蜂毒溶血肽改善非酒精性脂肪肝大鼠肝组织脂肪沉积作用及其机制研究  

Protective effect of bee venom hemolysin on rats with nonalcoholic fatty liver disease

作　　者：王艳 苏峰[1] 李园园 李舒 Wang Yan;Su Feng;Li Yuanyuan(Department of Gastroenterology,Huxi Hospital Affiliated to Jining Medical College,Shanxian 274300,Shandong Province,China)

机构地区：[1]济宁医学院附属湖西医院消化内科,山东省单县274300 [2]锦州医科大学附属第一医院消化内科

出　　处：《实用肝脏病杂志》2019年第4期474-477,共4页Journal of Practical Hepatology

基　　金：山东省医药卫生科技发展计划项目(编号:2015WS0467)

摘　　要：目的探讨蜂毒溶血肽对非酒精性脂肪性肝病(NAFLD)大鼠肝脂肪变性的保护作用及其机制。方法随机将40只SD大鼠分成对照组、模型组、小剂量蜂毒溶血肽处理组和大剂量蜂毒溶血肽处理组。采用高脂饲料喂养建立NAFLD模型,再分别给予蜂毒溶血肽10μg·kg^-1·d^-1和100μg·kg^-1·d^-1或生理盐水皮下注射,连续12w。采用Westernblot法检测核转录因子E2相关因子2(Nrf2)和血红素加氧酶-1(HO-1)表达。结果大剂量蜂毒溶血肽处理组大鼠体质量和肝质量分别为(380.2±20.8)g和(10.4±1.3)g,显著低于模型组【分别为(435.2±22.1)g和(14.3±1.4)g,P<0.05】,血清AST和ALT水平分别为(88.0±10.4)U/L和(49.3±6.2)U/L,显著低于模型组【分别为(159.7±18.9)U/L和(77.7±6.8)U/L,P<0.05】,血糖、TC、TG和LDL-C水平分别为(8.7±1.8)mmol/L、(1.6±0.2)mmol/L、(0.8±0.1)mmol/L和(0.3±0.1)mmol/L,显著低于模型组【分别为(18.3±2.4)mmol/L、(2.8±0.3)mmol/L、(1.5±0.2)mmol/L和(0.5±0.1)mmol/L,P<0.05】,血清超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)水平分别为(82.1±6.6)U/L、(6.3±0.8)nmol/mL和(8.7±0.9)mmol/L,与模型组的(30.4±5.3)U/L、(13.1±1.6)nmol/mL和(2.3±0.5)mmol/L比,差异显著(P<0.05),肝组织Nrf2和HO-1表达分别为(1.4±0.2)和(1.2±0.1),显著高于模型组【分别为(0.3±0.1)和(0.3±0.1),P<0.05】。结论蜂毒溶血肽可以调节NAFLD大鼠血糖和血脂代谢,减轻肝脂肪变程度,改善肝功能,其机制可能与调控Nrf2和HO-1表达,缓解氧化应激损伤有关。Objective To explore the protective effect of bee venom hemolysin on rats with nonalcoholic fatty liver disease(NAFLD).Methods Forty male SD rats were randomly divided into control,model,low-dose and high dose of bee venom hemolysin-intervened groups.Rats were fed with high fat to establish the NAFLD models,and the bee venom hemolysin peptide at doses of 10μg·kg^-1 and 100μg·kg^-1 or saline were subcutaneously injected daily for 12 weeks.Hepatic expression of nuclear factor-erythroid 2 p45-related factor 2(Nrf2)and heme oxygenase-1(HO-1)were detected by Western bloting.Results The body weight and liver mass of rats in high dose of bee venom hemolysin-intervened group were(380.2±20.8)g and(10.4±1.3)g,significantly lower than(435.2±22.1)g and(14.3±1.4)g in the model(P<0.05),serum AST and ALT levels were(88.0±10.4)U/L and(49.3±6.2)U/L,much lower than(159.7±18.9)U/L and(77.7±6.8)U/L in the model(P<0.05),blood glucose,TC,TG,and LDL-C levels were(8.7±1.8)mmol/L,(1.6±0.2)mmol/L,(0.8±0.1)mmol/L and(0.3±0.1)mmol/L,significantly lower than(18.3±2.4)mmol/L,(2.8±0.3)mmol/L,(1.5±0.2)mmol/L and(0.5±0.1)mmol/L,respectively in the model(P<0.05),serum superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione(GSH)levels were(82.1±6.6)U/L,(6.3±0.8)nmol/mL and(8.7±0.9)mmol/L,significantly different as compared to(30.4±5.3)U/L,(13.1±1.6)nmol/mL and(2.3±0.5)mmol/L in the model(P<0.05),hepatic expression of Nrf2 and HO-1 were(1.4±0.2)and(1.2±0.1),significantly intensified as compared to(0.3±0.1)and(0.3±0.1)in the model(P<0.05).Conclusion Bee venom hemolytic peptide might alleviate hepatic steatosis in rats with non-alcoholic fatty liver disease and improve liver function,and the mechanism might be related to the regulation of Nrf2 and HO-1 expression and relieve oxidative stress injury.

关 键 词：肝脂肪变 蜂毒溶血肽 核转录因子E2相关因子2 血红素加氧酶-1 大鼠 

分 类 号：R575[医药卫生—消化系统]