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为探讨PI3K/Akt信号通路在眼镜蛇毒神经生长因子(NGF)诱导肝星状细胞凋亡中的作用,本实验分别采用CCK8和流式细胞术检测NGF对HSC-T6细胞增殖及凋亡作用,从而找出NGF作用HSC-T6细胞的最小有效浓度,同时应用Western Blot法分析NGF对细胞蛋白Akt磷酸化水平的影响。结果发现NGF浓度为4μg/m L时为诱导HSC-T6细胞凋亡的最小有效浓度,并且在作用HSC-T6细胞后,P-Akt的表达水平降低,Akt的表达量却增加。将该浓度NGF与信号通路抑制剂LY294002联合使用则协同作用增强。因此,眼镜蛇毒神经生长因子诱导HSC-T6细胞凋亡作用与PI3K/Akt信号通路有关。
In order to investigate the role of PI3K / Akt signaling pathway in the induction of hepatic stellate cell apoptosis by cobra venom nerve growth factor (NGF), CCK8 and flow cytometry were used to detect the proliferation and apoptosis of HSC-T6 cells, In order to find out the minimum effective concentration of NGF on HSC-T6 cells, Western Blot method was used to analyze the effect of NGF on Akt phosphorylation. The results showed that the concentration of NGF 4μg / m L induced apoptosis in HSC-T6 cells the minimum effective concentration, and the role of HSC-T6 cells, P-Akt expression decreased Akt expression increased. The concentration of NGF and signal pathway inhibitor LY294002 used in synergy enhanced. Therefore, cobra venom nerve growth factor induced HSC-T6 apoptosis and PI3K / Akt signaling pathway.