藤黄酸诱导人胃腺癌SGC-7901细胞的凋亡作用

目的：探讨藤黄酸(gambogic acid，GA)诱导体外培养人胃腺癌SGC-7901细胞凋亡的作用。方法：通过MTT比色法分析藤黄酸对人胃癌SGC-7901细胞在24，48，72 h增殖的影响，并通过光镜、电镜观察细胞形态学的改变及流式细胞术检测藤黄酸对SGC-7901肿瘤细胞周期动力学和凋亡诱导率的影响，用免疫组化方法检测凋亡相关基因bax和bcl-2的蛋白表达变化。结果：藤黄酸可明显抑制SGC-7901细胞的增殖，48h半数生长抑制剂量(IC50)为1．47，1．6 μmol／L的藤黄酸可导致7901细胞形态学的改变，流式细胞术显示细胞周期亦发生变化，G2／M期细胞增加，凋亡率呈时间-剂量相关性。同剂量的藤黄酸还可增加抑癌基因bax和减少诱癌基因bcl-2的蛋白表达量。结论：藤黄酸可明显抑制SGC-7901肿瘤细胞的生长，诱导细胞凋亡，其分子机制可能与其减少Bcl-2／Bax的比值相关。

Gambogic Acid Inducing Apoptosis in Human Gastric Adenocarcinom SGC-7901 Cells

AIM: To study the inducing apoptosis of Gambogic Acid (GA) on human gastric adenocarcinom SGC-7901 cells. METHOD: Inhibition of proliferation(24,48,72 h)was measured with MTT (3-4,5-dimethyl thiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. The marked morphological changes were confirmed by microscopy. A great quantity of apoptotic cells and the increasing G2/M phase cells were observed by flow cytometry. The expression of bax and bcl-2 genes were detected by immunohistochemistry.RESULT: GA has obvious inhibition on the growth of SGC-7901 cells. The value of IC50 for 48 h was 1.47 μmol/L. After treatment of SGC-7901 cells with GA 1.6 μmol/L,marked morphological changes and the increased apoptosis cells were observed. GA can also increase the proportion of G2/M phrase cells. The expressions of bax gene increased and bc1-2 gene decreased. The activation of bax and the suppression of bc1-2 may contribute to the apoptosis mechanism. CONCLUSION: GA inhibited proliferation and induced apoptosis of SGC-7901 cells.