Journal Article

Maresin 1, a Proresolving Lipid Mediator, Mitigates Carbon Tetrachloride-Induced Liver Injury in Mice

Deng, Meizhou, Shi, Liang, Wang, Yaxin, Li, Ruidong, Zhang, Peng, Wu, Ke, Zhao, Ende, Tao, Kaixiong, Li, Wei, Yin, Yuping, Xie, Gengchen, Wang, Di

2016

Overview

Maresin 1 (MaR 1) was recently reported to have protective properties in several different animal models of acute inflammation by inhibiting inflammatory response. 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-treated mice liver. MaR 1 decreased indices of inflammatory mediators such as tumor necrosis factor-α, interleukin-6, interleukin-1β, monocyte chemotactic protein 1, myeloperoxidase, cyclooxygenase-2, and inducible nitric oxide synthase. Administration of MaR 1 inhibited activation of nuclear factor kappa B (NF-κb) and mitogen-activated protein kinases (MAPKs) in the liver of CCl4 treated mice. In conclusion, these results suggested the antioxidative, anti-inflammatory properties of MaR 1 in CCl4 induced liver injury. The possible mechanism is partly implicated in its abilities to inhibit ROS generation and activation of NF-κb and MAPK pathway.

• Publisher: Hindawi Publishing Corporation,John Wiley & Sons, Inc
• Subject: Alanine Transaminase - blood / Animals / Antioxidants - metabolism / Aspartate Aminotransferases - blood / Carbon / Carbon Tetrachloride / Cell Nucleus - drug effects / Cell Nucleus - metabolism / Chemicals / Colleges & universities / Cyclooxygenase 2 - metabolism / Cytokines / Cytokines - blood / Docosahexaenoic Acids - administration & dosage / Docosahexaenoic Acids - pharmacology / Enzymes / Fatty acids / Glutathione - metabolism / Hep G2 Cells / Humans / Inflammation / Inflammation Mediators - metabolism / Interleukins / Kinases / Laboratories / Lipid peroxidation / Lipids / Liver / Liver - drug effects / Liver - pathology / Liver diseases / Male / Mice, Inbred BALB C / Mitogen-Activated Protein Kinases - metabolism / NF-KappaB Inhibitor alpha - metabolism / Nitric oxide / Nitric Oxide Synthase Type II - metabolism / Oxidative stress / Oxidative Stress - drug effects / Peroxidase - metabolism / Phosphorylation / Phosphorylation - drug effects / Reactive Oxygen Species - metabolism / Rodents / Science / Thiobarbituric Acid Reactive Substances - metabolism / Transcription Factor RelA - metabolism