AIM To investigate the protective effect of bisoprolol against burn-induced myocardial injury and explore its mechanism.

METHODS The burn model was established by subjecting rats to third degree burns on the back. Forty male SD rats were randomly divided into Sham, Burn, Burn+BIS, Burn+CQ and Burn+BIS+CQ groups, with 8 rats in each group. Twelve hours after the burn treatment, cardiac function of the rats was evaluated by echocardiography imaging system, morphology and structure changes of myocardium were observed by HE staining and transmission electron microscopy, and the apoptotic rate of cardiomyocytes was examined by apoptosis kit. The protein expressions of Bcl2-associated X protein (Bax), B-cell lymphoma 2 (Bcl2), dynamin-related protein 1 (Drp1), PTEN-induced putative kinase 1 (PINK1) and E3 ubiquitin-protein ligase enzyme Parkin were detected by Western blot.

RESULTS There were obvious disordered myocardium fibers and myocyte necrosis in the Burn group. Besides, electron microscopy observed broken and loose myofilaments, mitochondrial swelling and vacuolization. The structural damage of myocardium induced by burn was alleviated with bisoprolol treatment. Compared with those in the Sham group, interventricular septal thickness in diastole (IVSd), interventricular septal thickness in systole (IVSs), left ventricular posterior wall thickness at end-diastole (LVPWd), left ventricular posterior wall thickness at end-systole (LVPWs), left ventricular ejection fraction (LVEF) and fractional shortening (FS) were decreased, while left ventricular internal diameter at end-diastole (LVIDd) and left ventricular internal diameter at end-systole (LVIDs) were increased in the Burn group (P<0.01). The changes of the above indices were improved by bisoprolol (P<0.05, P<0.01). Compared with those in the Sham group, the apoptotic rate of cardiomyocytes and the protein expressions of Bax and Drp1 were increased and the expressions of Bcl2, PINK1 and Parkin were down-regulated in the Burn group (P<0.05, P<0.01). The alterations of the above indicators were ameliorated with bisoprolol treatment (P<0.05, P<0.01). However, the apoptotic rate of cardiomyocytes and the protein expressions of Bax and Drp1 were further increased and the expressions of Bcl2, PINK1 and Parkin were further decreased after chloroquine treatment (P<0.05, P<0.01).

CONCLUSION Bisoprolol improves myocardial injury and cardiac dysfunction induced by severe burn through reinforcing mitophagy via Drp1/PINK1/Parkin pathway.