Dl-3-n-Butylphthalide Ameliorates Concanavalin-Induced Autoimmune Hepatitis in Mice via Inhibiting Oxidative Stress and Inflammation

Dl-3-n-Butylphthalide (NBP) has been approved by the State Food and Drug Administration of China in 2002 to treat anticerebral ischemia and the related neurological diseases. The purpose of the current study was to investigate the protective effect of NBP against concanavalin A (ConA)-induced autoimmune hepatitis (AIH) and its underlying molecular mechanism. Our results found that treatment with NBP significantly reduced ConA-induced hepatotoxicity by decreasing the alanine transaminase and aspartate aminotransferase levels, alleviating histopathological liver changes, increasing the antioxidant capacity and attenuating the expression of inflammatory cytokines. Furthermore, NBP induced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced the expressions of antioxidant enzymes. The anti-inflammatory effect of NBP may be mediated by inhibition of mitogen-activated protein kinase (MAPKs) and nuclear factor κappa-B ( NF-κB ) inflammasome pathways. Taken together, our study suggested that NBP had protective potential against ConA-induced hepatotoxicity, which might be closely associated with concomitant anti-oxidative stress and anti-inflammatory.