Interleukin-2 confers cardioprotection by inhibiting mitochondrial permeability transition pore

C-M Cao; J-Z Chen; Q Xia; S-Z Zhang; G-H Lin; T-M Wong

doi:10.1109/IEMBS.2004.1404017

Interleukin-2 confers cardioprotection by inhibiting mitochondrial permeability transition pore

Conf Proc IEEE Eng Med Biol Soc. 2004:2004:3618-21. doi: 10.1109/IEMBS.2004.1404017.

Authors

C-M Cao¹, J-Z Chen, Q Xia, S-Z Zhang, G-H Lin, T-M Wong

Affiliation

¹ Department of Cardiology, the First Affiliated Hospital; Department of Physiology, The University of Hong Kong, Hong Kong SAR, China.

PMID: 17271075
DOI: 10.1109/IEMBS.2004.1404017

Abstract

In the present study, we determined whether interleukin-2 (IL-2) confers cardioprotection by inhibiting mitochondria permeability transition pore (MPTP) opening. In isolated rat hearts subject to 30 min ischemia and 120 min reperfusion (IR), IL-2 (50 U/ml) decreased the infarct size and LDH release, effects blocked by a selective kappa-opioid receptor antagonist, Nor-BNI (5 microM) or an opener of MPTP, atractyloside (Atr, 20 microM). In isolated ventricular myocytes subjected to anoxia and reoxygenation (AR), which reduced both the amplitude of the electrically induced [Ca2+]i transient and diastolic [Ca2+]i, IL-2 attenuated the AR-induced alterations and their effects were abolished by Atr. In addition, IL-2 attenuated the reduction in calcein fluorescence in myocytes subject to AR and reduced calcium-induced swelling in mitochondria of rat hearts subjected to IR, which were similar to effect of inhibitor of MPTP. The observations indicated that IL-2 confers cardioprotection by inhibiting the MPTP opening.