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目的 :探讨氧化砷 (As2 O3)对人肝癌细胞诱导凋亡作用的分子机制。方法 :以As2 O3 作用于体外培养的人肝癌细胞株HepG2 ,通过免疫组化技术对bcl- 2、bax、p5 3、Fas及c -myc五种基因编码蛋白的表达进行检测。结果 :经As2 O3 作用的人肝癌细胞bcl- 2基因编码蛋白表达减少 ,bax、Fas基因编码蛋白表达增加 ,p5 3、c -myc基因编码蛋白表达改变不明显。结论 :As2 O3 诱导肝癌细胞凋亡分子机制可能是下调bcl- 2基因编码蛋白表达 ,增强bax、Fax基因编码蛋白表达。
Objective: To investigate the molecular mechanism of arsenic trioxide (As 2 O 3) on human hepatoma cell apoptosis. Methods: Human hepatocellular carcinoma cell line HepG2 was treated with As2 O3, and the expressions of bcl-2, bax, p5 3, Fas and c-myc were detected by immunohistochemistry. Results: The expression of bcl-2 gene in human hepatocellular carcinoma cells treated with As2 O3 was decreased, while the expression of bax and Fas genes was increased. The expression of p5 3 and c-myc gene was not significantly changed. CONCLUSION: The molecular mechanism of As2 O3-induced hepatocellular carcinoma cell apoptosis may be down-regulation of bcl-2 gene-encoding protein expression and enhancement of bax, Fax gene-encoded protein expression.