Zhongguo Zhong Xi Yi Jie He Za Zhi
July 2012
Objective: To explore the effects of Tanshinone II A (Tan II A) on the myocardial apoptosis in rats with heart failure and its mechanisms for regulating the miR- 133 levels.
Methods: The heart failure rat model was established by thoracic aorta constriction (TAC). Tan II A Injection was applied for 12 successive weeks.
Objective: To study the effect of tanshinone II A on the cell signal transduction system protein kinase B (Akt) in rats with hypertrophy of the myocardium induced by partial constriction of the thoracic aorta.
Methods: Rat models of myocardial hypertrophy were established by the thoracic aorta partial constriction method. Forty-eight rats were randomly divided into the sham-operative group, the model group, the valsartan treatment group, and the low-, medium-, and high-dose tanshinone treatment groups.
Cardiac fibrosis occurs after pathological stimuli to the cardiovascular system. One of the most important factors that contribute to cardiac fibrosis is angiotensin II (AngII). Accumulating studies have suggested that reactive oxygen species (ROS) plays an important role in cardiac fibrosis and sodium tanshinone IIA sulfonate (STS) possesses antioxidant action.
View Article and Find Full Text PDFObjective: To explore the molecular biological mechanism for tanshinone II A reversing left ventricular hypertrophy, it would be studying the effect of tashinone on the endothelial nitric oxide synthase (eNOS) and protein kinase C (PKC) in the hypertrophic cadiocyte of rats suffered abdominal aorta constriction.
Method: SD rats were operated with abdominal aorta constriction and 8 rats were done with sham surgery. After 4 weeks, all rats were divided into 4 groups: myocardial hypertrophy group, low dose tanshinone II A group (10 mg x kg(-1) x d(-1)), high dose tanshinone II A group (20 mg x kg(-1) x d(-1)) and valsartan group (10 mg x kg(-1) d(-1) intragastric administration).
Objective: To observe the effects of sodium tanshinone II A sulfonate (STS) on angiotensin II (Ang II)-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase (p-ERK1/2).
Methods: In the primary culture of neonatal rat myocardial cells, the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by [3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells. The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling.
Objective: To investigate the changes of proto-oncogene c-fos, c-jun mRNA expression in angiotensin II (Ang II)-induced hypertrophy and effects of tanshinone II A (Tan) in the primary culture of neonatal rat cardiomyocytes.
Method: Twelve neonatal Wistar rats aged one day old of clean grade and both sexes were selected to isolate and culture cardiomyocytes. The cardiomyocytes were divided into: normal control group, Ang II (10(-6) mol x L(-1)) group, Ang II (10(-6) mol x L(-1)) +Tan (10(-8) g x L(-1)) group, Ang II (10(-6) mol x L(-1)) + valsartan (10(-6) mol x L(-1)) group, Tan (10(-8) g x L(-1)) group, valsartan (10(-6) mol x L(-1)) group.
Objective: To investigate the protective effect of tanshinone II A on porcine aortic endothelial cells (PAEC).
Methods: PAEC were stimulated with angiotensin II (Ang- II) for different acting time (1 h, 6 h and 24 h) and Tanshinone II A was added along with Ang- II stimulation (Group A) or 6 h after it (Group B). The nitric oxide (NO) level, the protein and mRNA expression of nitric oxide synthase (cNOS) in PAEC were measured by nitric acid deoxidizing assay, RT-PCR and immunohistochemical assay, respectively.