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Eur J Cardiothorac Surg 2005;27:117-121
© 2005 Elsevier Science NL

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

^a Department of Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
^b Department of Post-Genomics and Diseases, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan

Received 18 May 2004; received in revised form 6 September 2004; accepted 9 September 2004.

^* Corresponding author. Tel.: +81 6 6879 3151; fax: +81 6 6879 3163. (E-mail: sawa{at}surg1.med.osaka-u.ac.jp).

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°C) for 30min followed by 60min 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.

Key Words: Apoptosis • Cardiomyocytes • Ischemia/reperfusion injury • Heart surgery

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