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首页> 外文期刊>Tropical Journal of Pharmaceutical Research >Green tea polyphenol induces significant cell death in human lung cancer cells
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Green tea polyphenol induces significant cell death in human lung cancer cells

机译:绿茶多酚诱导人肺癌细胞明显死亡

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Purpose: To investigate the dose–response relationship of green tea polyphenol in an animal model of lung cancer. Methods: The effects of epigallocatechin-3-gallate (EGCG) on the inhibition of xenograft tumor growth, the accumulation of 8-hydroxy-2'-deoxyguanosine (8-OHdG), and apoptosis based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay were evaluated in non-small cell lung cancer (NSCLC) cell lines, namely, H1155, H661, and A427 (a human lung carcinoma-derived cell line). The dose-dependent effects of EGCG on H1155 xenograft tumor growth, as well as the levels of EGCG in plasma and tissue, were also determined in male nude mice. Results: EGCG inhibited the growth of NSCLC-derived cell lines (H1155) over a 45-day period. There was a significant reduction (57 %) in tumor weight in EGCG-fed (0.5 %) animals compared with the control group (p 0.05). Linear regression analysis revealed a dose-dependent reduction in tumor size. MTT assay results revealed inhibition of H1155 cell growth (25 %, p 0.05) after 24 h treatment with EGCG. The addition of superoxide dismutase (5 U/mL) and catalase (30 U/mL) reduced the inhibitory effect of EGCG. Mice administered 30 mg/kg EGCG via intraperitoneal injection exhibited the least amount of oxidative stress. Conclusion: The results demonstrate the concentration-dependent inhibitory effects of EGCG on lung cancer cells, including H1155 cells, both in vitro and in vivo. The induction of reactive oxygen species, oxidative DNA damage, and apoptosis were evident following EGCG treatment.
机译:目的:探讨绿茶多酚在肺癌动物模型中的剂量反应关系。方法:基于3-(4,5-二甲基噻唑)对表没食子儿茶素-3-没食子酸酯(EGCG)抑制异种移植瘤的生长,抑制8-羟基-2'-脱氧鸟苷(8-OHdG)的积累和凋亡。在非小细胞肺癌(NSCLC)细胞系,即H1155,H661和A427(人类肺癌衍生的细胞系)中评估了-2-yl)-2,5-二苯基四唑溴化物(MTT)分析。还测定了雄性裸鼠中EGCG对H1155异种移植肿瘤生长的剂量依赖性作用以及血浆和组织中的EGCG水平。结果:EGCG在45天内抑制了NSCLC衍生细胞系(H1155)的生长。与对照组相比,EGCG喂养的动物(0.5%)的肿瘤重量显着减少(57%)(p <0.05)。线性回归分析显示肿瘤大小呈剂量依赖性降低。 MTT分析结果显示,EGCG处理24小时后,H1155细胞生长受到抑制(25%,p <0.05)。超氧化物歧化酶(5 U / mL)和过氧化氢酶(30 U / mL)的加入降低了EGCG的抑制作用。通过腹膜内注射施用30mg / kg EGCG的小鼠表现出最小量的氧化应激。结论:结果表明,EGCG对肺癌细胞(包括H1155细胞)的体内和体外浓度依赖性抑制作用。 EGCG处理后,明显诱导了活性氧,氧化性DNA损伤和细胞凋亡。

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