摘要
目的观察丹参酚酸B(Sal B)对db/db小鼠血管功能的影响及机制。方法 20只雄性db/db小鼠随机分为对照组及Sal B组,每组10只;另选取10只同龄雄性C57BL/Ks J小鼠作为正常对照组。Sal B组用Sal B以100 mg/(kg·d)的剂量进行灌胃;db/db对照组和C57BL/KsJ对照组给予等体积生理盐水灌胃,每周测体质量、血压、心率及空腹血糖,干预6周后取胸主动脉观察:血管舒张功能,血管内膜超氧阴离子和NO水平;e NOS,p-e NOS,AMPK,p-AMPK水平。结果 Sal B可显著降低db/db小鼠体质量,空腹血糖;对血压及心率无显著影响;可减少超氧阴离子水平,增加NO水平,改善血管内皮依赖性舒张功能;增加p-e NOS及p-AMPK的水平。结论 Sal B可降低db/db小鼠血管超氧阴离子水平,增加NO水平,从而改善血管内皮依赖性舒张功能,其机制可能与其激活AMPK通路有关。
Objective To investigate the effect of Salvianolic Acid B（Sal B）on vascular function of db/db mice and reveal the potential mechanism. Methods 20 male db/db mice were divided into 2 groups,the con-trol group（n = 10）and Sal B group（n = 10）. 10 age-matched male C57 BL/Ks J mice were used as the wild typecontrol. Mice in Sal B group were given Sal B,100 mg/（kg·d）by tube. Mice in db/db control group and in wildtype control were given the same volume of saline. Body weight,tail blood pressure,heart rate and fasting bloodglucose level were measured every week. After 6-weeks treatment,thoracic aorta was obtained and used to detectthe levels ofsuperoxide anion and NO,vascular function,e NOS,p-e NOS,AMPK and p-AMPK. Results Sal Bcould reduce the body weight and fasting blood glucose level of db/db mice,but had no effect on blood pressure.Sal B could decrease the level of superoxide inon,increased NO level,and improved endothelium-dependent butnot endothelium-independent diastolic function. Sal B could increase phosphorylation levels of e NOS and AMPK.Conclusion Sal B can reduce the oxidative stress,increases NO level in vasculature,and improves the endo-thelium-dependent vasodilation in the diabetic mice,which may be associated with the promotion of AMPK phos-phorylation.
出处
《实用医学杂志》
CAS
北大核心
2017年第20期3367-3371,共5页
The Journal of Practical Medicine
基金
国家自然科学基金项目(编号:81400289)
四川省杰出青年学术技术带头人资助计划(编号:2016JQ0032)
四川省卫生计生委科研项目(编号:150047)
四川省教育厅自然科学重点项目(编号:16ZA0277)
成都医学院科研创新团队项目(编号:CYTD16-01)
关键词
糖尿病
丹参酚酸B
血管功能
氧化应激
腺苷酸活化的蛋白激酶
diabetes
salvianolic acid B
endothelial function
oxidative stress
adenosine 5＇-mo-nophosphate-aetivated protein kinase
