cells was not significantly changed (P> 0.05), but the expression of p-JAK2, p-STAT3 and Bcl-2 protein were significantly decreased in the berberine group compared with the control group The expression level increased significantly (P <0.05). Conclusion: Berberine can induce the proliferation and apoptosis of K562 cells. The mechanism may be through the inhibition of JAK2 / STAT3 signal transduction pathway.