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

Abstract

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.

Maresin 1 improves insulin sensitivity and attenuates adipose tissue inflammation in ob/ob and diet‐induced obese mice

“…13S,14S-epoxy-maresin, an intermediate in the biosynthesis of MaR1, has been reported to switch human macrophages to the anti-inflammatory M2 phenotype, leading to a higher production of MaR1 (35), although the direct effects of MaR1 on macrophage phenotype had not been reported. In line with current results, Li et al (36) found that MaR1 administration reduced serum levels of the proinflammatory IL-1b, MCP-1, and TNF-a and increased IL-10 in a model of carbon tetrachloride-induced liver injury.…”

“…In line with current results, Li et al . (36) found that MaR1 administration reduced serum levels of the proinflammatory IL‐1β, MCP‐1, and TNF‐α and increased IL‐10 in a model of carbon tetrachloride–induced liver injury.…”

Maresin 1, a Proresolving Lipid Mediator, Ameliorates Liver Ischemia-Reperfusion Injury and Stimulates Hepatocyte Proliferation in Sprague-Dawley Rats

“…In addition, the metabolism of eicosanoids plays a crucial role in the anti-inflammatory pathways related to the conversion of EPA and DHA to E-resolvins and D-resolvins (series E and D, respectively) [5,6]. Resolvins have potent immunomodulatory properties, limiting inflammation through several mechanisms, including reduction of proinflammatory eicosanoids synthesis, decrease in leukocyte chemotaxis, inhibition of expression of adhesion molecules, and reduced activation of NF-κB [7,8].…”

Maresin 1 Mitigates Inflammatory Response and Protects Mice from Sepsis

“…Severe sepsis is frequently accompanied with acute respiratory distress syndrome (ARDS), hepatic dysfunction, and other organ failures, which lead to poor prognosis [10]. Many previous studies have demonstrated that proresolving mediators, like maresin 1, had protective effect in several organ specified injury models, such as acute lung injury, colitis, liver injury, and lung fibrosis [7, 11–14]. Cecal ligation and puncture (CLP) is an experimental model of lethal sepsis, which can simulate the whole pathology of sepsis which occurs in clinic patients [2].…”