In this study, we aim to develop a new, reproducible crush injury (CI) model in rabbits. Anesthetized rabbits were compressed on both hind limbs using a special instrument for 6 h followed by 3 h of reperfusion. Blood samples and injured muscles were collected for biochemical analysis and morphological evaluation.
View Article and Find Full Text PDFZhongguo Zhong Xi Yi Jie He Za Zhi
May 2010
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.
Objective: 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).