机构地区:[1]电子科技大学资源与环境学院,四川成都611731 [2]中国科学院深圳先进技术研究院,广东深圳518055 [3]中国农业大学食品科学与营养工程学院,北京100083
出 处:《食品与发酵工业》2021年第20期44-51,共8页Food and Fermentation Industries
基 金:国家自然科学基金(42077395);深圳市科技计划项目(JCYJ2017081816440501,YCYJ20180507182525623)。
摘 要:研究植物发酵液对慢性酒精性诱导小鼠肝损伤的保护作用及其机制。将雄性C57BL/6小鼠随机分为正常对照组、模型组、植物发酵液低、高剂量干预组[1.25和5.0 mL/kg体重(body weight,BW)]。每天正常对照组、模型组先灌胃无菌蒸馏水,植物发酵液干预组先灌胃相应剂量的植物发酵液,1 h后除正常对照组外各组小鼠均灌胃56°白酒(10 mL/kg BW)。实验结束后检测血清肝功能指标、细胞因子水平,肝脏乙醇代谢关键酶活力、抗氧化指标及有关基因mRNA表达水平等,并观察肝脏组织病理变化。结果表明,与慢性肝损伤模型组小鼠比较,干预8、10、12周后低高剂量植物发酵液均能够显著降低由慢性酒精摄入诱导的血清中天门冬氨酸氨基转移酶(aspartate aminotransferase,AST)、丙氨酸氨基转移酶(alanine transaminase,ALT)活性的升高;苏木精-伊红染色结果显示,与模型组相比,植物发酵液高剂量组小鼠肝组织破坏程度减轻。植物发酵液能抑制肝脏中乙醇诱导的乙醇脱氢酶(alcohol dehydrogenase,ADH)、乙醛脱氢酶(aldehyde dehydrogenase,ALDH)活性升高及细胞色素P450家族成员2E1(recombinant cytochrome P4502E1,Cyp2e1)mRNA表达下调,恢复机体乙醇代谢系统功能;提高肝组织中总超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、总抗氧化能力(total antioxidant capacity,T-AOC)酶活力,抑制肝组织中脂质过氧化物丙二醛(malondialdehyde,MDA)含量的增加,提高肝脏抗氧化能力;上调血清细胞因子白细胞介素-1β(interleukin-1β,IL-1β)水平及肝脏白细胞介素-6(interleukin-6,Il6)mRNA的表达,下调肝脏信号转导与转录激活因子3(signal transducer and activator of transcription 3,Stat3)mRNA的表达,减轻炎症反应。可见,植物发酵液对慢性酒精诱导的小鼠肝损伤具有保护作用,可能与其恢复机体酒精代谢功能、减轻酒精代谢对机体造成的氧化�Protective effects of plant fermentation extracts(PFE)against alcohol-induced liver injury in mice was investigated.Male C57BL/6 mice were randomly divided into four groups.The normal control group and the model group were given distilled water per day,and the PFE low and high dose groups were given the corresponding PFE(1.25 or 5.00 mL/kg·BW).After 1 h,all groups were given 56%vol liquor(10 mL/kg·BW)except the normal control group.The serum liver function indexes,cytokine levels,key enzyme activities of hepatic ethanol metabolism,antioxidant indexes and mRNA expression levels of related genes were detected,and the pathological changes of liver tissues were observed.PFE administration with ethanol resulted in prevention of ethanol-induced hepatotoxicity due to reductions of serum aspartate aminotransferase(AST)and alanine transaminase(ALT)levels in mice treated with PFE for 8,10,12 weeks.Results of hematoxylin-eosin staining showed that administration of PFE significantly alleviated alcohol-induced hepatocellular lesions in mice.Alcohol-induced upregulation of alcohol dehydrogenase(ADH),aldehyde dehydrogenase(ALDH)activity and downregulation of recombinant cytochrome P4502E1(Cyp2e1)mRNA expression in liver tissue were dramatically inhibited by PFE treatment.Mice treated with PFE showed increased hepatic antioxidant system with normal activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)and total antioxidant capacity(T-AOC),and reduced formation of malondialdehyde(MDA)in liver.Furthermore,PFE treatment also significantly inhibited the alcohol-induced inflammatory by increasing the hepatic interleukin-6(Il 6)mRNA expression and serum interleukin-1β(IL-1β)level,and the alcohol-induced increase of signal transducer and activator of transcription 3(Stat3)mRNA expression.This study showed that PFE exerted hepatoprotective effects against alcohol-induced hepatic injury by mediating ethanol metabolism,oxidation and inflammation.
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