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Open Access Research article

Anti-lipoapoptotic effect of Artemisia capillaris extract on free fatty acids-induced HepG2 cells

Eungyeong Jang1, Min-Hee Shin1, Ki-Suk Kim1, Yoomi Kim12, Yun-Cheol Na2, Hong-Jung Woo1, Youngchul Kim1, Jang-Hoon Lee1* and Hyeung-Jin Jang1*

Author Affiliations

1 College of Korean Medicine, Institute of Korean Medicine, Kyung Hee University, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea

2 Integrated Metabolomics Research Group, Seoul Center, Korea Basic Science Institute, 126-16 Anam-Dong, Seungbuk-Ku, Seoul 136-713, Republic of Korea

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BMC Complementary and Alternative Medicine 2014, 14:253  doi:10.1186/1472-6882-14-253

Published: 19 July 2014



Artemisia capillaris (AC) has been recognized as one of the promising candidates for hepatoprotective, hypoglycemic, hypolipidemic, antiobesitic and anti-inflammatory therapeutic effectiveness. This study evaluated the inherent mechanism and anti-apoptotic activity of 30% ethanol extract of AC (AC extract) 100 μg/ml on free fatty acids (FFAs)-induced HepG2 cellular steatosis and lipoapoptosis.


Hepatic steatosis was induced by culturing HepG2 cells with a FFAs mixture (oleic and palmitic acid at the proportion of 2:1) for 24 h, thus ultimately giving rise to lipoapoptosis. Cell viability and lipid accumulation were detected by MTT assay and Oil Red O staining method respectively and Caspase-3, −9, Bax, Bcl-2, p-JNK and PUMA were measured for lipoapoptosis after 24 hours.


AC extract significantly improved the FFAs-induced steatosis without cytotoxicity and Caspase-3, −9, Bax and Bcl-2 were modulated profitably to HepG2 cells after AC treatment. In addition, AC extract inhibited the activation of c-Jun NH2 terminal kinase (JNK) and PUMA, which mechanism is related to non-alcoholic steatohepatitis (NASH).


Combined together, AC extract exerted an obvious hypolipidemic and anti-apoptotic effect, indicating that AC extract might have potential therapeutic herb against NASH.

Artemisia capillaris (AC); HepG2; Non-alcoholic steatohepatitis (NASH); Lipoapoptosis; c-Jun NH2-terminal kinase (JNK); p53 up-regulated mediator of apoptosis (PUMA)