Effect of rhynchophylline on TGF-β1/Smad pathway for processing ven-tricular remodeling in spontaneously hypertensive rats
10.3969/j.issn.1000-4718.2015.08.004
- VernacularTitle:钩藤碱对自发性高血压大鼠心室重构过程中TGF－β1／Smad 通路的影响
- Author:
Hua HUANG
;
Yusheng LI
;
Xin JIN
;
Jiangtao WANG
;
Na LI
;
Zhengui HUANG
;
Boping DING
- Publication Type:Journal Article
- Keywords:
Rhynchophylline;
Spontaneouslyhypertensiverats;
TGF-β1/Smadpathway;
Ventricularremode-ling
- From:
Chinese Journal of Pathophysiology
2015;(8):1365-1370
- CountryChina
- Language:Chinese
-
Abstract:
AIM:Toinvestigatetheeffectofrhynchophylline(Rhy)onbloodpressure,cardiachypertrophy and myocardial fibrosis in spontaneously hypertensive rats ( SHR) .METHODS:Spontaneously hypertensive rats were ran-domly divided into model group , high dose (10 mg? kg-1? d-1 ) and low dose (2.5 mg? kg-1? d-1 ) group of rhyncho-phylline, captopril group (17.5 mg? kg -1? d-1).Wistar-Kyoto rats were used as normal control.Respectively, systolic blood pressure was measured by tail cuff every 2 weeks.After 10 weeks, heart weight index and left ventricular weight in-dex were calculated .The myocardial hydroxyproline and plasma angiotensin Ⅱwere detected .Moreover , basic myocardial histopathological changes and myocardial collagen fibres were observed by HE staining and Masson staining , respectively . The protein expression of TGF-β1 and Smad3 in the myocardium was measured by the methods of immunohistochemistry and Western blot .RESULTS:Compared with SHR model group , Rhy significantly reduced blood pressure ( P<0.05 ) , the levels of HYP in the myocardium (P<0.05) and the levels of AngⅡin the plasma (P<0.01).The pathological dama-ges of the myocardial tissues and collagen deposition were attenuated .The protein expression of TGF-β1 and Smad3 was sig-nificantly reduced by the treatment with Rhy (P<0.01).CONCLUSION:Rhynchophylline reduces blood pressure and adjusts to improve ventricular remodeling of SHR .The mechanism may be involved in the TGF-β1/Smad pathway and re-ducing AngⅡcontent.
