飞燕草素对人膀胱癌T24细胞增殖、凋亡的影响及机制研究

Study on Effect of Delphinidin on Proliferation and Apoptosis of Human Bladder Cancer T24 cells and Its Mechanism

关键词:  飞燕草素  人膀胱癌T24细胞  活性氧  JNK/STAT3信号通路

Key words:  delphinidin  human bladder cancer T24 cells  reactive oxygen species  JNK/STAT3 signaling pathway

摘要:

目的 探讨飞燕草素对人膀胱癌细胞株T24的增殖抑制作用、诱导凋亡作用及其相关的分子机制。方法 体外培养T24细胞，利用CCK-8试验检测飞燕草素对人膀胱癌T24细胞的杀伤作用；利用流式细胞术试验检测细胞凋亡情况、活性氧水平变化；利用Western blotting检测细胞凋亡相关蛋白和信号通路相关蛋白的表达。结果 飞燕草素能够有效抑制人膀胱癌T24细胞增殖，IC₅₀为（42.37±2.82）μmol·L^-1；飞燕草素能够通过线粒体依赖性途径诱导T24细胞发生凋亡，使Cyt-c、cleaved-Caspase-3、PARP和Bax蛋白表达量升高，Bcl-2表达量降低；飞燕草素能够降低T24细胞中的活性氧水平，并激活JNK/STAT3信号通路。结论 飞燕草素对人膀胱癌T24细胞具有良好的杀伤作用，并能够通过降低T24细胞内活性氧水平，进而调控JNK/STAT3信号通路来诱导T24细胞发生线粒体依赖性凋亡。

Abstract:

OBJECTIVE To explore the inhibitory effect of delphinidin on proliferation inhibition and apoptosis induction of human bladder cancer cell line T24 and its related molecular mechanism. METHODS T24 cells were cultured in vitro, and the killing effect of delphinidin on human bladder cancer T24 cells was detected by CCK-8 assay. Apoptosis and reactive oxygen species levels were detected by flow cytometry. Apoptosis correlation protein and signaling pathway-related proteins expression were detected by Western blotting. RESULTS Delphinidin could effectively inhibit the proliferation of human bladder cancer T24 cells with an IC₅₀ of (42.37±2.82)μmol·L^-1; delphinidin could induce apoptosis of T24 cells through mitochondria- dependent pathway, making Cyt-c, cleaved-Caspase-3, PARP and Bax protein expression increased, Bcl-2 expression decreased; delphinidin could reduce reactive oxygen species levels in T24 cells and activate JNK/STAT3 signaling pathway. CONCLUSION Delphinidin has a good killing effect on human bladder cancer T24 cells, and can induce mitochondria- dependent apoptosis in T24 cells by decreasing the level of reactive oxygen species in T24 cells and regulating JNK/STAT3 signaling pathway.