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However, its function in acute liver injury is still unknown. To address this question, we induced liver injury in BALB\/c mice with intraperitoneal injection of carbon tetrachloride with or without treatment of MaR 1. Our data showed that MaR 1 attenuated hepatic injury, oxidative stress, and lipid peroxidation induced by carbon tetrachloride, as evidenced by increased thiobarbituric acid reactive substances and reactive oxygen species levels were inhibited by treatment of MaR 1. Furthermore, MaR 1 increased activities of antioxidative mediators in carbon tetrachloride\u2010treated mice liver. MaR 1 decreased indices of inflammatory mediators such as tumor necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic>, interleukin\u20106, interleukin\u20101<jats:italic>\u03b2<\/jats:italic>, monocyte chemotactic protein 1, myeloperoxidase, cyclooxygenase\u20102, and inducible nitric oxide synthase. 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