Abstract: OBJECTIVE: We aimed to observe the regulatory effect of protein kinase Cε(PKCε) on injuries in primary cultured cardiomyocytes induced by hypoxia/reoxygenation (H/R). METHODS：H/R model was made by primary culture of neonatal rat cardiomyocytes. The translocation pattern of PKC activity was assessed by fractionated Western-blot analysis. Measurements including cardiac troponin I (cTnI) release were measured by two-site sandwich chemiluminescence enzyme immunoassay and levels of tumor necrosis factor-α (TNF-α)were measured by enzyme-linked sandwich immunosorbent assay (ELISA) method to assess the degree of injury in cultured cardiomyocytes. RESULTS：Compared with control group，in primary cultured cardiomyocytes exposed to H/R，PKCε translocation significantly increased after 2 h of hypoxia and 30 min of reoxygenation (P＜0.05)，the protein levels of PKCε decreased after 4 h of hypoxia (P＜0.05). Compared with H/R group，the PKCε inhibitor peptide εV1-2 increased cTnI release (P＜0.05) but did not influence TNF-α secretion from cardiomyocytes. CONCLUSION：Activation of PKCε could alleviate the cardiomyocyte cell damage induced by H/R.

Key words: cardiomyocytes, hypoxia/reoxygenation, protein kinase Cε