AIM To explore the expression of glucagon-like peptide-1 receptor (GLP-1R) and related molecular mechanism on hypoxic reoxygenation injury of cardiomyocytes in mice under high glucose conditions.

METHODS Hypoxic-reoxygenation model was established by cultured mice cardiomyocytes with high glucose and non-high glucose. The experiments were divided into six groups: group. control group with normal glucose (NG)、NG+ Hypoxic-reoxygenation (H/R)、NG+H/R+Exendin-4、control group with high glucose (HG)、HG+H/R、HG+H/R+Exendin-4. The expression GLP-1R was observed by Western blot. The oxidative stress marker of NOX4 and p22phox was observed by Western blot and RT-PCR. And exogenous GLP-1R agonist exendin-4 and PKC agonist (PMA) and PKC inhibitor (Go 6983) was treated according to the experimental groups to detect the expression changes of GLP-1R and the expression changes of oxidative stress marker NOX4 and p22phox.

RESULTS Compared to NG+H/R group, Exendin-4 reduced the oxidative stress injury（P<0.05）, but the anti-oxidative stress effect of GLP-1 on cardiomyocytes of mice was significantly reduced in high-glucose culture. The overexpression of PKC in mice cardiomyocytes of high-glucose culture down-regulated the expression of GLP-1R（P<0.05）. After inhibition of PKC by PKC inhibitor Go 6983, the protective effect of GLP-1 on mice cardiomyocytes of high-glucose culture could be partially restored（P<0.05）.

CONCLUSION Under high glucose conditions, PKC reduces the expression of GLP-1R on hypoxic reoxygenation injury of cardiomyocytes in mice and the antioxidant stress effect of GLP-1 is partly restored by down-regulating the active of PKC.