Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion / 中国实验方剂学杂志

ABSTRACT

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.