摘要
目的观察复方钩藤降压片对自发性高血压大鼠(SHR)心肌营养素-1(CT-1)/JAK-STAT通路蛋白表达影响,探讨其干预逆转高血压左室肥厚的机制。方法将50只SHR按随机数字表法分为5组,复方钩藤降压片高剂量组(H组,129. 6 mg/m L)、复方钩藤降压片中剂量组(M组,86. 4 mg/m L)、复方钩藤降压片低剂量组(L组,43. 2 mg/m L)、贝那普利组(B组,0. 9 mg/m L)、SHR模型对照组(S组),每组10只,另选取10只Wistar大鼠为正常对照组(W组),每天灌胃1次,持续干预24周后取材,采用免疫组化法检测心肌局部CT-1的含量,Western blot法检测心肌JAK1/STAT3蛋白表达水平。结果与W组比较,S组心肌组织中CT-1表达量和JAK1、STAT3蛋白表达水平均升高(P <0. 05)。与S组比较,B组、H组、M组及L组心肌组织中CT-1表达量降低(P <0. 05),JAK1、STAT3蛋白表达水平降低(P <0. 05)。各药物干预组间CT-1表达量差异无统计学意义(P> 0. 05),H组、M组、L组呈剂量依赖性JAK1、STAT3蛋白表达量递增,差异有统计学意义(P <0. 05)。与B组比较,H组、M组JAK1、STAT3蛋白表达水平均降低(P <0. 05)。结论复方钩藤降压片具有一定抑制SHR心肌CT-1/JAK-STAT通路蛋白表达的作用,可能通过降低心脏局部CT-1表达水平,抑制JAK-STAT通路,干预逆转左室肥厚。
Objective To explore the mechanism of reversing left ventricular hypertrophy in spontaneous hypertension rats( SHR) by the intervention of Compound Uncaria Antihypertensive Tablet from the point of view of interfering with the protein expression of cardiotrophin-1( CT-1)/JAK-STAT pathway in rats’ cardiac myocardium. Methods Totally 50 SHR were divided into 5 groups,the high dose group( group H,129. 6 mg/m L),the middle dose group( group M,86. 4 mg/m L),the low dose group( group L,43. 2 mg/m L),the benazepril group( group B,0. 9 mg/m L),and the SHR model control group( group S) according to the random number table,10 in each group. 10 Wistar rats were recruited in a normal control group( group W),then perfomed gastric lavage once a day,and continued the intervention for 24 weeks. The contents of partial myocardial CT-1 and protein expression level of myocardial JAK1/STAT3 were detected by immunohistochemistry and Western blot respectively. Results Compared with group W,the expression level of CT-1 and the protein expression level of JAK1 and STAT3 in myocardial tissue were uniformly increased in group S(P < 0. 05). Compared with group S,expression levels of CT-1 in myocardial tissue decreased(P < 0. 05),while protein expression level of JAK1 and STAT3 decreased in group B,H,M and L(P < 0. 05). There was no statistically significant difference in the expression of CT-1 among the intervention groups(P > 0. 05). The protein expression levels of dose-dependent JAK1 and STAT3 increased in group H,M and L,and the difference was statistically significant(P < 0. 05). Compared with group B,the expression level of JAK1 and STAT3 decreased,the difference was statistically significant(P < 0. 05). Conclusion Compound Uncaria Antihypertensive Tablet had a certain inhibitory effect on the protein expression of CT-1/JAK-STAT pathway protein,and its possible mechanism to reverse left ventricular hypertrophy is to reduce expression level of cardiac partial CT-1 and inhibit the JAK-STAT pathway,and then give full scope to reverse the left ventricular hypertrophy.
作者
曾勇
谭元生
任卫琼
陈偶英
段武磊
文爱珍
ZENG Yong;TAN Yuan-sheng;REN Wei-qiong;CHEN Ou-ying;DUAN Wu-lei;WEN Ai-zhen(First Affiliated Hospital of Hunan University of Chinese Medicine,Changsha (410007))
出处
《中国中西医结合杂志》
CAS
CSCD
北大核心
2019年第2期206-210,共5页
Chinese Journal of Integrated Traditional and Western Medicine
基金
国家自然科学基金项目(No.81473616)
湖南省中医药科研计划重点项目(No.201534)
湖南省教育厅重点项目资助(No.15A142)
中医内科学省部共建教育部重点实验室开放基金资助项目(No.ZYNK201507)
关键词
复方钩藤降压片
自发性高血压大鼠
心肌营养素-1
JAK—STAT通路
左室肥厚
Compound Uncaria Antihypertensive Tablet
spontaneously hypertensive rats
cardiot rophin-1
JAK-STAT pathway
left ventricular hypertrophy