AIM: To investigate the cardioprotective effects and the mechanisms of
delayed preconditioning of Allitridium on cultured
neonatal rat myocardiocytes subjected to H/R.METHODS: Cultured neonatal rat cardiomyoctytes were preconditioned using Allitridum in final concentrations 20μg/ml.Cell viability, lactate dehydrogenase (LDH) release and malondialdehyde (MDA) formation were measured 24h late to determine the protective effects against H/R injury.And the expressions of nPKC-ε, HSP70 and NF-κB were measured 24h after preconditioning by western blot analysis.RESULTS: Increased cell viability, decreased LDH release and MDA formation were observed in
cardiomyocytes treated with Allitridium.The delayed protection was abolished by pretreating with either PKC inhibitor H-7 or PD 98059(a upstream kinase inhibitor of MAPKs).And the expressions of nPKC-ε and HSP70 were significantly increased in APC group compared to control group which were abolished in APC+H-7 group, while only HSP70 increase was obviously restrained in APC+PD98059 group.CONCLUSION: Allitridium can mimick the delayed cardioprotection in rat neonatal cardiomyocytes.The protective mechanisms are associated with PKC and MAPKs signaling pathways.Allitridum induce delayed cardioprotective effects by activation of nPKC-ε, MAPKs(a dowmstream kinase of PKC) phosphorylation and followed increased expression of HSP70.