AIM To investigate the expression of lectin-like oxidized low-density lipoprotein receptor-1(LOX-1) and its correlation with autophagy-associated protein Beclin-1 and autophagy microtubule-associated protein light chain 3 antibody II (LC3-II) in an ethanol-induced rat cardiomyocyte model.

METHODS Rat cardiomyocytes in logarithmic growth phase were randomly divided into the following 6 groups: Blank group, ethanol group, ethanol+sh-NC group, ethanol+sh-LOX-1 group, ethanol+OE-LOX-1 group and ethanol+OE-LOX-1+si-NC group, and the cells of all the groups except those of blank control group were incubated with 200 mmol/L alcohol for 1d. The ethanol-induced rat cardiomyocyte model was constructed in vitro and the number of autophagy bodies was observed by electron microscopy. The expression levels of LOX-1, Beclin-1, LC3-I and LC3-II in each group were detected by real-time fluorescence quantitative PCR (Realtime PCR) and protein blotting (Western blot), respectively, and their expressions were compared and analyzed.

RESULTS Acute ethanol exposure resulted in significantly higher expressions of LOX-1, Beclin-1, LC3-I and LC3-II in rat cardiomyocytes at both gene and protein levels(P<0.01). After inhibition of LOX-1 expression, Beclin-1, LC3-I and LC3-II expressions were significantly down-regulated(P<0.01), whereas after over-expression treatment of LOX-1, the expression levels of Beclin-1, LC3-I and LC3-II increased(P<0.01). Under transmission electron microscopy, acute ethanol ingestion caused an increase in autophagy bodies in rat cardiomyocytes. Down-regulation of LOX-1 reduced the number of autophagy bodies, whereas over-expression of LOX-1 increased the number of autophagy bodies(P<0.01).

CONCLUSION LOX-1 expression is up-regulated in an acute ethanol-induced rat cardiomyocyte model and shows a synergistic trend with autophagy-related factors (Beclin-1 and LC3-II), suggesting that LOX-1 may contribute to the pathological process of alcohol-refined myocardial injury by up-regulating the expression levels of Beclin-1 and LC3-II, resulting in the over-activation of autophagy levels.