Abstract
Objective: To assess the effects of traditional Chinese medicine YiQiFuMai on cardiac function during the progression of ischemic heart failure. Methods: Rabbits were divided into sham, heart failure, and YiQiFuMai groups. The ischemic heart failure model was established in New Zealand white rabbits, which were intraperitoneally injected with YiQiFuMai injection and 0.9% sodium chloride after the operation. After six weeks, cardiac function was examined by ultrasound; serum BNP levels were measured by ELISA; p-AKT, eNOS, ICAM-1 and VEGF levels were evaluated by real-time PCR and Western-Blot; pathological changes of the myocardial tissue were observed by H&E staining; CD31 expression in tissue samples was analyzed by immunohistochemistry. The ultrastructure and microcirculation of myocardial tissue specimens from the three groups were assessed by transmission electron microscopy. Results: YiQiFuMai decreased serum BNP levels, and increased LVEF and reduced LVEDD at 6 weeks postoperatively. In addition, YiQiFuMai can improve myocardial damage and microcirculation structure, as assessed by histology and transmission electron microscope. At the molecular level, treatment with YiQiFuMai resulted in increased eNOS, VEGF and p-AKT levels but reduced ICAM-1 amounts compared with the heart failure group. Conclusion: Ischemic heart failure damages the microvascular structure and functions of the myocardium. Treatment with YiQiFuMai potentially ameliorates microcirculatory damage and alleviates cardiac failure by improving endothelial function and angiogenesis, and inhibiting inflammatory cell adhesion.
Highlights
After acute myocardial infarction, myocardial fibrosis and cardiac dilatation occur gradually in the infarcted myocardium, eventually leading to heart failure [1]
Cardiac function was examined by ultrasound; serum BNP levels were measured by ELISA; p-AKT, Endothelial Nitric Oxide Synthase (eNOS), ICAM-1 and VEGF levels were evaluated by real-time PCR and Western-Blot; pathological changes of the myocardial tissue were observed by H&E staining; CD31 expression in tissue samples was analyzed by immunohistochemistry
Two weeks after the surgical operation, we found that LVEF values in the heart failure, YiQiFuMai groups were significantly increased compared with preoperative values, while LVEDD values in these three groups were significantly decreased after modeling (Table 2)
Summary
Myocardial fibrosis and cardiac dilatation occur gradually in the infarcted myocardium, eventually leading to heart failure [1]. It has been highlighted that microcirculatory dysfunction plays a pivotal role in ischemic heart failure [3]. Its release is affected by a series of signaling pathways during endothelial injury, leading to coronary microvascular damage [4]. Microvascular angiogenesis is crucial to survival and functional recovery after ischemic heart disease. Angiogenesis is triggered by angiogenic factors binding to endothelial cell receptors, and VEGF is the major factor contributing to angiogenesis [6]. VEGF plays an important role in angiogenesis through three structurally related VEGF receptor tyrosine kinases, including VEGFR1, VEGFR2 and VEGFR3 [7]. VEGFR2, a major VEFG receptor in endothelial cells, is indispensable for the differentiation, proliferation and migration of endothelial cells, as well as angiogenesis. VEGF is critically involved in the maturation of newly formed blood vessels in ischemic myocardium, providing long-term blood supply for cardiomyocytes and limiting ventricular remodeling after myocardial infarction [8]
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