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机构地区:[1]广州医学院第一附属医院,广州510182 [2]广州市第十二人民医院
出 处:《山东医药》2011年第1期7-9,共3页Shandong Medical Journal
基 金:第八轮广东省高等学校重点扶持学科资助项目[粤科教(2007)26号]
摘 要:目的探讨维生素C对胃癌细胞株MKN45增殖、凋亡的影响及其相关机制。方法在体外培养的胃癌细胞株MKN45中加入不同浓度(0.05、0.1、0.5、1 mg/ml)的维生素C,通过MTT比色法检测维生素C对细胞生长活力的影响;应用荧光显微镜、流式细胞术、DNA Ladder分析法检测细胞凋亡情况;应用分光光度法检测Caspase-3活性;应用化学显色法测定维生素C作用MKN45 24 h后细胞内超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量。结果维生素C对胃癌细胞株MKN45有显著的生长抑制作用;与对照组比较,1 mg/ml维生素C处理后,细胞凋亡率升高(P<0.01),并呈现凋亡的形态学改变,DNA Ladder分析呈典型"梯状"条带;Caspase-3活性升高(P<0.05)。与对照组相比,维生素C处理组细胞内的SOD活性下降,MDA含量增加(P<0.05)。结论 1 mg/ml浓度的维生素C作用24 h后,可诱导胃癌细胞MKN45凋亡,其机制可能是通过提高Caspase-3的活性以及通过自身自氧化的氧化应激效应而诱导肿瘤细胞凋亡。Objective To investigate the effects of vitamin C on proliferation and apoptosis of gastric cancer cell line MKN45 and elucidate its related mechanisms. Methods Add different concentrations of vitamin C into gastric cancer cell line MKN45 which was cultured in vitro, the effection of vitamin C on growth activity was measured by MTT assay. Apoptosis was detected by fluorescence microscope, flow cytometry (FCM) and DNA Ladder analysis method. The activity of Caspase-3 was tested by spectrophotometry. The activity of SOD and the levels of MDA in gastric cancer cells after 24-h treatment were assayed by chemical staining method. Results Vitamin C had significantly effect on inhibiting the growth of human gastric cancer cell strain MKN45. The apoptosis rates in vitamin C treatment group were apparently higher than those of the control group, and the treatment group had shown the morphological changes of apoptesis. The result of DNA Ladder showed a typical "ladder" stripe. Compared to the control group, the activity of Caspase-3 of vitamin C group rose remarkably(P 〈 0. 05 ); SOD activity at vitamin C treatment group dropped, while quantity of MDA increased (P 〈0. 05). Conclusions 1 mg/ml concentration of vitamin C for 24 hours could induce apoptosis in human gastric cancer cell MKN45 strain, the mechanism of this effect may he regulated by increasing the activity of Caspase-3, through its own self-oxidation effects of oxidative stress to induce apoptosis of tumor ceils.
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