小金海棠多酚对肝纤维化的改善及机制研究  

Study on Induced Live Injury and Fibrosis By Malus xiaojinensis Polyphenols

作　　者：韦月平[1] 王鹏[1] WEI Yueping, WANG Peng(Agriculture college, Eastern Liaoning University, Dandongl 18003, China)

机构地区：[1]辽东学院农学院,辽宁丹东118003

出　　处：《食品与生物技术学报》2018年第7期764-768,共5页Journal of Food Science and Biotechnology

基　　金：辽东学院青年基金项目(QN030)

摘　　要：研究小金海棠多酚对CCl4诱导小鼠肝纤维化的改善作用及机制。采用皮下注射CCl4诱导小鼠肝纤维化,同时小金海棠多酚(MXP)灌胃给药(10 mg/kg、20 mg/kg)的方法。结果表明,皮下注射CCl4诱导小鼠肝脏发生明显的损伤。与模型组相比,喂食小金海棠多酚显著降低了血清和肝组织中ALT与AST活性,同时肝组织中SOD和GSH-PX活性显著提高。形态和组织学检测表明,小金海棠多酚显著逆转CCl4诱导的肝损伤。此外,喂食小金海棠多酚能显著抑制皮下注射CCl4引发的IL-1、IL-6和TNF-α等炎性细胞因子的生成。以上结果表明,小金海棠多酚可以明显减轻CCl4诱导产生的肝纤维化,其作用机制可能与其增强机体抗氧化能力、抑制炎性细胞因子合成有关。The aim of this study was to investigate the anti-hepatic fibrosis mechanism of Malus xiaojinensis polyphenols （MXP）.Mice with Subcutaneous injection of CC14 were set as the animal model of live injury and fibrosis while those treated with MXP by gavage（ 10 mg/kg, 20 mg/kg） was used as the prevention groups. The results showed that CC14 caused severe liver injury with increased activity of ALT and AST. Meanwhile the model mice had reduced activity of SOD and GSH-PX. Compared with the model group, MXP decreased the activity of ALT and AST in serum and liver and increased the activity of SOD and GSH-PX significantly. Both morphologic and histological detections indicated that MXP could ameliorate the degree hepatocyte injury and privation of the liver fibrosis. Moreover, feeding of MXP could inhibit the production of IL- 1, IL-6 and TNF-a. The study showed that MXP could partly reverse CC14 induced hepatic fibrosis by enhancing anti-oxidative function and down -regulating inflammatory cytokine synthesis. MXP may be developed as a novel antioxidant for prevention of the liver diseases.

关 键 词：小金海棠 多酚 保肝 肝纤维化 

分 类 号：TS201.4[轻工技术与工程—食品科学]