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

袁彬; 杨永红; 周海洋

doi:10.13386/j.issn1002-0306.2023020024

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

摘要

摘要: 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。

Abstract: 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-1β were 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-1β in liver, significantly decreased the levels of TG and TC in liver, significantly increased the level of PPARα in 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.