Key result
Oral administration of Shu-mai-tang significantly increased capillaries and arterioles, suppressed myocardial fibrosis, and improved cardiac function in rats with myocardial ischemia.
Why the study?
Does Shu-mai-tang improve angiogenesis, arteriogenesis, and cardiac function in a rat model of myocardial ischemia?
RCT (n=96)
randomized
Does Shu-mai-tang improve angiogenesis, arteriogenesis, and cardiac function in a rat model of myocardial ischemia?
Shu-mai-tang promotes angiogenesis and arteriogenesis and improves cardiac function in a rat model of myocardial ischemia, potentially via the PI3K/Akt signaling pathway.
Shu-mai-tang effects in rats should not alter clinical practice; hypothesis-generating for human myocardial ischemia trials.
Ischemic heart disease is one of the leading causes of morbidity and mortality worldwide. Shu-mai-tang (SMT) is a traditional Chinese medicine for the treatment of ischemic heart disease. To better understand the underlying cardioprotection mechanisms of SMT on myocardial ischemia (MI), the effect of SMT on angiogenesis, arteriogenesis and cardiac function was investigated in a rat model of MI, as well as the potential mechanism. Rats with a ligated left anterior descending coronary artery (MI model) were randomized (24 rats/group) to receive SMT/LY294002 [phosphatidylinositol 3-kinase (PI3K) inhibitor], SMT or no treatment. A sham-operation group was included. It was demonstrated that 2 and 4 weeks after treatment the oral administration of SMT significantly increased capillaries and arterioles, suppressed myocardial fibrosis, as well as significantly increased cardiac phosphorylation of Akt, vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF-BB) levels and functional improvement. PI3K inhibitor down-regulated SMT-induced angiogenesis and arteriogenesis. These novel therapeutic properties of SMT to induce the reconstitution of stable blood supply networks, reverse LV remodeling may offer an alternative therapy for the treatment of ischemic heart disease. The potential mechanism may be that SMT promotes VEGF and PDGF-BB-mediated angiogenesis and arteriogenesis through the PI3K/Akt signaling pathway.
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Yin et al. (2008) conducted an RCT in myocardial ischemia (n=96). Shu-mai-tang (SMT) vs. no treatment, SMT/LY294002, and sham-operation was evaluated on angiogenesis, arteriogenesis and cardiac function. Oral administration of Shu-mai-tang significantly increased capillaries and arterioles, suppressed myocardial fibrosis, and improved cardiac function in rats with myocardial ischemia.
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