Icariin Acts as a Potential Agent for Preventing Cardiac Ischemia/Reperfusion Injury.
In: Cell biochemistry and biophysics, Jg. 72 (2015-06-01), Heft 2, S. 589-97
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Zugriff:
Myocardial infarction is a leading cause of mortality and morbidity worldwide. Although essential for successful recovery, myocardium reperfusion is associated with reperfusion injury. Icariin, a major flavonoid of Epimedium koreanum Nakai, has been proven to exert efficacy for improving cardiovascular function. We investigated the molecular effect and signal pathway of icariin on cardiac ischemia/reperfusion injury. In an in vivo model of infarct in rats, icariin (10 mg/kg) significantly attenuated myocardial infarct size induced by ischemia/reperfusion (I/R). From the TUNEL assay, icariin reduced the apoptotic cell induced by I/R and decreased blood indicators of creatine kinase, ischemia-modified albumin, and lactate dehydrogenase. All this effect was antagonized by the PI3K inhibitor LY294002. Meanwhile, icariin activated the PI3K/Akt/eNOS pathway. The PI3K inhibitor LY294002 suppressed icariin-mediated protective effect. These results suggest that icariin protects against myocardial ischemia reperfusion injury in rats by activating the PI3K/Akt/eNOS-dependent signal pathways and may be a useful drug for angiogenic therapy.
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Icariin Acts as a Potential Agent for Preventing Cardiac Ischemia/Reperfusion Injury.
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Autor/in / Beteiligte Person: | Zhai, M ; He, L ; Ju, X ; Shao, L ; Li, G ; Zhang, Y ; Liu, Y ; Zhao, H |
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Zeitschrift: | Cell biochemistry and biophysics, Jg. 72 (2015-06-01), Heft 2, S. 589-97 |
Veröffentlichung: | Totowa, NJ : Humana Press, c1996-, 2015 |
Medientyp: | academicJournal |
ISSN: | 1559-0283 (electronic) |
DOI: | 10.1007/s12013-014-0506-3 |
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