高强度间歇运动通过调控Nrf2/ARE和NF-κB信号通路调节高脂饮食诱导肥胖大鼠的氧化应激和炎症反应

High-Intensity Intermittent Exercise Regulates Oxidative Stress and Inflammatory Response in Obese Rats by Regulating Nrf2/ARE and NF-κB Signaling Pathways in a High-fat Diet

为了揭示高强度间歇运动对肥胖大鼠的氧化应激和炎症反应的调节作用及机制,本研究将60只大鼠随机分为对照组、肥胖组、中强度持续运动组(MICE)和高强度间歇运动组(HIIE)。对照组大鼠采用标准饲料喂养,其他组大鼠采用高脂饲料喂养以建立肥胖大鼠模型。MICE组大鼠进行中强度持续运动,HIIE组大鼠进行高强度间歇运动,共运动4周。采用苏木精-伊红(HE)染色检测大鼠骨骼肌形态。采用TUNEL法检测骨骼肌细胞凋亡。通过商用试剂盒检测活性氧(ROS)水平。通过RT-PCR或Western blotting检测大鼠骨骼肌组织中Nrf2、SOD、GSH-PX、CAT、p65、p-p65、IκB、p-IκB、TNF-α、IL-1β和IL-6的表达。研究显示,与肥胖组比较,MICE组和HIIE组大鼠骨骼肌组织中的ROS水平均显著降低,HIIE组大鼠骨骼肌组织中的ROS水平显著低于MICE组。MICE组和HIIE组大鼠的骨骼肌形态基本正常,仅少量肌纤维排列异常。与肥胖组比较,MICE组和HIIE组大鼠骨骼肌细胞凋亡率均显著降低,HIIE组大鼠骨骼肌细胞凋亡率显著低于MICE组。与肥胖组比较,MICE组和HIIE组大鼠骨骼肌组织中Nrf2、SOD、GSH-PX和CAT的蛋白水平均显著升高,HIIE组均显著高于MICE组。与肥胖组比较,MICE组和HIIE组大鼠骨骼肌组织中p-p65、p-IκB、TNF-α、IL-1β和IL-6的蛋白水平均显著降低,HIIE组均显著低于MICE组。总之,HIIE运动可通过抑制NF-κB信号通路来抑制肥胖引起的慢性炎症。HIIE运动可通过激活Nrf2/ARE信号通路来提高机体抗氧化能力并减弱氧化应激损伤。

In order to reveal the regulation effect and mechanism of high-intensity intermittent exercise on oxidative stress and inflammatory response in obese rats,in this study,60 rats were randomly divided into the control group,obesity group,medium-intensity continuous exercise group(MICE)and high-intensity intermittent exercise group(HIIE).The control group rats were fed with standard feed,and the other groups were fed with high-fat feed to establish an obese rat model.The rats in the MICE group were subjected to continuous and moderate intensity exercise,and the rats in the HIIE group were subjected to high intensity intermittent exercise for 4 weeks.Hematoxylin-eosin(HE)staining was used to detect rat skeletal muscle morphology.Apoptosis was detected by TUNEL method.Reactive oxygen(ROS)levels were detected by a commercial kit.The expressions of Nrf2,SOD,GSH-PX,CAT,p65,p-p65,IκB,p-IκB,TNF-α,IL-1βand IL-6 in rat skeletal muscle tissue were detected by RT-PCR or Western blotting.The study showed that compared with the obese group,the ROS levels in the skeletal muscle tissue of the MICE group and the HIIE group were significantly reduced,and the ROS level in the skeletal muscle tissue of the HIIE group was significantly lower than that of the MICE group.The morphology of skeletal muscle of the rats in MICE group and HIIE group was basically normal,and only a small number of muscle fibers were abnormally arranged.Compared with the obese group,the apoptosis rate of skeletal muscle cells in the MICE group and the HIIE group was significantly reduced,and the apoptosis rate of the skeletal muscle cells in the HIIE group was significantly lower than that in the MICE group.Compared with the obese group,the protein levels of Nrf2,SOD,GSH-PX and CAT in the skeletal muscle tissue of the MICE group and the HIIE group were significantly increased,and the HIIE group was significantly higher than the MICE group.Compared with the obese group,the protein levels of p-p65,p-IκB,TNF-α,IL-1βand IL-6 in the skeletal muscle tissue of the MICE group and the HIIE group were significantly reduced,and the HIIE group was significantly lower than the MICE group.In conclusion,HIIE exercise can inhibit chronic inflammation caused by obesity by inhibiting the NF-κB signaling pathway.HIIE exercise can increase the body’s antioxidant capacity and reduce oxidative stress injury by activating the Nrf2/ARE signal pathway.