Activation of p38 MAPK induced by a multi-cycle ischaemic preconditioning protocol is associated with attenuated p38 MAPK activity during sustained ischaemia and reperfusion.

摘要: Abstract The role of p38 mitogen-activated protein kinase (MAPK) in ischaemic preconditioning remains controversial. Since most previous studies focussed on events only during sustained ischaemia, the aim this study was to establish activation pattern MAPK a multicycle protocol, ischaemia as well reperfusion and correlate these with functional recovery isolated perfused rat heart. Isolated hearts were preconditioned by 3×5 min global followed 25 30 reperfusion. Non-preconditioned subjected Hearts freeze-clamped tissue lysates assessed standard Western blotting techniques, using dual phospho-p38 antibody non-radioactive IP-kinase assay. results showed that transient phosphorylation occurs protocol: maximal first episode, becoming progressively lower second third episodes. significantly less both hearts, when compared non-preconditioned hearts. Attenuation activity associated improved recovery. effect inhibition cardioprotection further evaluated adult, cardiomyocytes. Administration SB 203580 (1–10 μ M ) before had no cell morphology viability after 2 h hypoxia, untreated When administered cells onset it caused significant improvement viability. In summary, suggest attenuation may be an essential element process.