葫芦素B抑制STAT3/Bcl-2表达诱导非小细胞肺癌H1975细胞凋亡  

Inhibition of STAT3/Bcl-2 expression by cucurbitacin B on apoptosis of non-small cell lung cancer H1975 cells

作　　者：何臣[1] 王菊辉 丘韶校[1] 徐羽中[1] 李元广[1] HE Chen;WANG Ju-hui;QIU Shao-xiao(Department of Respiratory Medicine,Bao’an People’s Hospital,Shenzhen 518101,China)

机构地区：[1]深圳市宝安区人民医院呼吸内科,518101

出　　处：《中国实用医药》2020年第13期196-198,共3页China Practical Medicine

摘　　要：目的探讨葫芦素B对非小细胞肺癌H1975细胞凋亡的影响及可能的机制。方法应用不同浓度葫芦素B作用H1975细胞不同时间,分别使用Annexin/7-AAD双染法检测细胞凋亡,Western blot法测定信号转导与转录活化因子3(STAT3)、B淋巴细胞瘤-2(Bcl-2)蛋白表达。结果0 nM的葫芦素B处理后24、48 h的细胞增殖抑制率分别为(2.86±0.11)、(3.21±1.26)%,20 nM的分别为(3.10±0.29)、(4.09±0.65)%,40 nM的分别为(4.09±0.12)、(7.59±0.74)%,80 nM的分别为(4.61±0.14)、(32.63±0.67)%。0、20 nM葫芦素B处理后24、48 h对H1975细胞增殖抑制率无明显影响;40、80 nM葫芦素B处理后24、48 h,对H1975细胞增殖抑制率均高于0 nM与20 nM,差异均有统计学意义(P<0.05)。葫芦素B处理后24 h的细胞增殖抑制率均低于处理后48 h,呈时间-剂量依赖性增加,80 nM葫芦素B作用48 h对H1975细胞的细胞凋亡诱导作用最为明显,差异有统计学意义(P<0.05)。40 nM以上浓度葫芦素B作用H1975细胞48 h后p-STAT3、STAT3、Bcl-2明显降低。结论葫芦素B通过抑制STAT3信号活化下调Bcl-2蛋白表达诱导H1975细胞凋亡的发生。Objective To discuss the effect of cucurbitacin B on the apoptosis of non-small cell lung cancer cell line h1975 and its possible mechanism. Methods The H1975 cells were treated with different concentrations of cucurbitacin B at different times, the cell apoptosis were detected by Annexin/7-AAD double staining, and the expression of signal transducer and activator of transcription 3(STAT3) and B-cell lymphoma-2(Bcl-2) protein expression were detected by Western blot method. and STAT3/BCL2 expression were analyzed by the and respectively. Results The cell proliferation inhibition rates of 0 nM cucurbitacin B at 24 and 48 h were(2.86±0.11),(3.21±1.26)%, respectively, 20 nM were(3.10±0.29) and(4.09±0.65)%, respectively, 40 nM were(4.09±0.12) and(7.59±0.74)%, respectively, and 80 nM were(4.61±0.14) and(32.63±0.67)%, respectively. After 0 and 20 nM cucurbitacin B treatment for 24 and 48 h, there was no significant effect on the proliferation inhibition rate of H1975 cells. After 40 and 80 nm cucurbitacin B treatment for 24 and 48 h, the proliferation inhibition rate of H1975 cells was higher than that of 0 nM and 20 nM, and the difference was statistically significant(P<0.05). The inhibition rate of cell proliferation at 24 h after treatment with cucurbitacin B was lower than that at 48 h after treatment, showing a time-concentration-dependent manner. The cell apoptosis of H1975 cells induced by 80 nM cucurbitacin B for 48 h was the most obvious, and the difference was statistically significant(32.63±0.67)%. H1975 cell was treated by Cucurbitacin B above 40 nM for 48 h, p-STAT3, STAT3 and Bcl-2 were significantly decreased. Conclusion Cucurbitacin B can induce apoptosis of H1975 cells by inhibiting STAT3 signal activation and down regulating Bcl-2 protein expression.

关 键 词：非小细胞肺癌 葫芦素B 信号转导与转录活化因子3 B淋巴细胞瘤-2 

分 类 号：R734.2[医药卫生—肿瘤]