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为了研究Ang-(1-7)通过Mas对人肝癌细胞增殖的影响及在Mas高、低表达模型中分析其表达差异、凋亡等细胞生理活性变化,我们采用药物(Mas激活剂Ang-(1-7),Mas抑制剂A779)干预Hep G2细胞,分别对Ang-(1-7)和A799进行剂量、时间效应实验,实时定量RT-PCR检测药物干预后细胞Mas的表达水平,最后流式细胞仪检测药物干预后细胞的凋亡变化。结果表明,Ang-(1-7)与A779的有效工作浓度为10-7mol/L,Ang-(1-7)促进Mas的表达,Mas表达水平高于对照组。相反,A779抑制Mas的表达,但作用不明显,主要为拮抗Ang-(1-7)的功能。Ang-(1-7)处理组细胞凋亡明显升高,揭示Mas表达提升诱导人肝癌细胞凋亡。
In order to study the effect of Ang- (1-7) on the proliferation of human hepatocellular carcinoma cells by Mas, and to analyze its expression difference and the changes of cell physiological activities such as apoptosis in Mas high and low expression models, 1-7) and Mas inhibitor A779 (Hep G2). The dose and time effect of Ang- (1-7) and A799 were tested respectively. The expression of Mas was detected by real-time quantitative RT-PCR. Cytometric detection of apoptosis after drug intervention. The results showed that the effective working concentration of Ang- (1-7) and A779 was 10-7mol / L, and Ang- (1-7) promoted the expression of Mas. The expression level of Mas was higher than that of the control group. In contrast, A779 inhibited the expression of Mas, but its effect was not obvious, mainly antagonizing the function of Ang- (1-7). Ang- (1-7) treated group significantly increased apoptosis, revealing the Mas expression increased induced apoptosis in human hepatoma cells.