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Effect of traditional Chinese medicine Shu‐mai‐tang on angiogenesis, arteriogenesis and cardiac function in rats with myocardial ischemia
Author(s) -
Yin Huiqiu,
Zhang Jidong,
Lin Haiqing,
Qiao Yun,
Wang Rong,
Lu Huixia,
Liang Su
Publication year - 2009
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2565
Subject(s) - arteriogenesis , medicine , angiogenesis , cardioprotection , cardiac function curve , pi3k/akt/mtor pathway , pharmacology , cardiology , coronary artery disease , vascular endothelial growth factor , protein kinase b , ischemia , heart failure , signal transduction , vegf receptors , biology , biochemistry
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. Copyright © 2008 John Wiley & Sons, Ltd.