頁籤選單縮合
題 名 | Calcium-Sensing Receptor Induced Myocardial Ischemia/Reperfusion Injury via the C-Jun NH₂-Terminal Protein Kinase Pathway |
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作 者 | Jiang, Chun-ming; Xu, Chang-qing; Mi, Yan; Li, Hong-zhu; Wang, Rui; Li, Wei-min; | 書刊名 | Acta Cardiologica Sinica |
卷 期 | 26:2 2010.06[民99.06] |
頁 次 | 頁102-110 |
分類號 | 415.3165 |
關鍵詞 | Apoptosis; Calcium-sensing receptor; Ischemia/reperfusion; JNK; Myocardium; Rat; |
語 文 | 英文(English) |
英文摘要 | Objective: Calcium-sensing receptor (CaSR) belongs to the family C of G-protein coupled receptors. This study was carried out to investigate the role of CaSR in a model of myocardial ischemia/reperfusion injury (MI/RI) in rats. Methods: To produce an MI/RI in rats, a branch of the left anterior descending coronary artery was occluded for 30min followed by a 6h reperfusion. Then, we measured cardiac function, noted morphologic alterations of the myocardium, and analyzed the the expression of caspase-3, Bcl-2, CaSR, and c-Jun NH2-terminal protein kinase (JNK) by Western blotting, respectively. Results: GdCl3, an activator of CaSR, further enhanced myocardial injury induced by ischemia/reperfusion, resulting in an increase in JNK phosphorylation, down-regulation of Bcl-2 expression, and up-regulation of caspase-3 expression. Inhibition of JNK activation with SP600125 partly converted the myocardial injury. Conclusion: The results demonstrated that CaSR may induce MI/RI via the JNK pathway. |
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