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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 investigate the effects of Tongxinluo on renal damage in spontaneously hypertensive rats (SHR) and its mechanism. Methods 10 SHR 48 male SHR were randomly divided into five groups: SHR control group (same age Wistar rats as control), amlodipine intervention group and amlodipine + different doses of Tongxinluo (0.5, 1.0, 1.5 g · kg- 1 · d-1) intervention group. Twenty weeks later, the blood pressure was measured and sacrificed after leaving the urine. The indexes of renal tissue were taken. Urine microalbuminuria (UMA) and β2 microglobulin (β2MG) were measured for Angiotensin Converting Enzyme 2 and Angiotensin Ⅱ Type 1 receptor gene expression. Results Compared with WKY rats of the same age, urinary β2MG, AT1R expression in renal tissue and ACE2 in 10-week-old SHR were significantly decreased. Compared with the single amlodipine group, the urinary β2MG, UMA and AT1R expression in the kidney of Wu Tong Tong Xin Luo group decreased significantly, while the expression of ACE2 in kidney increased significantly. Conclusion Amlodipine WU Tongxinluo can reduce proteinuria, reduce renal damage in hypertensive patients may be through increased renal ACE2, AT1R expression down to achieve.