摘要
目的:评价有氧运动和二甲双胍对糖尿病大鼠血管炎症反应的影响。方法:对糖尿病大鼠(通过高脂饮食+腹腔注射链脲佐菌素制备)分别进行8周有氧运动、二甲双胍与二甲双胍和运动联合治疗干预,检测干预后糖尿病大鼠糖脂代谢、血管内皮和血管炎症标志物的相关指标,并探讨影响血管炎症反应的途径。结果:糖尿病对照组血清IL-1β、TNF-α和MCP-1浓度均明显高于正常对照组,二甲双胍组血清IL-1β、TNF-α和MCP-1浓度与糖尿病对照组相比没有明显变化,运动组大鼠血清IL-1β、TNF-α和MCP-1浓度显著低于糖尿病对照组,二甲双胍+运动组血清TNF-α浓度明显低于糖尿病对照组、二甲双胍组和运动组,MCP-1浓度明显低于糖尿病对照组。3个干预组血清IL-10浓度均高于糖尿病对照组,但仅有二甲双胍+运动组具有显著性差异。结论:有氧运动和二甲双胍+运动联合干预均能有效缓解糖尿病大鼠血管炎症反应。
Objective： To evaluate the effects of aerobic exercise and metformin on vascular inflammatory reaction in diabetic rats. Methods： Diabetic rates, prepared through high-fat diet and intraperitoneal STZ injections, were treated with aerobic exercise, metformin and the combination of aerobic exercise and metformin respectively for 8 weeks. After receiving interventional treatment, diabetic rats were tested to obtain relevant indicators such as glycolipid metabolism, vascular endothelium and vascular inflammatory markers. Based on the experiment, the approach to influencing vascular inflammatory reaction is explored. Results： Serum concentrations of IL-1β, TNF-α and MCP-1 in DM group were significantly higher than those in Con group; serum concentrations of IL-1β, TNF-α and MCP-1 in DM＋Met group had no obvious change compared with those in DM group; serum concentrations of IL- 1β, TNF-α and MCP- 1 in DM＋Exe group were evidently lower than those in DM group; serum concentration of TNF-α in DM＋Exe＋Met group was greatly lower than it in DM, DM＋Met and DM＋Exe groups, and MCP-1 was lower markedly than it in DM group. Serum concentration of IL-10 in three interventional groups was higher than it in Con group, but there was a significant discrepancy only in the DM＋Exe＋Met group. Conclusion： Both aerobic exercise and the combination of aerobic exercise and metformin can effectively relieve the vascular inflammatory reaction in diabetic rats.
出处
《中国体育科技》
CSSCI
北大核心
2017年第3期41-47,共7页
China Sport Science and Technology
基金
福建省自然科学基金资助项目(2016J01150)
南京信息工程大学126工程资助项目(2016tyb003)
关键词
糖尿病
有氧运动
二甲双胍
炎症
diabetes mellitus
aerobic exercise
metformin, inflammation
