AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by ...AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.展开更多
目的研究SD大鼠在听觉剥夺后Bcl-2、Bax、Fas在听皮层的表达。方法选择生后3周龄SD大鼠48只,按体重将其分为6组(8只/组):分别为7天、14天、28天手术组和其相对应的对照组。手术组大鼠双侧耳蜗行捣毁术,对照组耳后切口。采用免疫组织化...目的研究SD大鼠在听觉剥夺后Bcl-2、Bax、Fas在听皮层的表达。方法选择生后3周龄SD大鼠48只,按体重将其分为6组(8只/组):分别为7天、14天、28天手术组和其相对应的对照组。手术组大鼠双侧耳蜗行捣毁术,对照组耳后切口。采用免疫组织化学方法和 Western Blot技术分别检测大鼠听皮层部位Bcl-2、Bax、Fas的变化。结果免疫组化结果显示表达促凋亡基因Bax和Fas对应细胞有所增幅,而抑制凋亡的基因bcl-2却呈现出衰减趋势。Western Blot检测结果显示促凋亡基因蛋白Bax和Fas表达升高,抑凋亡蛋白Bcl-2表达降低。结论Bcl-2、Bax、Fas基因参与了幼年大鼠发育过程中听皮层神经元凋亡的过程。展开更多
基金Supported by The National Natural Science Foundation of China (No. 30872481)the Scientific and Technological Planning Foundation of Shaanxi Province (No. 2006K09-G7-1)
文摘AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.
文摘目的研究SD大鼠在听觉剥夺后Bcl-2、Bax、Fas在听皮层的表达。方法选择生后3周龄SD大鼠48只,按体重将其分为6组(8只/组):分别为7天、14天、28天手术组和其相对应的对照组。手术组大鼠双侧耳蜗行捣毁术,对照组耳后切口。采用免疫组织化学方法和 Western Blot技术分别检测大鼠听皮层部位Bcl-2、Bax、Fas的变化。结果免疫组化结果显示表达促凋亡基因Bax和Fas对应细胞有所增幅,而抑制凋亡的基因bcl-2却呈现出衰减趋势。Western Blot检测结果显示促凋亡基因蛋白Bax和Fas表达升高,抑凋亡蛋白Bcl-2表达降低。结论Bcl-2、Bax、Fas基因参与了幼年大鼠发育过程中听皮层神经元凋亡的过程。
