Baicalin provides protection against fluoxetine-induced hepatotoxicity by modulation of oxidative stress and inflammation

Core Tip

Core Tip: Prolonged treatment with the antidepressant drug fluoxetine causes severe hepatic damage. This study evaluated fluoxetine-induced liver damage in male albino Wistar rats. Oral fluoxetine was administered (10 mg/kg) for 28 d and caused significant alterations in serum and tissue biomarkers. Baicalin and silymarin were co-administered to facilitate the amelioration of oxidative stress-mediated hepatic damage and inflammation. The biochemical markers (total protein, albumin, total bilirubin, alanine transaminase, aspartate transaminase, alkaline phosphatase, superoxide dismutase, catalase, glutathione, glutathione-S-transferase, malondialdehyde and advanced oxidation protein products) and inflammatory markers [tumor necrosis factor-α, interleukin (IL)-6, IL-10 and interferon-γ] were markedly restored to near normal levels after treatment with the natural flavonoid compound baicalin. Histopathological examination of liver slices showing cellular degeneration and increased vacuolation in the fluoxetine-treated rats also corroborated the results obtained for biomarkers of liver function, oxidative stress and inflammation. The baicalin-treated rats demonstrated normal vacuolation and cellular pattern. Thus, baicalin acts as an antioxidant, anti-inflammatory and hepatoprotective agent in mitigating fluoxetine-induced toxicity. To the best of our knowledge, this is the first study to report the hepatoprotective efficacy of baicalin in fluoxetine-induced liver damage.