Literature DB >> 15621482

BH4 peptide derivative from Bcl-xL attenuates ischemia/reperfusion injury thorough anti-apoptotic mechanism in rat hearts.

Masamichi Ono1, Yoshiki Sawa, Masahiro Ryugo, Alexei N Alechine, Shigeomi Shimizu, Rie Sugioka, Yoshihide Tsujimoto, Hikaru Matsuda.   

Abstract

OBJECTIVE: To prevent apoptosis is thought to be promising for myocardial protection in cardiac surgery. Recently, we showed that BH4 domain of Bcl-xL is essential for the prevention of apoptosis, and that BH4 fused to HIV TAT protein (TAT-BH4) prevented apoptotic cell death. Then, we hypothesized TAT-BH4 may attenuate ischemia/reperfusion injury in rat hearts.
METHODS: The isolated rat hearts in the TAT-BH4 preconditioning group (BH4 group, n=8) or control group (C group, n=8) were subjected to warm ischemia (37 degrees C) for 30 min followed by 60 min of reperfusion using Langendorff perfusion system.
RESULTS: Left ventricular developed pressure and maximum dP/dt after reperfusion were significantly improved in the BH4 group than those in the C group (P<0.01). Recovery of mitochondrial respiration was significantly better in the BH4 group (P<0.05). Moreover, expression of caspase-3 and TUNEL-positive myocardium were decreased in the BH4 group than those in the C group.
CONCLUSIONS: These results demonstrated that TAT-BH4 attenuates myocardial ischemia/reperfusion injury through preventing myocardial apoptosis. Thus, TAT-BH4 may be a novel therapeutic agent for myocardial protection in cardiac surgery.

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Year:  2005        PMID: 15621482     DOI: 10.1016/j.ejcts.2004.09.025

Source DB:  PubMed          Journal:  Eur J Cardiothorac Surg        ISSN: 1010-7940            Impact factor:   4.191


  11 in total

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