Biomedical Research

Objective: To investigate the effects of shenfuqiangxin on the expression of factors related to TGF-beta/ Smads signaling pathway in cardiac tissue of rats with Heart Failure (HF) post myocardial infarction, and explore its significance.

Methods: 45 Sprague-Dawley healthy male rats were divided randomly into Sham group, HF group and shenfuqiangxin group, 15 rats in each group. HF model was reproduced with myocardial infarction which was created by ligating the left anterior descending coronary artery. In sham group, the coronary artery was not ligated. 2 w after operation, sham group and HF group rats were administrated with saline by intragastric administration for 8 w, while in shenfuqiangxin group, shenfuqiangxin (14 g/kg) was used. Echocardiography was performed at 2 w after surgery (before gavage) and repeated at 8 w post gavage to measure Left Ventricular End Systolic Volume (LVESD), Left Ventricular End Diastolic Volume (LVEDD), Left Ventricular Ejection Fraction (LVEF) and Fractional Shortening (FS). After 8 w of intragastric administration, Hematoxylin and Eosin (HE) staining was adopted to show the morphology of myocardium, and Masson staining was used to determine the degree of myocardial fibrosis. The mRNA expression of TGF-β1, Smad2, Smad3 and Smad7 were detected using real-time PCR and the protein expression of TGF-β1, Smad2, Smad3 and Smad7 were detected by Western blot.

Results: Before intragastric administration, LVEDD and LVESD in Shenfuqiangxin group and HF group were both increased compared with sham group, while EF and FS were decreased (P<0.05). 8 w after intragastric administration, EF and FS in shenfuqiangxin group were higher than those in HF group (P<0.05). HE staining showed that, in sham group, there were no degeneration, necrosis, atrophy or hypertrophy in the myocardium and there were no mesenchymal inflammatory cell infiltration or hyperplasia of fibrous tissue. Myocardial cells were homogeneously stained and had clear boundary with intact membrane, and cross striation was arranged evenly. In HF group, myocardial cell swollen was observed and some of the myocardial fibers were broken and dissolved. Striations disappeared, and vacuolar degeneration of cytoplasm, interstitial edema, fibrous hyperplasia and inflammatory cell infiltration were also observed. Shenfuqiangxin group showed different degrees of myocardial cell swelling, slightly blurred cross striation and slight inflammatory cell infiltration. Pathological changes of myocardium in Shenfuqiangxin group were mild and similar to that of sham group. Myocardium was red, collagen fibers were blue and nuclei were black or blue in Masson trichrome staining. No obvious left ventricular fibrosis was observed in sham group. In HF group, there was patchy or small focal fibrosis in the left ventricle. Different degrees of focal necrosis or scattered fibrosis were found in shenfuqiangxin group and were similar to that of Sham group. The mRNA and protein expression level of TGF-β1, Smad2, Smad3 and Smad7 were highest in HF group followed by shenfuqiangxin group and sham group (P<0.05).

Conclusion: Application of shenfuqiangxin could inhibit the expression of factors related to TG-beta/ Smads signaling pathway in myocardium of rats with heart failure after myocardial infarction, which may be one of the important mechanisms to improve myocardial fibrosis.

Author(s): Yunfei Qu, Ning Zhang, Jianrong Zhang
Abstract | Full-Text | PDF

Share this