摘要
试验旨在研究黄芪甲苷对力竭运动大鼠心肌损伤及炎症反应的影响。SD大鼠分为对照组、运动模型组、运动模型+低剂量黄芪甲苷组(100 mg/kg)及运动模型+高剂量黄芪甲苷组(200 mg/kg),除对照组外,均需给予运动训练,随后检测相关指标变化情况。结果表明:(1)黄芪甲苷可以使力竭运动大鼠心肌组织病理变化减轻,显著降低CK、CK-MB、LDH及AST活性(P<0.05);(2)黄芪甲苷能显著降低力竭运动大鼠iNOS活性及NO、IL-1β、IL-6、TNF-α含量(P<0.05),升高IL-10含量(P<0.05);(3)黄芪甲苷也可以显著下调力竭运动大鼠TLR4、MyD88及NF-κBp65蛋白表达(P<0.05)。研究结果表明,黄芪甲苷具有抑制力竭运动大鼠TLR4/MyD88/NF-κB通路及炎症反应作用,该作用是其保护心肌损伤的潜在原因。
To study the effects of astragaloside IV on myocardial injury and inflammatory reaction in exhaustive exercise rats,SD rats were divided into 4 groups,namely control(CON)group,exercise model(EM)group,EM+low dose astragaloside IV(L-Astr IV)group(100 mg/kg)and EM+high dose astragaloside IV(H-Astr IV)group(200 mg/kg),and all rats were given exercise training to establish exhaustion exercise model except for control group.Subsequently,the change of related indicators was detected.The results showed that:(1)astragaloside IV alleviated the pathological changes of myocardium and significantly decreased the activities of CK,CK-MB,LDH and AST in exhaustive exercise rats(P<0.05);(2)astragaloside IV significantly decreased iNOS activity and the contents of NO,IL-1β,IL-6 and TNF-αin exhaustive exercise rats(P<0.05),but increased IL-10 content(P<0.05);(3)astragaloside IV significantly down-regulated the expressions of TLR4,MyD88 and NF-κBp65 protein in exhaustive exercise rats(P<0.05).These results suggest that astragaloside IV can inhibit the TLR4/MyD88/NF-κB pathway and inflammatory reaction in exhausted exercise rats,which may be the potential cause of its protective effect on myocardial injury.
作者
王冠锦
赵暘
WANG Guanjin;ZHAO Yang(Graduate School,Beijing Sport University,Beijing 100084,China;Physical Education Department,Beijiang Jiaotong University,Beijing 100044,China)
出处
《家畜生态学报》
北大核心
2022年第9期43-47,共5页
Journal of Domestic Animal Ecology
基金
首都高校重点培育专项研究项目(2014JBW002)。