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作 者:李翔[1] 易继林[1] 万亚峰[1] 李兴睿[1]
机构地区:[1]华中科技大学同济医学院附属同济医院普外科,武汉430030
出 处:《华中医学杂志》2007年第3期198-200,共3页Central China Medical Journal
摘 要:目的研究血卟啉衍生物光动力作用诱导人肝癌细胞HepG2凋亡及其机制。方法应用流式细胞仪分析光动力作用后细胞凋亡及免疫组化染色检测凋亡相关蛋白bcl-2蛋白、bax蛋白表达水平。结果血卟啉衍生物光动力组人肝癌细胞HepG2凋亡率达(25.28±1.52)%,与对照组相比,差异有极显著意义(P<0.01);并且光动力作用后凋亡相关蛋白bcl-2表达显著高于对照组(P<0.05)。结论血卟啉衍生物光动力作用具有诱导人肝癌细胞HepG2凋亡的生物学效应,而凋亡调控蛋白bcl-2表达水平的降低可能是血卟啉衍生物光动力作用诱导人肝癌细胞HepG2凋亡的一个重要机制。Objective To investigate the apoptosis of human hepatocellular carcinoma ceils induced by photodynamic therapy with hematoporphyrin and its mechanism. Methods The apoptosis of human hepatocellular carcinoma cell-line HepG2 was detected by flow cytometry with P1 staining and the translational levels of bcl-2 gene and bax gene by immunohistochemical staining. Results The apoptotic rate of hepatocellular carcinoma cell line HepG2 after photodynamic therapy with hematoporphyrin was significantly increased, which was higher than that in the controls(P〈0. 01). The expression of bcl-2 protein in hematoporphyrin group was lower than that in the controls(P〈0. 05). Conclusion Photodynamic therapy with hematoporphyrin might obviously trigger apoptosis of HepG2 cells by down-regulating the translational level of bcl-2 gene.
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