Protective effect of AE3 on anoxia preconditioning via NO pathway in rat cardiomyocytes

Aim To investigate the role of AE3 in anoxic preconditioning of primary cultured neonatal rat cadiomyocytes and the underlying mechanism related to NO pathway.Methods Cardiomyocytes were randomly divided into four groups as follows: control,anoxia/reoxygenation(A/R),anoxia preconditioning(APC) and L-NAME groups.RT-PCR and Western blotting were used to measure AE3 mRNA and protein expression in A/R and APC model respectively.Cell viability was determined by MTT assay.The activity of LDH and CPK in culture medium was measured with an automatic biochemical analyzer.Results Both AE3 mRNA transcription and protein expression had upward tendency in A/R group,and had more abundance after APC,compared with A/R group and control group.However,L-NAME,an inhibitor of NO synthase inhibitor,could suppress the expression of AE3 in APC and abolished the cardioprotection of APC on cell injury and viability.Conclusion AE3 may be involved in the cardioprotection of APC via NO pathway in rat cardiomyocytes.