黄芩苷对大鼠肾脏细胞NRK-52E增殖的影响及相关机制研究

Effect of baicalin on the proliferation of NRK-52E cells in rats and its mechanism

目的探究黄芩苷对大鼠肾脏细胞NRK-52E增殖的影响及相关机制。方法体外培养NRK-52E细胞,并给予不同浓度黄芩苷处理,通过CCK-8试剂盒检测细胞增殖,采用Hoechst染色检测细胞凋亡,利用Western blot检测凋亡相关蛋白表达,使用ELISA检测炎症因子的水平。结果黄芩苷可时间和剂量依赖性抑制NRK-52E细胞增殖。89.274 mg·L^-1及178.548 mg·L^-1黄芩苷可诱导NRK-52E细胞凋亡,Western blot检测结果显示黄芩苷可通过抑制Bcl-2表达,增加Bax水平,激活caspase 3和PARP-1等凋亡相关蛋白,进而诱导细胞凋亡。ELISA结果显示黄芩苷处理的NRK-52E细胞中的炎症因子IL-6、TNF-α的表达水平无明显变化。结论高剂量黄芩苷可抑制大鼠肾脏NRK-52E细胞增殖,并诱导其凋亡,且对炎症因子IL-6、TNF-α的表达无明显影响。

Objective To determine the effect of baicalin on the proliferation of NRK-52 E cells and its mechanism. Methods NRK-52 E cells were cultured and treated with baicalin of different concentrations. The proliferation of NRK-52 E cells was detected by CCK-8, the apoptosis rate was measured by Hoechst, the expression of apoptosis-related protein was analyzed with Western blot, and the cytokine release and expression were determined with ELISA. Results Baicalin suppressed the proliferation of NRK-52 E cells in a dose-and time-dependent manner. The apoptosis rate was raised after treatment with baicalin, especially at 89.274 mg·L^-1 and 178.548 mg·L^-1. Baicalin induced the apoptosis in NRK-52 E cells, as shown by the inhibited expression of Bcl-2, increased level of Bax, and activated apoptosis-related proteins such as caspase 3 and PARP-1. There were no significant changes in the levels of inflammatory cytokines IL-6 and TNF-α after treatment with baicalin. Conclusion High dose baicalin may suppress the proliferation of NRK-52 E cells, and induce their apoptosis. but with no significant effect on the expression of inflammatory cytokine IL-6 and TNF-α.