研究动态
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香茅酮鼠尾草乙醇根提取物通过内源性凋亡诱导HepG2细胞的细胞毒性。

Coleus vettiveroides ethanolic root extract induces cytotoxicity by intrinsic apoptosis in HepG2 cells.

发表日期:2023 Sep 03
作者: Kadmad Abdul Hameed Mohamed Azar, Devaraj Ezhilarasan, Karthik Shree Harini
来源: Cellular & Molecular Immunology

摘要:

肝细胞癌(HCC)是全球所有原发癌症中占比80%以上的肿瘤,因缺乏有效、明确的治疗药物而在与癌症相关的死亡中排名第四。斑叶草(CV)在印度传统医药中被用来治疗糖尿病、肝病、皮肤病、白癜风和麻风病。本研究探讨了CV乙醇根提取物对HepG2细胞的抗癌效应。HepG2细胞经CV提取物处理后,用MTT法分析其细胞毒性。通过AO/EB染色、丙碘胺染色、DCFH-DA法、鬼笔草素染色、流式细胞仪和qPCR研究对ROS表达、细胞凋亡和细胞周期进行分析。植物化学分析证实CV根提取物中存在槲皮素和月桂素。结果显示CV抑制了HepG2细胞的增殖,引起细胞和核形态的改变。CV还发现增加了HepG2细胞内的细胞内ROS水平和氧化应激标志物。CV显著改变了HepG2细胞中肌动蛋白微丝分布,并引起亚G0-G1阶段的细胞周期阻滞。CV还通过增加p53、Bax、细胞色素C、Apaf-1、PARP、caspase-3和caspase-9的表达,以及下调Bcl-2的表达诱导了线粒体介导的细胞凋亡。因此,CV通过引起线粒体功能障碍、氧化应激、细胞骨架紊乱、细胞周期阻滞和线粒体介导的细胞凋亡发挥其抗癌作用,并且可能是治疗HCC的有潜力的选择。© 2023 John Wiley & Sons Ltd.
Hepatocellular carcinoma (HCC) contributes to more than 80% of all primary cancers globally and ranks fourth in cancer-related deaths, due to the lack of an effective, definite therapeutic drug. Coleus vettiveroides (CV) has been used in Indian traditional medicine to treat diabetes, liver ailments, skin diseases, leukoderma, and leprosy. This study investigates the anticancer effect of CV ethanolic root extract in HepG2 cells. HepG2 cells were treated with CV extract, and its cytotoxicity was analyzed by MTT assay. AO/EB staining, propidium iodide staining, DCFH-DA assay, phalloidine staining, flow cytometry, and qPCR studies were performed for ROS expression, apoptosis and cell cycle analysis. The phytochemical analysis confirmed the presence of quercetin and galangin in CV root extract. The results showed that CV inhibited the proliferation of HepG2 cells, with altered cellular and nuclear morphology. CV was also found to increase intracellular ROS levels and oxidative stress markers in HepG2 cells. CV significantly altered the actin microfilament distribution in HepG2 cells and caused cell cycle arrest at the sub G0 -G1 phase. CV also induced mitochondria-mediated apoptosis, as evidenced by increased expression of p53, Bax, cytochrome C, Apaf-1, PARP, caspase-3 and caspase-9, and downregulated Bcl-2 expression. Therefore, CV exerts its anticancer effect by inducing mitochondrial dysfunction, oxidative stress, cytoskeletal disorganization, cell cycle arrest, and mitochondria-mediated apoptosis, and it could be a potent therapeutic option for HCC.© 2023 John Wiley & Sons Ltd.