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目的探讨没食子酸(gallic acid,GA)对胃癌MGC-803细胞侵袭能力的影响及机制。方法体外培养胃癌MGC-803细胞,噻唑蓝(MTT)法检测细胞的抑制率;Transwell小室法检测GA对MGC-803细胞侵袭能力的影响;Western blotting检测没食子酸对PI3K/AKT通路相关因子(PI3K、p-PI3K、AKT、p-AKT)及细胞基质金属蛋白酶(MMP2、MMP9)蛋白表达的影响。结果 MTT法检测表明6.250~50.000μmol·L~(-1)GA可抑制MGC-803细胞的生长,并呈剂量依赖性(P<0.05);Transwell小室法显示,与对照组比较,经GA处理后MGC-803细胞侵袭能力明显降低(P<0.05);Western blotting结果显示,没食子酸处理后的MGC-803细胞p-PI3K、p-AKT、MMP2、MMP9蛋白表达下降,同时加入PI3K抑制剂后,可抑制PI3K/AKT通路活化,抑制MMP2和MMP9的表达。结论没食子酸可有效抑制胃癌MGC-803细胞侵袭能力,其机制可能是与通过调控PI3K/AKT信号通路,抑制MMP2和MMP9的表达有关。
Objective To investigate the effect and mechanism of gallic acid (GA) on invasion of gastric cancer cell line MGC-803. Methods The gastric cancer cell line MGC-803 was cultured in vitro. The inhibitory rate of MGC-803 cells was determined by MTT assay. The invasion ability of MGC-803 cells was detected by Transwell chamber assay. The effect of gallic acid on the PI3K / AKT pathway-related factors , P-PI3K, AKT, p-AKT) and matrix metalloproteinase (MMP2, MMP9) protein expression. Results The results of MTT assay showed that the proliferation of MGC-803 cells was inhibited by 6.250 ~ 50.000μmol·L -1 GA in a dose-dependent manner (P <0.05). Transwell chamber assay showed that compared with the control group, (P <0.05). The results of Western blotting showed that the expression of p-PI3K, p-AKT, MMP2 and MMP9 in MGC-803 cells after treatment with gallic acid decreased, and the PI3K inhibitor , Can inhibit PI3K / AKT pathway activation, inhibit the expression of MMP2 and MMP9. Conclusion Gallic acid can effectively inhibit the invasion of gastric cancer cell line MGC-803. The mechanism may be related to the inhibition of the expression of MMP2 and MMP9 through the regulation of PI3K / AKT signaling pathway.