Effect of apelin-13 on glucose deprivation-induced autophagy of cardiomyocytes in suckling mice and its mechanism

Objective To observe the effect of angiotensin 1 receptor-related apelin-13 on glucose deprivation (GD)-induced autophagy of injured cardiomyocytes and its mechanism. Methods Cardiomyocytes from 3 days old SD suckling mice were incubated in vitro. A cardiomyocyte injury model was induced by GD. The cardiomyocytes were divided into control group, GD group, GD+apelin-13 group, GD+apelin-13+tricribine group, and tricribine group. Intracellular autophagosomes were observed under transmission electron microscope. Activity of phosphoinositide-3-kinase (PI3K) was tested by immunoprecipitation lipid kinase assay. Expressions of autophagy-related microtubule light chain protein 3 (LC3) and signal pathway-related proteins (Akt, p-Akt, mTOR and p-mTOR) were detected by Western blot. Results GD increased the number of autophagosomes and the LC3-II/LC3-I ratio(P< 0.01). Apelin-13 pretreatment attenuated the GD-induced injury of cardiomyocytes, reduced the number of autophagosomes and the LC3-II/LC3-I ratio, up-regulated the activity of PI3K and the phosphorylation levels of Akt and mTOR (P< 0.01). However, tricribine blocked the protective effect of apelin-13(P< 0.01). Conclusion Apelin-13 can inhibit GD-induced autophagy of cardiomyocytes at a certain extent by activating the signaling pathway of PI3K, Akt and mTOR.