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目的:研究熊果酸抑制HepG2细胞增殖的分子机制。方法:应用CDK2试剂盒检测熊果酸对CDK2的抑制效果以及浓度和时间等影响因素,用流式细胞术验证CDK2抑制所造成的细胞周期阻滞,并用Annexin V/PI检测细胞凋亡。结果:CDK2试剂盒实验显示熊果酸对CDK2具有抑制作用,并呈时间和浓度依赖性;细胞周期检测结果表明熊果酸能将HepG2细胞周期阻滞在G0/G1期,Annexin V/PI细胞凋亡检测其早期凋亡率达24.12%。结论:熊果酸能抑制CDK2活性,将HepG2细胞周期阻滞于G0/G1期,从而抑制HepG2细胞增殖,并进一步诱导细胞凋亡。
Objective: To study the molecular mechanism of ursolic acid inhibiting the proliferation of HepG2 cells. Methods: The inhibitory effect of ursolic acid on CDK2 and the influencing factors such as concentration and time were detected by CDK2 kit. Cell cycle arrest induced by CDK2 inhibition was examined by flow cytometry. Cell apoptosis was detected by Annexin V / PI. Results: The results of CDK2 kit showed that ursolic acid inhibited CDK2 in a time-and-concentration-dependent manner. The results of cell cycle assay showed that ursolic acid could arrest HepG2 cells in G0 / G1 phase and Annexin V / PI cells Apoptosis detection rate of early apoptosis reached 24.12%. Conclusion: UA can inhibit the activity of CDK2 and block the HepG2 cell cycle in G0 / G1 phase, thus inhibiting HepG2 cell proliferation and inducing apoptosis.