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Cytotoxic effects of Urtica dioica radix on human colon (HT29) and gastric (MKN45) cancer cells mediated through oxidative and apoptotic mechanisms

机译:荨麻对氧化和凋亡机制介导的人结肠癌(HT29)和胃癌细胞(MKN45)的细胞毒性作用

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Defects in the apoptotic pathways are responsible for both the colorectal cancer pathogenesis and resistance to therapy. In this study, we examined the level of cellular oxidants, cytotoxicity and apoptosis induced by hydroalcoholic extract of U. dioica radix (0-2000 mu g/mL) and oxaliplatin (0-1000 mu g/mL, as positive control) in human gastric (MKN45) and colon (HT29) cancer, as well as normal human foreskin fibroblast (HFF) cells. Exposure to U. dioica or oxaliplatin showed a concentration dependent suppression in cell survival with IC50 values of 24.7, 249.9 and 857.5 mu g/mL for HT29, MKN45 and HFF cells after 72 h treatment, respectively. ROS formation and lipid peroxidation were also concentration-dependently increased following treatment with U. dioica, similar to oxaliplatin. In addition, the number of apoptotic cells significantly increased concomitantly with concentration of U. dioica as compared with control cells, which is similar to oxaliplatin and serum-deprived cancer cells. In conclusion, the present study demonstrated that U. dioica inhibited proliferation of gastric and colorectal cancer cells while posing no significant toxic effect on normal cells. U. dioica not only increased levels of oxidants, but also induced concomitant increase of apoptosis. The precise signaling pathway by which U. dioica induce apoptosis needs further research.
机译:凋亡途径中的缺陷与结直肠癌的发病机理和对治疗的抗性有关。在这项研究中,我们检查了人类U. dioica radix(0-2000μg / mL)和奥沙利铂(0-1000μg / mL,作为阳性对照)的水醇提取物诱导的细胞氧化剂水平,细胞毒性和凋亡。胃癌(MKN45)和结肠癌(HT29),以及正常人包皮成纤维细胞(HFF)。处理72 h后,暴露于U. dioica或奥沙利铂显示浓度依赖性抑制细胞存活,HT29,MKN45和HFF细胞的IC50值分别为24.7、249.9和857.5μg / mL。类似于草酸铂,用U. dioica处理后,ROS的形成和脂质过氧化作用也随浓度而增加。另外,与对照细胞相比,凋亡细胞的数量与U.dioica浓度显着增加,这与奥沙利铂和血清缺乏的癌细胞相似。总之,本研究表明,U。dioica抑制胃和结肠直肠癌细胞的增殖,同时对正常细胞没有明显的毒性作用。 U.dioica不仅增加了氧化剂的水平,而且还诱导了细胞凋亡的同时增加。 U.dioica诱导凋亡的确切信号途径尚待进一步研究。

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