Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158

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Baicalin attenuates acute myocardial infarction of rats via mediating the mitogen-activated protein kinase pathway
Xiaobing LiuJianmin GuYuqi FanHuihua ShiMier Jiang
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ジャーナル フリー 早期公開

論文ID: b13-00021

この記事には本公開記事があります。
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抄録
Baicalin is a bioactive ingredient from the herb and has possessed various pharmacological actions. The present study was performed to evaluate the cardioprotective potential of baicalin against myocardial infarction and explore the potential mechanism. Baicalin was intraperitoneally injected into the rats by the doses of 50, 100 and 200 mg/kg, respectively, once a day for 7 days and, thirty minutes after the last administration, the left coronary artery was ligated. Infarct size was measured to analyze the myocardial damage. Myocardial specific enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) were determined with the colorimetric method. Evidence for myocardial apoptosis was detected by caspase-3 activity measurement and Western blot analysis. We also examined the protein levels of three major subgroups of mitogen-activated protein kinases (MAPKs), namely, ERK, JNK and p38 by Immuoblotting. Our results indicated that baicalin significantly reduced the infarct size and myocardial enzymes (CK, CK-MB, LDH and cTnT). Administration of baicalin also suppressed the activity and protein expression of caspase-3. Moreover, the protein level of phosphorylated ERK (p-ERK) was found to be evidently augmented while the phosphorylated JNK (p-JNK) and phosphorylated p38 (p-p38) were strikingly diminished in infarcted rats with baicalin treatment. These findings suggest that the baicalin's cardioprotection associates with mediation of MAPK cascades in acute myocardial infarction of rats.
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© 2013 The Pharmaceutical Society of Japan
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