Tanshinone ⅡA Inhibit Pressure Load Induced Left Ventricular Hypertrophys and Myocardial JAK1/STAT3 in Rats
- VernacularTitle:丹参酮ⅡA磺酸钠盐抑制腹主动脉缩窄高血压大鼠的心肌肥厚
- Author:
Li YAN
;
Qiansheng LIANG
;
Guangtian YANG
- Publication Type:Journal Article
- Keywords:
Aorta constriction;
Left ventricular hypertrophy;
Tanshinone ⅡA;
JAK/STAT
- From:
Chinese Journal of Hypertension
2007;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Background Left ventricular hypertrophy(LVH) is a cardiovascular risk factor independent of the blood pressure. JAK/STAT pathway has been confirmed to participate in cardiac hypertrophy and hyperplasia. Our previous reports have shown that sodium tanshinone ⅡA sulfonate(STS) reversed LVH,inhibited the myocardial cells Ca2+ influx,lowered left ventricular myocardial tumor necrosis factor-?(TNF-?)and the proto-oncogene c-fos,Bcl-2,and p53 protein expression. Objective To study the effect of sodium tanshinone ⅡA sulfonate(STS) on JAK/STAT pathway in left ventricular hypertrophy(LVH) induced by abdominal aorta stenosis in rats. Methods Twenty-four 9-weeks-old rats submitted to abdominal aorta constriction,were randomized to receive STS 10 mg/(kg?d)(n=8)or sterilized distilled water (1 mL/d)(n=8),or valsartan 10 mg/(kg?d) by gavage(n=8),with age and sex matched sham operated rats(n=8) as control. HE,VG and immunohistonchemical staining were used to evaluate the myocardial fiber dimension(MFD). Expressions of JAK1 and STAT3 were assessed by using Western blot. Results Compared with the control group,pressure loaded rats had higher SBP[(117.3?8.3) vs LVH: (186.5?13.5)mmHg,P
