基于p38 MAPK/NF-κB信号通路探讨淫羊藿多糖对运动性疲劳小鼠的影响及作用机制  

Effect and Mechanism of Action of Epimedii Folium Polysaccharides on Mice with Exercise-induced Fatigue Based on p38 MAPK/NF-κB Signaling Pathway

作　　者：邹悦 萧闵[2,3] 孟宇豪 唐琨洋 江晓翠 方志鹏 ZOU Yue;XIAO Min;MENG Yuhao;TANG Kunyang;JIANG Xiaocui;FANG Zhipeng(College of Physical Education and Health,Hubei University of Chinese Medicine,Wuhan 430065,China;Experimental Centre of Traditional Chinese Medicine,Hubei University of Chinese Medicine,Wuhan 430065,China;Hubei Shizhen Laboratory,Wuhan 430065,China;College of Basic Medical Sciences,Hubei University of Chinese Medicine,Wuhan 430065,China)

机构地区：[1]湖北中医药大学体育健康学院,武汉430065 [2]湖北中医药大学中医药实验中心,武汉430065 [3]湖北时珍实验室,武汉430065 [4]湖北中医药大学基础医学院,武汉430065

出　　处：《中国实验方剂学杂志》2024年第10期20-28,共9页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：国家自然科学基金青年基金项目(82104704);湖北省自然科学基金面上项目(2023AFB990);湖北省卫生健康委员会中医药科研项目(ZY2021M021);湖北省中医药管理局2023—2024年度中医药重点项目(ZY2023Z024);2022年度湖北省教育厅科学研究计划项目(D2022006);湖北省中医药管理局2023—2024年度中医药指导性项目(ZY2023F134)。

摘　　要：目的:研究淫羊藿多糖对运动性疲劳小鼠的影响并探讨其可能的作用机制。方法:将游泳训练筛选后的ICR雄性小鼠随机分为正常组、模型组、维生素C组和淫羊藿多糖低、中、高剂量组,每组8只。除正常组外各组通过负重游泳训练建立运动性疲劳模型。负重游泳2周后,淫羊藿多糖低、中、高剂量组分别给予100、200、400 mg·kg^(-1)淫羊藿多糖灌胃,维生素C组给予200 mg·kg^(-1)维生素C灌胃,正常组和模型组灌服等量的生理盐水,连续2周。实验结束后,纪录各组小鼠体质量、末次力竭游泳时间;试剂盒检测各组小鼠血清尿素氮(BUN)、乳酸(LA)、乳酸脱氢酶(LDH)、丙二醛(MDA)、过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)水平,骨骼肌中肌糖原(MG)、肝脏中肝糖原(HG)含量,苏木素-伊红(HE)染色法观察肌组织病理形态变化;蛋白免疫印迹法(Western blot)检测肌组织中p38丝裂原活化蛋白激酶(p38 MAPK)、磷酸化(p)-p38 MAPK、细胞外信号调节激酶1/2(ERK1/2)、核转录因子-κB(NF-κB)、p-NF-κB、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)的蛋白表达;免疫荧光法(IF)检测各组小鼠骨骼肌组织中肿瘤坏死因子-α(TNF-α)的表达。结果:与正常组比较,模型组小鼠体质量下降、游泳力竭时间降低(P<0.01),血清中疲劳代谢产物LA、LDH、BUN和脂质过氧化产物MDA含量显著升高(P<0.01),MG、HG、SOD、GSH-Px水平下降(P<0.01),骨骼肌组织p-p38 MAPK、ERK1/2、p-NF-κB、IL-1β、IL-6、TNF-α蛋白表达显著升高(P<0.01);与模型组比较,淫羊藿多糖低、中、高剂量组和维生素C组小鼠体质量、游泳力竭时间增加(P<0.05,P<0.01),LA、LDH、BUN、MDA含量明显下降(P<0.05,P<0.01),MG、HG、SOD、GSH-Px水平升高(P<0.05,P<0.01),骨骼肌组织p-p38 MAPK、ERK、p-NF-κB、IL-1β、IL-6、TNF-α蛋白表达水平降低(P<0.05,P<0.01)。结论:淫羊藿多糖可通过抑制p38 MARK/NF-κB信号通路,从而减少�Objective:To study the effects of Epimedii Folium polysaccharides on mice with exerciseinduced fatigue and explore its possible mechanism of action.Method:ICR male mice screened by swimming training were randomly divided into a control group,model group,vitamin C group,and low,medium,and high dose groups of Epimedii Folium polysaccharides,with eight mice in each group.The exercise-induced fatigue model was established by weight-bearing swimming training in each group except for the control group.After two weeks of weight-bearing swimming,the Epimedii Folium polysaccharide groups were given 100,200,400 mg·kg^(-1) of Epimedii Folium polysaccharides by gavage,and the vitamin C group was given 200 mg·kg^(-1) of vitamin C by gavage.The control group and the model group were given equal amounts of saline for 14 d.At the end of the experimental period,the body mass of the mice in each group and the time of last swimming due to exhaustion were recorded.Serum urea nitrogen(BUN),lactic acid(LA),lactate dehydrogenase(LDH),malondialdehyde(MDA),superoxide dismutase(SOD),glutathione peroxidation(GSH-Px),myoglycogen(MG)in skeletal muscle,hepatic glycogen(HG)in the liver were detected by kits.Hematoxylin-eosin(HE)staining was used to observe the pathological changes in muscle tissue.Western blot was used to detect the protein expression of p38 mitogen-activated protein kinase(p38 MAPK),phosphorylation(p)-p38 MAPK,extracellular signal-regulated kinase1/2(ERK1/2),nuclear factor-κB(NF-κB),p-NF-κB,interleukin-1β(IL-1β),and interleukin-6(IL-6)in muscle tissue.The immunofluorescence(IF)method was used to detect the expression of tumor necrosis factor-α(TNF-α)in skeletal muscle tissue of mice in each group.Result:Compared with the control group,the body mass of mice in the model group decreased,and the time of last swimming due to exhaustion decreased(P<0.01).In addition,there were significantly higher serum levels of the fatigue metabolites LA,LDH,BUN,and lipid peroxidation product MDA(P<0.01)and decreased levels of MG,HG,SOD

关 键 词：运动性疲劳 淫羊藿多糖 p38丝裂原活化蛋白激酶(p38 MAPK)/核转录因子-κB(NF-κB)信号通路 氧化应激 炎症 

分 类 号：R2-0[医药卫生—中医学] R22R285.5R289R33