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Buxus Microphylla var. Koreana Nakai Extract for the Treatment of Gastric Cancer

机译:小叶黄杨大韩中性提取物治疗胃癌

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Objectives: Buxus Microphylla var. Koreana Nakai Extract (BMKNE) is used as a folk remedy for malaria and veneral disease. In the present study, we investigated the effects of BMKNE in the growth and the survival of AGS cells, the most common human gastric adenocarcinoma cell lines. Methods: The AGS cells were treated with varying concentrations of BMKNE. Analyses of the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial depolarization were conducted to determine whether AGS cell death occured by apoptosis. Also, to identify the role of transient receptor potential melastatin (TRPM) 7 channels in AGS cell growth and survival, we used human embryonic kidney (HEK) 293 cells overexpressed with TRPM7 channels. Results: Experimental results showed that the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial depolarization were increased. Therefore, BMKNE was found to induce the apoptosis of these cells, and this apoptosis was inhibited by SB203580 (a p38 mitogen-activated protein kinase (MAPK) inhibitor), and by a c-jun NH2-terminal kinase (JNK) II inhibitor. Furthermore, BMKNE inhibited TRPM7 currents and TRPM7 channel over-expressions in HEK 293 cells, exacerbating BMKNE-induced cell death. Conclusions: These findings indicate that BMKNE inhibits the growth and the survival of gastric cancer cells due to a blockade of the TRPM7 channel's activity and MAPK signaling. Therefore, BMKNE is a potential drug for treatment of gastric cancer, and both the TRPM7 channel and MAPK signaling may play an important role in survival in gastric cancer cells.
机译:目标:小叶黄杨变种。大韩民国中毒提取物(BMKNE)被用作疟疾和小肠疾病的民间疗法。在本研究中,我们研究了BMKNE在AGS细胞(最常见的人胃腺癌细胞系)的生长和存活中的作用。方法:用不同浓度的BMKNE处理AGS细胞。进行了亚G1峰,caspase-3和-9活性以及线粒体去极化的分析,以确定AGS细胞是否因凋亡而死亡。同样,为了确定瞬时受体潜在褪黑素(TRPM)7通道在AGS细胞生长和存活中的作用,我们使用了TRPM7通道过表达的人胚肾(HEK)293细胞。结果:实验结果表明,亚G1峰,caspase-3和-9活性以及线粒体去极化均增加。因此,发现BMKNE诱导了这些细胞的凋亡,并且SB203580(p38丝裂原活化蛋白激酶(MAPK)抑制剂)和c-jun NH2末端激酶(JNK)II抑制剂抑制了该凋亡。此外,BMKNE抑制HEK 293细胞中TRPM7电流和TRPM7通道过表达,加剧了BMKNE诱导的细胞死亡。结论:这些发现表明,由于阻断TRPM7通道的活性和MAPK信号传导,BMKNE抑制了胃癌细胞的生长和存活。因此,BMKNE是治疗胃癌的潜在药物,TRPM7通道和MAPK信号传导均可能在胃癌细胞的存活中起重要作用。

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