The aim of this study was to observe the protective effect and mechanism of Yiqi Wenyang Huoxue Lishui components compatibility (YWHL) on myocardial microvascular injury in chronic heart failure (CHF) rats. A rat model of CHF was prepared by aortic arch constriction. The serum levels of endothelins 1 (ET-1), vonwillebrand factor (vWF), angiotensin II (Ang II) and norepinephrine (NE) were measured by enzyme-linked immunosorbent assay. Transmission electron microscopy was used to observe myocardial ultrastructure and myocardial microvascular ultrastructure; The expression levels of occludin, zonula occluden-1 (ZO-1), vascular endothelial ZO-1, vascular endothelial cadherin (VE-cadherin), filamentous actin (F-actin) and matrix metalloproteinase-9 (MMP-9) were detected by Western blot. Using the hypoxia-induced rat cardiomyocyte injury model, the apoptosis level of cardiomyocytes and the change of mitochondrial membrane potential were detected by flow cytometry; the mitochondrial respiratory chain complexes I-IV enzyme activity were measured by biochemical assay kits; the expression levels of adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator activated receptor gama coactivator 1 alpha (PGC-1α), nuclear respiratory factor-1 (NRF1), mitochondrial transcription factor A (mtTFA) were detected by Western blot. The results of animal experiments showed that compared with the model group, YWHL significantly reduced the levels of serum ET-1, vWF, Ang Ⅱ, NE, attenuated myocardial and myocardial microvascular injury, increased the protein expression levels of Occludin, ZO-1, VE-cadherin, F-actin and reduced the protein expression level of MMP-9. The results of cellular experiments showed that, compared with the control group, the apoptosis rate of cells in the hypoxia group increased; mitochondrial membrane potential decreased; respiratory chain complexes I-IV enzyme activity decreased; the protein expression levels of PGC-1α, NRF1, and mtTFA decreased, and the degree of AMPK phosphorylation fell. After YWHL and AMPK agonist intervention, all of the above conditions improved. And AMPK inhibitors serve to block the potency of YWHL. YWHL was effective in ameliorating myocardial microvascular injury, and this effect may be realized by regulating the AMPK/PGC-1α pathway.

"> chronic heart failure, Yiqi Wenyang Huoxue Lishui components compatibility, energy metabolism, F-actin depolymerization, AMPK/PGC-1α pathway