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首页> 外文期刊>International Journal of Pharmacology >Unveiling the Anti-cancer Efficiency of Chebulagic Acid-Mediated Apoptotic Mechanisms in HepG2 Cell Line
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Unveiling the Anti-cancer Efficiency of Chebulagic Acid-Mediated Apoptotic Mechanisms in HepG2 Cell Line

机译:揭示乳蛋白酸介导的HepG2细胞凋亡机制的抗癌效率

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Background and Objective: Hepatocellular carcinoma (HCC) is a predominant type of Cancer in the liver than other cancers. World Health Organization predicted that the maximum mortality rate was caused by HCC (6th leading cause of death) and also by 2030, 1 million affected patients will die due to HCC. The molecular mechanism and treatment with plant-derived remedies/drugs giving better efficacy/resistance against HCC causing genes and its induced apoptosis. In the present (in vitro) study was designed to check the antitumor activity of the Chebulagic acid on HepG2 cells. Materials and Methods: Terminalia chebular derived Chebulagic acid anticancer activity on HepG2 cells was assessed by MTT assay, followed by DCFH-DA, Rhodamine123, acridine orange, Acridine orange/Ethidium bromide and DAPI fluorescent staining was done to check the apoptosis which was induced by Chebulagic acid on HepG2 cells. Results: The MTT assay revealed that Chebulagic acid treatment significantly inhibited cell proliferation and controlling ROS. Simultaneously, it shows a better effect on cells were pre-treatment with Chebulagic acid with dose and time-dependent based. Increased apoptotic cells (%) were found in mitochondrial membrane-associated and it's potential by Chebulagic acid on HepG2 cells. Conclusion: Overall findings of the study proposed that Chebulagic acid able to induce apoptosis HCC in human HepG2 cells by its apoptotic mechanisms.
机译:背景和目的:肝细胞癌(HCC)是肝脏的主要癌症,而不是其他癌症。世界卫生组织预测,最大的死亡率是由HCC(第6次死亡原因)造成的,并且在2030年,100万名受影响的患者将因HCC而死亡。植物衍生的补救措施/药物的分子机制和治疗给药患有更好的疗效/抗性导致基因及其诱导的细胞凋亡。在本发明(体外)的研究中,设计用于检查HepG2细胞对雪柱酸的抗肿瘤活性。材料和方法:通过MTT测定评估HepG2细胞上的末端乳白乳白乳酸抗癌活性,其次是DCFH-DA,罗丹明123,吖啶橙,吖啶橙/乙酸溴和DAPI荧光染色,检查诱导的凋亡乳蛋白酸在hepg2细胞上。结果:MTT测定显示薄丁酸治疗显着抑制细胞增殖和控制ROS。同时,它表明对细胞的更好效果与雪尿酸预处理,其剂量和时间依赖性。在线粒体膜相关的增加的凋亡细胞(%)增加,并且在HepG2细胞上受苯脲酸的潜力。结论:该研究的总体调查结果提出了薄泛酸能够通过其凋亡机制诱导人HepG2细胞的凋亡HCC。

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