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QiShenYiQi Pills® Attenuates the Myocardial Injury and Microvascular Hyperpermeability Induced by Ischemia‐reperfusion in Rat, via Regulation of Myocardial Energy
Author(s) -
Han JingYan,
Lin SeQi,
Wei XiaoHong,
Liu YuYing,
Hu BaiHe,
Chang Xin,
Li Quan,
Pan ChunShui,
Yang XiaoYuan,
Fan JingYu
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.687.17
Subject(s) - pinacidil , medicine , myocardial infarction , cardiology , evans blue , cardiac function curve , reperfusion injury , pharmacology , ischemia , endocrinology , heart failure , glibenclamide , diabetes mellitus
QiShenYiQi Pills® (QSYQ) is a compound Chinese medicine used for alleviating cardiac function. However, it is unknown whether QSYQ is favorable for I/R‐induced myocardial injury. This study explored the effect and mechanism of QSYQ on I/R‐induced myocardial injury. SD rats were subjected to 30 min occlusion of the left anterior descending coronary artery and followed by reperfusion with or without QSYQ. Albumin leakage, myocardial blood flow (MBF), and cardiac function were evaluated. Myocardial energy, myocardial infarction and apoptosis, myocardial histological and ultrastructural evidence were assessed. Tight junction‐related proteins and myocardial skeleton protein were examined. Pre‐treatment with QSYQ attenuated I/R‐induced MBF decrease, albumin leakage increase, and cardiac dysfunction. Moreover, myocardial infarct size and apoptotic cells, the ratio of ADP/ATP and AMP/ATP, the phosphorylation of Myosin Light Chain (MLC), Src, and Caveolin‐1, and Aquaporin (AQP)‐1 level increased significantly in response to I/R, and the augmented junction of endothelial cells, the reduction of ATP 5D, ZO‐1, Occludin, and Claudin‐5 were observed after reperfusion, all of which were significantly ameliorated by pre‐treatment with QSYQ. Pre‐treatment with QiShenYiQi Pills ameliorates I/R‐induced myocardial injury and microvascular permeability damage in rats via the regulation of myocardial energy.