Apoptotic activity of alpha-mangostin in acetaldehyde- induced LX2 hepatic stellate cell lines

Abstract

Previous studies have shown that alpha-mangostin has cytotoxic potentials by increasing apoptotic and promoting arrest in the cell cycle process in hepatocellular carcinoma in vitro. Prior research has also shown that alpha- mangostin ameliorates alcohol's toxicity in hepatic stellate cells in vitro; however, whether alpha-mangostin exerts its effect by inducing apoptosis is still unknown. The study was aimed to analyze the apoptotic properties of alpha-mangostin in acetaldehyde-induced hepatic stellate cells in vitro. Immortalized human hepatic stellate (HSC) cells with LX2 cell line were treated with acetaldehyde in the presence or absence of alpha-mangostin (10 and 20 μM). After treatments, cells were harvested, isolated for RNA, and analyzed for mRNA expressions of apoptotic markers: Bax, Bcl-2, caspase-3, and caspase-9 using qRT-PCR. Acetaldehyde treatment caused a significant reduction in the mRNA expressions of Bax and caspase-3 and a slight decrease in the expressions of caspase-9. The addition of alpha-mangostin increased the mRNA expressions of Bax, caspase-9, and caspase-3 significantly. Increased mRNA expressions of Bcl-2 in alpha-mangostin- treated cells were observed. These effects displayed a dose-dependent tendency. Alpha-mangostin demonstrates apoptotic activity in acetaldehyde-induce hepatic stellate cells in a dose-dependent manner.