Objective: Alcohol accumulation in the liver can cause pathological disorders such as liver fibrosis that can develop into hepatocellular carcinoma, one of the main causes of mortality associated with liver disease. The previous studies have shown that a plant compound, alpha-mangostin, has an antioxidant effect in the inhibition of pancreatic tumor growth in vitro. This study aimed to analyze the antioxidative properties of alpha-mangostin in acetaldehyde-induced liver fibrosis in vitro. Methods: Immortalized hepatic stellate cells (HSCs), of the LX-2 cell line, were incubated with acetaldehyde in the presence or absence of alphamangostin (10 and 20 μM). The cells were then counted and lysed, and LX-2 cell viability was determined with the trypan blue exclusion method. The malondialdehyde levels, superoxide dismutase activity, and glutathione (GSH) levels were also determined using the cell lysates. Results: Acetaldehyde treatment resulted in a significant increase in HSC cell viability and decreased the production of GSH. Alpha-mangostin treatment resulted in reduced cell viability of the HSCs and prevention of the loss of intracellular GSH. Conclusion: Alpha-mangostin reduced acetaldehyde-induced cell proliferation, and this was affected at least in part by its antioxidative properties.