Objective To investigate the effect of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) on the expression of apoptosis-related proteins in an alcohol cardiomyopathy (ACM) cell model. Methods A number of cells of logarithmic growth phase were selected and randomly divided into the following six groups: normal control group (Blank group), alcoholic cardiomyopathy group (ACM group), ACM+sh-NC inhibition control group (ACM+sh-NC group), ACM+sh-LOX-1 group, ACM+OE-LOX-1 overexpression group (ACM+OE-LOX-1 group), ACM+OE-LOX-1+si-NC group. Except for the blank group, all groups of cells were incubated with 200 mmol/L alcohol for 1 d to induce alcoholic cardiomyopathy cell model in vitro. The expression levels of LOX-1, Bax, Cleaved Caspase-3 were detected at the protein and gene levels by Western blot and real-time quantitative PCR, respectively, and the correlation was analyzed by Pearson product moment correlation coefficient.Results The expression of LOX-1, Bax and Cleaved Caspase-3 in myocardial tissue was significantly increased in the ACM group compared with the Blank group (P＜0.01); the protein expression was also significantly increased (P＜0.05). After intervening with LOX-1 expression, the expression of Bax and Cleaved Caspase-3 in myocardial tissue was significantly decreased in the ACM+sh-LOX-1 group compared with the ACM and ACM+sh-NC groups (P＜0.01).（The expression of Bax and Cleaved Caspase-3 in myocardial tissues was significantly increased in the ACM+OE-LOX-1 group compared with the ACM group (P＜0.01); correlation analysis suggested that the expression of LOX-1 was positively correlated with the expression of Bax and Cleaved Caspase-3 (r＜0.01). Expression was positively correlated with the expression of Bax and Cleaved Caspase-3 (r=0.663, P＜0.05; r=0.604, P＜0.05).Conclusion The expression of LOX-1 is increased in the alcoholic cardiomyopathy cell model, and is positively correlated with the expression of cardiomyocyte apoptosis proteins Bax and CleavedCaspase-3, and participates in the alcohol-induced apoptosis of cardiomyocytes by interfering with the expression of Bax and CleavedCaspase-3