The results support the possibility that Ala-Gln may diminish oxidative stress by enhancing SOD and GPX activities, reducing lipid accumulation via regulating the expression of CD36 and FXR, alleviating inflammation by decreasing the number of activated macrophages and proinflammatory mediators, and suppressing the progression of liver fibrosis through inhibiting hepatic stellate cells activation. This evidence concerns the gene SOD1 and Hepatic fibrosis.