Essential Oil from Siegesbeckia pubescens Induces Apoptosis through the Mitochondrial Pathway in Human HepG2 Cells

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2017-02, Vol.37 (1), p.87-92
• Main Author: 吕丹 郭凯文 徐婵 黄密 郑思建 麻新华 潘丽红 王强 杨新洲
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis Regulatory Proteins - metabolism; Carcinoma, Hepatocellular - drug therapy; Carcinoma, Hepatocellular - metabolism; Caspase-3; Cell Proliferation - drug effects; Cell Survival - drug effects; Drugs, Chinese Herbal - chemistry; Gene Expression Regulation, Neoplastic - drug effects; Hep G2 Cells; HepG2细胞; Humans; Liver Neoplasms - drug therapy; Liver Neoplasms - metabolism; Medicine; Medicine & Public Health; Mitochondria - drug effects; Oils, Volatile - pharmacology; Plant Oils - pharmacology; Signal Transduction - drug effects; Western印迹法; 流式细胞术检测; 精油; 线粒体; 细胞凋亡; 诱导
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-017-1699-7

Siegesbeckia pubescens（SP） has been used as a traditional medicine for the treatment of and inflammatory diseases. However, the activities of SP against hepatocellular carcinoma and the related mechanisms remain unclear. The present study aimed to examine the effects of the essential oil of SP（SPEO） on the proliferation of hepatocellular carcinoma cells and the possible mechanisms. The growth inhibition of Hep G2 cells was analyzed by MTT assay. Hoechst 33258 and fluorescence microscopy were utilized to observe the nuclear morphological changes of apoptotic cells. Flow cytometry was used to detect cell apoptosis and cell cycle. The expressions of the target proteins were detected by Western blotting. The results showed that SPEO obviously inhibited the proliferation of Hep G2 cells in a dose-dependent manner. SPEO activated a series of apoptotic proteins in Hep G2 cells, increasing expression levels of Bax, caspase-3 and caspase-9, and decreasing the bcl-2 expression level. SPEO displayed promising anti-hepatocellular carcinoma activities in vitro, partly by inducing apoptosis in Hep G2 cells through activating the mitochondrial pathway.