PMID- 20681280
OWN - NLM
STAT- MEDLINE
DCOM- 20130124
LR  - 20191210
IS  - 1003-5370 (Print)
IS  - 1003-5370 (Linking)
VI  - 30
IP  - 5
DP  - 2010 May
TI  - [Effect of tanshinone II A on the transforming growth factor beta1/Smads signal 
      pathway in rats with hypertensive myocardial hypertrophy].
PG  - 499-503
AB  - OBJECTIVE: To investigate the molecular mechanism of tanshinone II A (TSN) for 
      preventing left ventricular hypertrophy (LVH) by studying the expressions of 
      angiotensin I type 1 receptor (AT1R), transforming growth factor beta1 
      (TGF-beta1) and intracellular signal protein gene (Smads gene) in the 
      hypertrophic myocardium of hypertensive rat models induced by pressure 
      over-loading. METHODS: SD rat model of LVH was established by abdominal aorta 
      constriction. The model animals were randomly divided into 4 groups 4 weeks after 
      modeling, the untreated model control group (C1), the two tested groups (T1 and 
      T2) treated respectively with high (20 mg/kg) and low (10 mg/kg) dose of TSN II A 
      per day via intraperitoneal injection, and the positive control group (C2) 
      treated with 10 mg/kg of Valsartan per day by gastric perfusion, with 8 animals 
      in each group. Besides, 8 SD rats managed with sham operation were set up as the 
      sham-operated control group (C3) After an 8-week treatment, the caudal arterial 
      pressure, left ventricular mass index (LVMI), myocardial fiber dimension (MFD, by 
      pathologic examination with HE staining) in rats were measured. Meanwhile, mRNA 
      expression of AT1R, protein expression of TGF-beta1 and activity of Smad-3, 4, 7 
      in the ventricular tissue were detected by RT-PCR analysis and Western blotting 
      respectively. RESULTS: (1) Blood pressure in Group T1 and T2 was unchanged after 
      treatment, which was significantly higher than that in Group C2 and C3 (P < 0.01, 
      P < 0.05). (2) LVMI and MFD in Group T1, T2 and C2 were higher than that in Group 
      C3 (P < 0.01), but remarkably lower than that in Group C1 (P < 0.01). (3) Levels 
      of AT1R, TGF-beta1 and Smad-3 expression increased significantly in the model 
      rats (P < 0.01), but they were down-regulated in Group T1 and C2, and the 
      TGF-beta1 regulating effect in the C2 was more potent than that in Group T1 and 
      T2 (P < 0.05). (4) Protein expression of Smad-7 was up-regulated in Group T1, T2 
      and C2 obviously (P < 0.01), and the effect in Group T1 was superior to that in 
      C2 (P < 0.05). CONCLUSION: The myocardial hypertrophy inhibition effect of TSN II 
      A is a blood pressure independent process, and it may be related to the 
      inhibition of AT1R mRNA expression and blocking of TGF beta1/Smads signal 
      pathway.
FAU - Li, Yong-Sheng
AU  - Li YS
AD  - Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong Science and Technology University, Wuhan. ysli@tjh.tjmu.edu.cn
FAU - Yan, Li
AU  - Yan L
FAU - Yong, Yong-Quan
AU  - Yong YQ
LA  - chi
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - China
TA  - Zhongguo Zhong Xi Yi Jie He Za Zhi
JT  - Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese 
      journal of integrated traditional and Western medicine
JID - 9211576
RN  - 0 (Abietanes)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Smad Proteins)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 03UUH3J385 (tanshinone)
SB  - IM
MH  - Abietanes/*pharmacology
MH  - Animals
MH  - Cardiomegaly/etiology/*metabolism
MH  - Drugs, Chinese Herbal/pharmacology
MH  - Hypertension/complications/*metabolism
MH  - Myocardium/*metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Angiotensin, Type 1/metabolism
MH  - Signal Transduction/*drug effects
MH  - Smad Proteins/metabolism
MH  - Transforming Growth Factor beta1/metabolism
EDAT- 2010/08/05 06:00
MHDA- 2013/01/25 06:00
CRDT- 2010/08/05 06:00
PHST- 2010/08/05 06:00 [entrez]
PHST- 2010/08/05 06:00 [pubmed]
PHST- 2013/01/25 06:00 [medline]
PST - ppublish
SO  - Zhongguo Zhong Xi Yi Jie He Za Zhi. 2010 May;30(5):499-503.