目的 研究构树绿原酸样化合物诱导胃癌SGC-7901细胞凋亡的作用及机制。方法 采用MTT法检测构树绿原酸样化合物对SGC-7901细胞增殖的影响，DAPI染色法观察细胞形态，Annexin V/PI双染色法结合流式细胞术检测细胞凋亡，PI染色结合流式细胞术检测细胞周期，DCHF-DA探针荧光显微镜观察细胞内活性氧（ROS）变化，JC-1染色荧光显微镜观察细胞线粒体膜电位变化，Western blotting检测细胞p53、Bcl-2、Bax、Cytochrome C、p-p38、p-JNK、JNK、细胞外调节蛋白激酶（ERK）、p-ERK蛋白表达量。结果 构树绿原酸样化合物能显著抑制SGC-7901细胞增殖，且呈时间和剂量依赖性；给药组细胞内出现染色质浓缩和凋亡小体，细胞周期被阻滞在G₂/M期，且线粒体膜电位显著下降（P<0.05、0.01），ROS水平显著升高（P<0.05、0.01）。构树绿原酸样化合物能显著上调SGC-7901细胞p53、Bax、Cytochrome C和p-p38蛋白表达水平（P<0.05、0.01、0.001），显著下调p-ERK和Bcl-2表达水平（P<0.01、0.001）。结论 构树绿原酸样化合物可能通过p38-MAPK和ERK-MAPK信号通路介导线粒体氧化应激途径诱导胃癌细胞SGC-7901凋亡。

Objective To explore the mechanism of gastric carcinoma cell SGC-7901 apoptosis induced by chlorogenic acid-like compounds extracted from Broussonetia papyrifera (CALCBP) bark. Methods The SGC-7901 cells were used to evaluate the anti-tumour activity of the extract in vivo, and the proliferation of cells was examined by MTT assay. The cell morphological changes of cells were observed by DAPI staining; The cell apoptosis and the cell cycle were detected respectively by flow cytometry after PI and Annexin V/PI staining; The intracellular ROS were determined under the fluorescence microscope using DCHF-DA probe, the changes of mitochondrial membrane potential were observed by JC-1 staining. The protein expression of p53, Bcl-2, Bax, and Cytochrome C, p-p38, p-JNK, JNK, p-ERK, ERK were analyzed by Western blotting. Results The proliferation of SGC-7901 cells was inhibited significantly by CALCBP in dose-dependent and time-dependent manner, the condensed chromosome and apoptotic body can be observed in the treated cells and the cell cycle was arrested in G₂/M phase, the mitochondrial membrane potential was significantly decreased, whereas the cellular ROS levels of the treated cells were significantly increased. Moreover, the protein expression of p53, Bax, Cytochrome C, and p-p38 were significantly up-regulated and p-ERK and Bcl-2 expression were significantly down-regulated. Conclusion The apoptosis of gastric cancer cell SGC-7901 induced by CALCBP was probably related to oxidative stress of the cell mitochondrial via p38-MAPK and ERK-MAPK signal pathways.

广东省农业科技计划项目"构树综合加工利用技术研究"（0809035）