Estrogen protects cardiomyocytes against lipopolysaccharide by inhibiting autophagy

Autophagy has a significant role in myocardial injury induced by lipopolysaccharide (LPS). Estrogen (E2) has been demonstrated to protect cardiomyocytes against apoptosis; however, it remains to be determined whether it exhibits anti-autophagic effects. The aim of the present study was to investigate whether estrogen-regulated autophagy attenuates cardiomyocyte injury induced by LPS. The cardiomyocytes of neonatal rats were randomized to the control (Con), LPS and estrogen + LPS groups. The LPS group was treated with 1 mu g LPS for 24 h and the estrogen + LPS group was treated with 10(-8) M estrogen 30 min prior to treatment with LPS. Cardiomyocyte autophagy was quantitated by investigating the mRNA and protein level of autophagy-related genes (Atgs). The mRNA expression of Atg5 and Beclin1 were measured by quantitative polymerase chain reaction and the microtubule-associated protein light chain 3 (LC3) protein expression was measured by western blot analysis. To demonstrate the cardiomyocyte protection of estrogen, cell vitality and serum lactate dehydrogenase (LDH) levels were measured following LPS treatment. It was identified that LPS induced cardiomyocyte injury, together with the upregulation of Atg5, Beclin1 mRNA and LC3-II protein. Furthermore, estrogen attenuated the effect of LPS. The present study provides evidence that estrogen has a myocardial protective role against injury induced by LPS by regulating autophagy.