眼镜蛇毒NGF通过PI3K/AKT信号通路对肝星状细胞的影响  

Effects of Obra Venom NGF on Hepatic Stellate Cells through PI3K/Akt Signal Pathway

作　　者：张可星[1] 张学荣[1] 侯瑞雪[1] 孙林[1] 蔡凤桃 廖明[1] 班建东[1] 陈缨[1] 

机构地区：[1]广西医科大学医学科学实验中心,广西医科大学蛇毒研究所,南宁530021

出　　处：《基因组学与应用生物学》2016年第5期1031-1035,共5页Genomics and Applied Biology

基　　金：国家自然科学基金(No.81360078,No.81460128)资助

摘　　要：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。To investigate the PI3K/Akt signaling pathway in cobra venom nerve growth factor（NGF） induces apoptosis of hepatic stellate cells, CCK8 and flow cytometry detected HSC-T6 cell proliferation and apoptosis to identify the minimum effective concentration of NGF in HSC-T6 cells, while applying Western Blot analysis NGF on cell protein Akt phosphorylation level. The result was that the concentration 4 μg/m L was the minimum effective concentration which reducing the level of expression of p-Akt and increasing that of Akt after induced HSC-T6 apoptosis. Moreover, the effect of NGF was stronger in combination with LY294002, the inhibitor of the PI3K/Akt signaling. The apoptosis of HSC-T6 induced by cobra venom NGF was related to the PI3K/Akt signal pathway.

关 键 词：眼镜蛇毒NGF HSC-T6 凋亡 PI3K/AKT信号通路 

分 类 号：R575.2[医药卫生—消化系统]