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Objective:To investigate the expressions of cardiac cycle, myocardial pathology, galectin-3 (Gal-3),transforming growth factor-β (TGF-β),Smad homologue 3 recombinant protein (Smad3) in rats with heart failure and heart failure after ischemia-reperfusion, and the intervention effect of Dendrobii Officinalis Caulis (DOC) myocardial fibrosis in model rats. Method:A rat model of heart failure and Qi deficiency was established through ligation of the left anterior descending coronary artery. The rats were divided into blank group, model group, valsartan group (9.43 mg·kg-1) and DOC group (10 mg·kg-1), with 10 in each group. The blank group and the model group were given an equal volume of physiological saline. The changes in left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic dimension(LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS) of the cardiac cycle of rats in each group were recorded by high-resolution ultrasound system. The carboxyterrninal propeptide of type I procollagen (PICP), and carboxyterrninal propeptide of type Ⅲ procollagen (PⅢNP)were detected by enzyme-linked immunosorbent assay (ELISA) kit. The morphological changes of myocardial cells were observed by hematoxylin-eosin (HE) staining. The changes of myocardial fiber tissue and collagen were observed by Masson staining. Western blot was used to detect the protein expressions of Gal-3, TGF-β, Smad3. Result:Compared with the blank group, the levels of LVEDD, LVEF, and LVFS were lower in the model group (PPβ, and Smad3 were decreased (PPPPβ and Smad3 were lower than those in the model group (PPConclusion:DOC can effectively inhibit myocardial fibrosis in rats with heart failure and heart Qi deficiency syndrome after ischemia-reperfusion. The mechanism may be correlated with the reduction of the expressions of Gal-3, TGF-β and Smad3.
ABSTRACT
[Objective] To observe the influence of rats serum SOD and cardiac function with qi deficiency syndrome through the factors of the acupuncture point injection with different reinforcing and reducing methods. [Methods] To establish SD rat heart-qi deficiency syndrome model with the compound factors of the feeding, load forced swimming and large dose propranolol. The rats were randomly divided into blank control group, model group, Zusanli(St. 36) Shenqi Fuzheng injection reinforcing method group, Zusanli(St. 36) Shenqi Fuzheng injection reducing method group. Each acupoint injection of 0.20ml, one time a day, for 10 consecutive days. Determine of serum SOD activity values respectively and detect cardiac function correlated hemodynamic indexes. [Results] (1) The activity of serum SOD in model group rats was significantly lower than control group( P<0.01);Treated groups and model group had significant difference(P<0.05 or P<0.01);Zusanli(St. 36) injection reinforcing method group and Zusanli(St. 36) reducing method group had significant differences(P<0.01);(2) The cardiac function of rats in model group decreased significantly, corresponding heart function index of each treatment groups had changes and obvious differences. The maximum ventricular rats model of the internal pressure, left ventricular systolic pressure ,the maximum rate of rise of left ventricular pressure, heart rate and other indicators of Zusanli(St. 36) Shenqi Fuzheng injection reinforcing method group were more than indexes of Zusanli(St. 36) Shenqi Fuzheng injection reducing method group( P<0.01). [Conclusion] Acupoint injection of different reinforcing-reducing manipulations had different effect on the treatment of disease, and Zusanli(St. 36) injection reinforcement treatment of heart-qi deficiency syndrome model rats was significantly better than the other groups.
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[Objective] Using gene chip to detect the influence on gene expression due to replicate Heart-Qi Deficiency Syndrome on Wistar Rat caused by complex factor including slimming, forced swimming and large dosage of propanolol. [Methods] Every animal in experiment group took food according to 5g/100g body weight, and was forced to swim by taking weight according to its 5% body weight until sank beyond 10 seconds. From 17th day ig propanolol 24mg/Kg and lasted for 4 days. At 21st day we took out hearts and picked up general DNA to prepare probe, then cross with gene chip. [Results] Compared with control group, expression of gene NM-017329,NM-016997 and NM-030850 showed down regulation obviously, expression of gene NM-031345 and NM-024349 showed up-regulation significantly. [Conclusion] Repression of immunological function and damage of vascular endothelium may be the main mechanism resulting in Heart-Qi Deficiency Syndrome.