首页> 中文期刊> 《海南医学院学报》 >维生素D干预对自发性高血压大鼠RAAS系统活性、心血管重构的影响

维生素D干预对自发性高血压大鼠RAAS系统活性、心血管重构的影响

         

摘要

目的:研究维生素D干预对自发性高血压大鼠RAAS系统活性、心血管重构的影响.方法:选择健康SD大鼠作为对照组,自发性高血压大鼠并随机分为高血压组和VitD组,对照组和高血压组给予丙二醇腹腔注射,VitD给予维生素D溶解于丙二醇腹腔注射.干预后6、12、18周时,处死大鼠后收集血清并测定RAAS系统分子的含量,收集心肌组织并测定心血管重构相关分子的含量.结果:干预后6、12、18周时,高血压组大鼠血清中PRA、AngII、ALD的含量以及肌组织中Col-I、Col-III、TGF-β1、α-actin、Myom-1的含量均呈逐步升高趋势且均显著高于对照组;VitD组大鼠血清中PRA、AngII、ALD的含量以及肌组织中Col-I、Col-III、TGF-β1、α-actin、Myom-1的含量均呈逐步降低趋势且均显著低于高血压组.结论:自发性高血压大鼠接受维生素D干预后能够降低RAAS系统活性、改善心血管重构.%Objective: To study the effect of vitamin D intervention on the RAAS system activity and cardiovascular remodeling in spontaneously hypertensive rats.Methods: Healthy SD rats were selected as the control group, spontaneously hypertensive rats were randomly divided into hypertension group and VitD group, control group and hypertension group received intraperitoneal injection of propylene glycol, and VitD group received intraperitoneal injection of vitamin D and propylene glycol solution.6 weeks, 12 weeks and 18 weeks after intervention, the rats were put to death, serum was collected to determine the levels of RAAS system molecules, and the myocardial tissue was collected to determine the levels of cardiovascular remodeling-related molecules.Results: Of 6 weeks, 12 weeks and 18 weeks after intervention, serum PRA, AngII and ALD levels as well as myocardial tissue Col-I, Col-III, TGF-β1, α-actin and Myom-1 levels of hypertension group gradually increased and were significantly higher than those of control group;serum PRA, AngII and ALD levels as well as myocardial tissue Col-I, Col-III, TGF-β1, α-actin and Myom-1 levels of VitD group gradually decreased and were significantly lower than those of hypertension group.Conclusions: Vitamin D intervention for spontaneously hypertensive rats can reduce the RAAS system activity and improve the cardiovascular remodeling.

著录项

相似文献

  • 中文文献
  • 外文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号