芹菜素诱导人胃癌细胞凋亡作用及机制研究

目的：研究芹菜素（apigenin, API）致人胃癌细胞凋亡作用及其机制。方法：培养人胃癌BGC823细胞株，加入不同浓度的API，孵育48 h。PI染色流式细胞术（FCM）分析测定凋亡率；罗丹明染色FCM分析测定细胞线粒体跨膜电位(Δψm)；Caspase-9分光光度法检测试剂盒测定caspase-9活性；Western印迹检测线粒体凋亡信号转导通路相关蛋白的表达，包括bax，bcl-2，caspase-9和caspase-3。结果： API（20，40和80 μg/mL）作用48 h能呈浓度依赖性地诱导BGC823细胞凋亡。而且，API也能降低BGC823细胞的Δψm，增加caspase-9活性，促进细胞色素c（Cyt c）释放，上调bax，caspase-9和caspase-3蛋白的表达，同时下调bcl-2蛋白表达，且呈剂量依赖性。结论：API通过活化线粒体信号转导途径诱导人胃癌细胞凋亡。

Study on pro-apoptotic effect of apigenin on human gastriccancer cells and its underlying mechanisms

ObjectiveTo determine the effect of apigenin (API) on induction of apoptotic death in human gastric cancer cells and its underlying mechanisms. MethodsHuman gastric cancer BGC823 cells line was cultured and treated with different concentrations of API for 48 h. Cell apoptosis and mitochondrial membrane potential was determined by flow cytometery (FCM) labeled with propidium iodide (PI) and Rhodamine123, respectively. Caspase-9 activity was determined by caspase-9 colorimetric assay kit. Western blot was used to analyze the expressions of apoptosis mitochondrial signal transduction pathway related proteins including bax, bcl-2, caspase-9 and caspase-3. ResultsTreatment with API (20, 40 and 80μg/mL) for 48 h could concentration-dependently induce the apoptotic death of BGC823 cells. Moreover, API could also decrease the cellular Δψm, increase the activity of caspase-9 and enhance the releasing of cytochrome c. The protein expressions of bax, caspase-9 and caspase-3 were upregulated by treatment with API, associated with a downregulation of the protein expression of bcl-2. ConclusionAPI can induce the apoptosis of human gastric cancer cells via activating mitochondrial signal transdution pathway.