通心络对自发性高血压大鼠肾损害的保护作用及机制  

Protection effect of Tong Xin Luo on the renal damage in spontaneously hypertensive rats and its potential mechanism

作　　者：陈申杰[1] 叶武[1] 朱敏[1] 陈洁[1] 冯培芳[1] 

机构地区：[1]浙江中医药大学附属第一医院心内科,杭州310006

出　　处：《中国临床药理学杂志》2015年第7期501-504,共4页The Chinese Journal of Clinical Pharmacology

基　　金：浙江省自然科学基金资助项目(Y13H270037)

摘　　要：目的研究通心络对自发性高血压大鼠(SHR)肾损害的干预作用及机制。方法 10周龄雄性SHR 48只随机分成5组:SHR对照组(同龄Wistar大鼠作对照),氨氯地平干预组和氨氯地平+不同剂量通心络(0.5,1.0,1.5g·kg-1·d-1)干预组。20周后,测血压、留尿后处死,取肾组织检测指标。测尿微量白蛋白(UMA)和β2微球蛋白(β2MG),测血管紧张素转化酶2、血管紧张素Ⅱ1型受体基因表达。结果与同龄京都威斯特(WKY)大鼠比较,10周龄SHR的尿β2MG、肾组织AT1R表达明显增加而ACE2明显减少。与单用氨氯地平组比较,伍用通心络组大鼠的尿β2MG、UMA及肾组织AT1R表达明显减少而肾组织ACE2表达明显增加。结论氨氯地平伍用通心络能降低蛋白尿、减轻高血压病肾损害的作用可能是通过增加肾组织ACE2、下调AT1R表达来实现的。Objective To explore the effect of Tong Xin Luo （ TXL） on the renal damage by hypertension in spontaneously hypertensive rats （ SHR）.Methods Ten week -old male SHR （ n=48 ） were randomly divided into 5 groups：control group , the amlodipine group , the amlodi-pine and different dose TXL groups.The same old male Wistor -Kyoto （ WK） rats was as control group .At the time of 20 weeks later after treatment, blood pressure, urine microalbumin, urine β2 -microglobulin were detected , the gene expression of angiotensin -converting enzyme 2 （ACE2） and angiotensin II type 1 receptor （AT1R） in rats kidney were determined.Results Compared with Wistar -Kyoto （ WKY ） control group, 10 week -old SHR showed higher levels of urine β2 MG and ACE2 , but less AT1 R.After treatment for 20 weeks, compared with the amlodipine group , amlodipine with TXL reduced urinary β2 -microglo-bulin and urine microalbumin , decreased AT 1 R expression and increased ACE2 expression.Conclusion Taking high-dose TXL with antihyper-tensive therapy could prevent renal damage progression , and its effect may be through lowering albuminuria , increasing renal ACE 2 expression , and decreasing AT 1 R expression.

关 键 词：通心络 自发性高血压大鼠 血管紧张素转化酶2 氨氯地平 

分 类 号：R285.5[医药卫生—中药学] R965.1[医药卫生—中医学]