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目的:探讨香芹酚(carvacrol,CV)对人肝癌细胞(HepG2)的抗癌作用及其分子机制.方法:予以不同浓度的香芹酚(0.00、0.05、0.10、0.20、0.40mmol/L)处理肝癌细胞HepG2后,采用四甲基偶氮唑蓝(MTT)比色法检测细胞活力;Hoechst33258染色法及流式细胞仪(FCM)技术检测细胞凋亡;Western blot检测MAPK蛋白水平的变化.结果:香芹酚对肝癌细胞株HepG2的抑制作用呈浓度依赖性及时间依赖性;在作用24h后,随着浓度的递增,细胞数目减少,凋亡细胞逐步增多,流式细胞仪检测的细胞凋亡率逐步升高,随着香芹酚浓度的增加(0.00、0.05、0.10、0.2、0.40mmol/L)细胞的凋亡比率明显升高,依次为:3.70%±0.22%、13.50%±1.59%、25.80%±2.18%、30.50%±0.25%、50.60%±3.81%.进一步的Western blot实验表明,香芹酚选择性地改变了MAPK家族成员的磷酸化,对磷酸化ERK有明显的浓度依赖性抑制作用,同时能激活p38的磷酸化,而JNK激酶磷酸化却没有改变.结论:香芹酚可通过MAPK信号通路诱导肝癌细胞株HepG2凋亡.
Objective: To investigate the anticancer effect of carvacrol (CV) on HepG2 cells and its molecular mechanism.Methods: Carvacrol (0.00,0.05,0.10,0.20,0.40mmol / L) After treated with HepG2, MTT assay was used to detect cell viability. Hoechst33258 staining and flow cytometry (FCM) were used to detect cell apoptosis. Western blot was used to detect the protein level of MAPK. Results: Carvacrol inhibited the proliferation of HepG2 cells in a concentration-dependent manner and in a time-dependent manner. After 24 h, the number of cells decreased and the number of apoptotic cells increased gradually. The cells detected by flow cytometry The apoptotic rate increased gradually with the increase of the concentration of carvacrol (0.00,0.05,0.10,0.2,0.40mmol / L), the apoptosis rate was significantly increased, followed by: 3.70% ± 0.22%, 13.50% ± 1.59%, 25.80% ± 2.18%, 30.50% ± 0.25%, 50.60% ± 3.81% respectively.Further Western blot showed that carvacrol selectively changed the phosphorylation of MAPK family members and had obvious phosphorylation ERK Concentration-dependent inhibition, while activating p38 phosphorylation, whereas JNK kinase phosphorylation did not Variable Conclusion: carvacrol can induce apoptosis of HepG2 cells lines by MAPK pathway.