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目的:探讨绿原酸诱导人肝癌细胞HepG2凋亡作用及机制。方法:采用噻唑蓝(MTT)法测定绿原酸对HepG2的生长抑制作用,倒置显微镜观察绿原酸对HepG2细胞作用后的形态改变,TUNEL实验和流式细胞术检测细胞凋亡情况,罗丹明123荧光染色实验观察线粒体膜电位的改变,免疫印迹实验探讨绿原酸的作用机制。结果:与空白组相比较,不同浓度绿原酸(1~10mmol/L)能够抑制HepG2肝癌细胞增殖并呈时间-浓度依赖性,绿原酸(1~10 mmol/L)作用24 h后能够显著降低SIRT1、HO-1、Bcl-2和NF-κB蛋白表达,同时上调p53和Bax蛋白表达。结论:绿原酸能够显著抑制HepG2肝癌细胞增殖并通过调控SIRT1/HO-1依赖的凋亡途径发挥作用。
Objective: To investigate the apoptosis of HepG2 cells induced by chlorogenic acid and its mechanism. Methods: The inhibitory effect of chlorogenic acid on HepG2 was measured by thiazolyl blue (MTT) method. Morphological changes of chlorogenic acid on HepG2 cells were observed by inverted microscope. TUNEL assay and flow cytometry were used to detect the apoptosis of Rhodamine. The changes of mitochondrial membrane potential were observed by fluorescence staining in 123, and the mechanism of action of chlorogenic acid was investigated by Western blotting. RESULTS: Compared with the blank group, different concentrations of chlorogenic acid (1-10 mmol/L) could inhibit the proliferation of HepG2 hepatoma cells in a time-and-concentration-dependent manner. Chlorogenic acid (1-10 mmol/L) could act for 24 h. Significantly reduced SIRT1, HO-1, Bcl-2, and NF-κB protein expression and up-regulation of p53 and Bax protein expression. CONCLUSION: Chlorogenic acid can significantly inhibit the proliferation of HepG2 hepatocellular carcinoma cells and play a role by regulating the SIRT1/HO-1 dependent apoptotic pathway.