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BML-111， A Lipoxin A4 Receptor Agonist， Regulated the Balance of Oxidation and Antioxidation in Rat Model with Hepatic Fibrosis
Yu Zhongjian1,3#, Hu Quandong1#, Xu Fangyun2, Huang Yonghong2, Zhu Jun2, Zhou Xiaoyan2*
1Department of Pharmacology, Medical College of Nanchang University, Nanchang 330006, China;
2Department of Pathophysiology, Medical College of Nanchang University, Nanchang 330006, China;
3Jiangxi Province Cancer Hospital l, Nanchang 330006, China
2Department of Pathophysiology, Medical College of Nanchang University, Nanchang 330006, China;
3Jiangxi Province Cancer Hospital l, Nanchang 330006, China
Abstract: In order to confirm the effect of BML-111， a lipoxin A4 receptor agonist， in regulating the balance of oxidation and antioxidation in CCl4-induced experimental hepatic fibrosis， forty Sprague-Dawley (SD) rats were used to build the model of hepatic fibrosis through hypodermic injection of 40% CCl4. And 1 mg/kg BML-111 was administrated via subcutaneous for prevention and treatment. These SD rats were respectively divided into 4 groups via treating with different ways: control group， CCl4 group， treatment group and prevention group. The severity of hepatic fibrosis was defined by observing the change in color， surface glossy and the extent of nodule in rat liver. The degree of hepatic injury and inflammatory infiltration was assessed by hematoxylin-eosin (HE) staining for the hepatic tissue sections. The liver function was evaluated by detecting the activities of alanine transaminase (ALT) and aspartate transaminase (AST) in hepatic homogenate. The balance of oxidation and antioxidation was evaluated by detecting the content of malondialdehyde (MDA)， the activities of antioxidant enzyme， including GSH-Px， superoxide dismutase (SOD) and catalase (CAT)， and the total antioxidative capacity (T-AOC). Through the above experiments， several results were found. When compared to the control group， the livers of CCl4 treated rats looked obviously slant yellow， lost surface glossy， and performed lots of nodules， which could be improved by BML-111， both in the prevention and the treatment groups. BML-111 could inhibit CCl4-induced hepatic injury and inflammatory cell infiltration in rats. CCl4 treated rats performed obviously lower activity of AST and ALT in hepatic homogenate， which was reversed when BML-111 was injected (P<0.05). BML-111， both in the prevention and the treatment groups， the content of CCl4-induced MDA was decreased， but the level of T-AOC and the activities of SOD， GSH-Px and CAT were all increased. The results showed that BML-111 could inhibit CCl4-induced experimental hepatic fibrogenesis by regulating redox homeostasis in rat liver tissue.
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