OBJECTIVETo elucidate whether ZFP580 is involved in the cardioprotective effects of intermittent hypobaric hypoxia (IHH) against myocardial ischemia/reperfusion (I/R) injury.

METHODSThirty two male Wistar rats were randomly divided into 2 groups (n = 16): normoxia control group and IHH preconditioning group. Rats in IHH group were exposed in a hypobaric chamber (equivalent to an altitude of 5 000 m) for a 6 h period each day for 42 d. Plasma was collected and lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) were measured after 2 h of myocardial I/R injury. ZFP580 protein expression in myocardial tissue was assayed by Western blot. Other 8 rats in each group were used to evaluate I/R-induced cardiac infarction by TTC staining. Lentivirus-mediated gene transfection was performed in H9c2 cells 72 h prior to simulated ischemia/reperfusion (SI/R) exposure. The degree of cell apoptosis was determined by annexin V/7-AAD staining and flow cytometry analysis.

RESULTSCompared with normoxia control group, adaptation to IHH attenuated infarct size and plasma leakage of LDH and CK-MB. In addition, ZFP580 expression in the myocardium was up-regulated by IHH. The results of gene transfection showed that ZFP580 overexpression significantly inhibited cells apoptosis induced by SI/R.

CONCLUSIONOur findings demonstrate that the cardioprotective effect of IHH against I/R injury is mediated via ZFP580, a novel transcription factor, with anti-apoptotic roles in myocardial cells.