红芸豆多糖联合运动改善饮食诱导的肥胖小鼠糖脂代谢紊乱

Polysaccharide from Red Kidney Bean Combined with Exercise Improves Diet-induced Metabolic Disorders in Obese Mice

目的:观察红芸豆多糖(Polysaccharides from red kidney bean,PRK)联合运动(Exercise,E)改善饮食诱导的肥胖小鼠代谢紊乱,并分析其机制。方法:40只C57BL/6小鼠随机分为5组:对照组(正常饮食)、模型组(高脂饮食)、PRK组(400 mg/kg PRK)、E组(运动)、PRK+E组(400 mg/kg PRK+运动),连续干预12周,并进行口服葡萄糖耐量试验(OGTT),生化分析仪测定血糖、胰岛素、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、肝脏TC、TG、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)水平。酶联免疫试剂盒检测胰岛素、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、IL-1β含量。H&E染色对肝脏进行病理分析,Western Blot实验检测PPARα、FASN、Nrf2、NQO1、HO-1水平。结果:与对照组比较,模型组小鼠的体重和肝质量极显著增加(P<0.01);与模型组比较,PRK联合运动极显著降低肥胖小鼠的体重和脂质,降低血糖和胰岛素水平(P<0.01)。与模型组比较,PRK联合运动极显著降低血清中TG、TC、LDL含量,极显著增加HDL,极显著降低肝脏TNF-α、IL-6和IL-1β水平,极显著下调肝脏TG、TC水平,极显著增加肝脏中PPARα水平,极显著降低FASN水平(P<0.01)。与模型组比较,PRK、E或PRK+E联合干预极显著提高肝脏GSH-Px和SOD水平,极显著降低MDA含量,极显著增加Nrf2、NQO1和HO-1蛋白水平,尤其PRK+E联合干预更加明显(P<0.01)。结论:PRK联合运动通过减少脂质积累、抑制炎症、氧化应激改善肥胖引起的代谢障碍,其机制与调节PGC-1α、FASN、Nrf2/NQO1/HO-1信号通路相关。

Objective:Observing the effects of polysaccharide from red kidney beans(PRK)combined with exercise(E)to improve the diet induced obese mice metabolic disorders,and analyzing its mechanism.Methods:C57BL/6 mice were randomly divided into 5 groups:Control group(normal diet),model group(high fat diet),PRK group(400 mg/kg PRK),E group(exercise),PRK+E group(400 mg/kg PRK+exercise).After continuous intervention for 12 weeks,oral glucose tolerance test(OGTT)was performed,and blood glucose,insulin,total cholesterol(TC),triglyceride(TG),low density lipoprotein(LDL),high density lipoprotein(HDL)were measured by biochemical analyzer.TC,TG,superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione peroxidase(GSH-Px)were analyzed in liver.The contents of insulin,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and IL-1βwere determined by enzyme-linked immunoassay kit.The levels of PPARα,FASN,Nrf2,NQO1 and HO-1 were detected by western blot.Results:Compared with the control group,the body weight and liver weight of model group were significantly increased(P<0.01).Compared with the model group,PRK combined with exercise significantly decreased the body weight,lipid,blood glucose and insulin levels in obese mice(P<0.01).Compared with model group,PRK combined exercise significantly decreased the contents of TG,TC and LDL in serum,significantly increased HDL,significantly decreased the levels of TNF-α,IL-6 and IL-1βin liver,significantly decreased the levels of TG and TC in liver,significantly increased the level of PPARαin liver and significantly decreased the level of FASN(P<0.01).Compared with model group,PRK,E or PRK+E combined intervention extremely significantly increased liver GSH-Px and SOD levels,extremely significantly decreased MDA content,and extremely significantly increased Nrf2,NQO1 and HO-1 protein levels,especially PRK+E combined intervention(P<0.01).Conclusion:PRK combined exercise could reduce lipid accumulation,inhibit inflammation and oxidative stress to improve metabolic disorders caused by obesity,and its mechanism was related to the regulation of PGC-1α,FASN,Nrf2/NQO1/HO-1 signaling pathways.