Effects of paeonol on RAS occurred on the development of ventricular remodeling after acute myocardial infarction in rats
10.11958/j.issn.0253-9896.2015.05.006
- VernacularTitle:丹皮酚对急性心肌梗死后心室重构模型大鼠RAS的影响
- Author:
Yuanyuan GU
;
Xiaohui ZHOU
;
Qian XU
;
Jingyi ZHAO
- Publication Type:Journal Article
- Keywords:
myocardial infarction;
ventricular remodeling;
renin-angiotensin system;
angiotensinogen;
angiotensin Ⅱ receptor type1;
endothelin-1;
peptidyl-dipeptidase A;
angiotensin Ⅱ;
paeonol
- From:
Tianjin Medical Journal
2015;43(5):470-473
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of paeonol on renin-angiotensin system (RAS) occurred on the development of ventricular remodeling after acute myocardial infarction (AMI) in rats. Methods The left anterior descending coronary artery was ligated to establish the model of AMI in male SD rats. Six groups were set up:sham-operation group, AMI model group, captopril control group, paeonol low dose group (6 mg/kg), paeonol middle dose group (9 mg/kg) and paeonol high dose group (12 mg/kg). Rats were given treatment for 4 weeks after the AMI model was established. HE staining was used to observe changes of myocardial tissue. Real-time PCR was used to detect the mRNA levels of angiotensinogen (AGT), angiotensin Ⅱ receptor type1(AGTR1) and endothelin (ET)-1 of six groups. Western blot assay was used to detect the protein levels of peptidyl-dipeptidase A (ACE), angiotensin Ⅱ(Ang)-Ⅱand AGTR1 in six groups. Results The transcription of AGT, AGTR1, ET-1mRNA and the expressions of ACE, Ang-Ⅱ and AGTR1 protein were significantly higher in myocardial tissue of AMI rats than those of sham-operation rats (P＜0.05). Compared with model group, the expressions of AGT, AGTR1, ET-1mRNA and ACE, Ang-Ⅱ, AGTR1 protein were significantly decreased in paeonol high dose group and captopril control group (P＜0.05). Paeonol reduced the expressions of those mRNA and protein levels in a significant dose dependent manner. Conclusion Paeonol can slow down the deterioration of the ventricular remodeling after AMI in rats, which may be related to the inhibition of over-activation of RAS.
