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