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首页> 外文期刊>Brazilian Journal of Pharmaceutical Sciences >Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction
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Essential oil from Euphorbia esula inhibits proliferation and induces apoptosis in HepG2 cells via mitochondrial dysfunction

机译:来自大戟属的精油Esula抑制了通过线粒体功能障碍诱导HepG2细胞中的细胞凋亡

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摘要

Hepatocellular carcinoma is one of the most prevalent malignancies and a leading cause of cancer-related mortality worldwide. However, the therapies to prevent hepatocellular carcinoma are still limited and the emergence of drug resistance leads to the development of new anti-cancer drugs and combinational chemotherapy regimens. Our study was aimed to explore the anticancer effects of the essential oil extract (EEEO) from Euphorbia esula which has been widely used in traditional Chinese folk medicine and possessed potential cytotoxic effects in several human tumor cells. However, the mechanisms of EEEO-induced anti-proliferation and apoptosis have not been completely elucidated. In this study, EEEO was prepared by hydro-distillation and the main chemical component of EEEO was identified by GC-MS. HepG2 cells were treated with EEEO in vitro and then evaluated with respect to proliferation, apoptosis, and levels of reactive oxygen species (ROS) and apoptotic proteins. Our studies showed that EEEO decreased cell viability, elevated ROS levels, and induced apoptosis of HepG2 cells in a concentration- and time-dependent manner. Furthermore, Bcl-2 was down-regulated, while Bax was up-regulated in HepG2 after EEEO treatment. These results suggest that EEEO induced apoptosis of HepG2 cells and indicate that this apoptosis might be mediated by the mitochondrial pathway.
机译:肝细胞癌是最普遍的恶性肿瘤之一,是全世界癌症相关死亡率的主要原因之一。然而,预防肝细胞癌的疗法仍然有限,耐药性的出现导致新的抗癌药物和组合化疗方案的发育。我们的研究旨在探讨来自大戟属Euphorbia Esula的基本油提取物(EEEO)的抗癌效应,这些抗eSula在传统的中国民间医学中被广泛应用于几种人类肿瘤细胞中具有潜在的细胞毒性作用。然而,EEEO诱导的抗增殖和细胞凋亡的机制尚未完全阐明。在该研究中,通过水蒸馏制备EEEO,通过GC-MS鉴定EEEO的主要化学成分。用EEEO在体外处理HEPG2细胞,然后相对于增殖,细胞凋亡和反应性氧(ROS)和凋亡蛋白的水平评估。我们的研究表明,EEEO降低了细胞活力,升高的ROS水平,并以浓度和时间依赖的方式诱导HepG2细胞的凋亡。此外,Bcl-2被下调,而Eeeo治疗后,Bax在HepG2中升高。这些结果表明Eeeo诱导HepG2细胞的凋亡,表明该细胞凋亡可能由线粒体途径介导。

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