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目的:研究迷迭香酸诱导HepG_2细胞凋亡的作用机制。方法:MTT法检测不同浓度的迷迭香酸作用于HepG_2细胞48 h后,对细胞生长的抑制作用;流式细胞术检测不同浓度迷迭香酸分别作用于HepG_2细胞24 h及48 h后的细胞凋亡;Western Blotting法检测迷迭香酸作用HepG_2细胞48 h对P53和c-Myc蛋白表达的影响。结果:12.50,25.00,50.00,100.00μg·ml~(-1)浓度的迷迭香酸作用48 h后对HepG_2的生长有抑制作用,半抑制浓度(IC50)为43.48μg·ml~(-1)。对比不同浓度迷迭香酸作用HepG_2细胞24 h及48 h,当作用48 h时对HepG_2细胞的早期凋亡产生作用。不同浓度迷迭香酸作用于HepG_248 h后,cMyc的表达随迷迭香酸浓度的增加而降低,P53的表达随迷迭香酸浓度的增加而增高。结论:迷迭香酸对HepG_2细胞增殖的抑制作用呈剂量依赖性,可通过对抑癌基因P53的激活及对原癌基因c-Myc蛋白的切割,促进HepG_2细胞发生凋亡。
Objective: To study the mechanism of rosmarinic acid-induced apoptosis in HepG2 cells. Methods: MTT assay was used to detect the inhibitory effect of different concentrations of rosmarinic acid on HepG_2 cells for 48 h. Flow cytometry was used to detect the effect of different concentrations of rosmarinic acid on HepG_2 cells for 24 h and 48 h The apoptosis of HepG2 cells was detected by Western Blotting. The expression of P53 and c-Myc protein in HepG2 cells treated with rosmarinic acid for 48 h were measured. Results: Rosmarinic acid (12.50,25.00,50.00,100.00μg · ml -1) inhibited the growth of HepG 2 after 48 h, and the IC50 was 43.48 μg · ml -1 ). HepG_2 cells were treated with different concentrations of rosmarinic acid for 24 h and 48 h, respectively. When treated with different concentrations of rosmarinic acid for 48 h, HepG 2 cells induced early apoptosis. After treated with different concentrations of rosmarinic acid for 24 h, the expression of cMyc decreased with the increase of rosmarinic acid concentration, while the expression of P53 increased with the increase of rosmarinic acid concentration. CONCLUSION: Rosmarinic acid inhibits the proliferation of HepG2 cells in a dose-dependent manner. The apoptosis of HepG2 cells can be promoted by activating the tumor suppressor gene P53 and cutting the proto-oncogene c-Myc.