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

被引:2
作者
Azar, Kadmad Abdul Hameed Mohamed [1 ,2 ]
Ezhilarasan, Devaraj [2 ,3 ]
Harini, Karthik Shree [2 ]
机构
[1] Koppal Inst Med Sci, Dept Pharmacol, Koppal, India
[2] Saveetha Inst Med & Tech Sci SIMATS, Saveetha Dent Coll, Dept Pharmacol, Chennai, India
[3] Saveetha Inst Med & Tech Sci, Saveetha Dent Coll, Dept Pharmacol Hepatol & Mol Med Lab, 162 PH Rd, Chennai 600077, Tamil Nadu, India
关键词
anticancer; apoptosis; cytotoxicity; hepatocellular carcinoma; HEPATOCELLULAR-CARCINOMA; CYCLE ARREST; TUBEIMOSIDE-I; CANCER; ASSAY; MITOCHONDRIA; ANTIOXIDANT; SORAFENIB; DISCOVERY; SILYMARIN;
D O I
10.1002/jat.4536
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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 G(0)-G(1) 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.
引用
收藏
页码:245 / 259
页数:15
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