胶红酵母胞外多糖抗氧化活性及对药物性肝损伤的护肝机制

Antioxidant activity of exo-polysaccharide from Rhodotorula mucilaginosa CM-1 and its protective mechanism against drug-induced liver injury

目的:研究胶红酵母(Rhodotorula mucilaginosa CM-1)胞外多糖对小鼠药物引起肝损伤的保护作用,分析其潜在的分子机制。方法:在多糖抗氧化活性的基础上评估胶红酵母胞外多糖组分RmEPS-11对小鼠异烟肼(INH)和利福平(RIF)引起的肝脏毒性的影响。结果:与INH和RIF处理的小鼠相比,RmEPS-11给药后血清丙氨酸转氨酶(ALT)、天门冬氨酸氨基转移酶(AST)水平和肝脏丙二醛(MDA)含量显著降低,肝脏超氧化酶(SOD)活性和谷胱甘肽过氧化物酶(GSH)含量显著恢复;此外,肝脏的组织病理学损伤和凋亡肝细胞数量改善显著;保护作用主要是由于细胞色素P4502E1(CYP2E1)mRNA表达水平的调节,导致有害自由基和活性氧的形成减少,同时伴随着其抗氧化能力的显著诱导。结论:由胶红酵母R.mucilaginosa CM-1菌株提取的多糖RmEPS-11能够对INH和RIF引起的小鼠急性肝损伤有一定的保护作用。

Objective:To study the protective effects of exo-polysaccharide of Rhodotorula mucilaginosa on drug-induced liver injury in mice and analyze its potential molecular mechanism,so as to provide scientific basis for the application of exo-polysaccharide of Rhodotorula mucilaginosa in functional food and drugs.Methods:Based on the antioxidant activity of polysaccharides,the effects of exo-polysaccharide component RmEPS-11 from Rhodotorula mucilaginosa on liver toxicity induced by INH and RIF in mice were evaluated.Results:Compared with the mice treated with INH and RIF,the levels of ALT and AST in serum and the content of MDA in liver were significantly decreased,while the activity of SOD and the content of GSH in liver were significantly restored.In addition,the histopathological damage of liver and the number of apoptotic hepatocytes were also significantly improved.The mechanism study showed that the protective effect was mainly due to the regulation of CYP2 E1 mRNA expression level,resulting in the reduction of harmful free radicals and ROS formation,accompanied by the significant induction of antioxidant capacity.Conclusion:The polysaccharide RmEPS-11 extracted from R.mucilaginosa CM-1 can protect mice from acute liver injury induced by INH and RIF.