Effects of intermittent hypoxia exposure on renal tubular epithelial cell injury and autophagy in rats

Abstract

Objective: To investigate the effects of intermittent hypoxia (IH) exposure on renal tubular epithelial cell injury and autophagy in rats. Methods: A total of 12 Sprague Dawley (SD) rats were randomly divided into two groups: normal control (NC) group and IH group, with 6 rats in each group. An IH animal model was established to observe the effects of IH on renal tubular epithelial cell damage and autophagy in rats. Microalbumin (mAlb) was detected by immunoturbidimetry. Neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1(KIM-1)in urine were assessed by enzyme-linked immunosorbent assay (ELISA) test. The pathological damage of renal tubules was observed by hematoxylin-eosin (HE) staining. The expression of autophagy marker protein light chain 3 (LC3) and Beclin-1 were detected by immunohistochemistry and immunoblotting. Results: At the end of the test, the levels of mAlb [(34.7±6.7) mg/L vs (11.1±3.3) mg/L, P=0.011], NGAL [(17.3±3.9) ng/ml vs(4.0±1.7)ng/ml, P=0.011] and KIM-1 [ (10.8±2.7) ng/ml vs (2.6±1.0) ng/ml, P=0.016] in urine of IH group were higher than those of control group, and the differences were statistically significant (all P<0.05). Pathological injury was showed by HE staining in IH group. The increase of autophagy in IH group was more obvious than that in NC group. Besides, the expression level of autophagy markers (protein LC3 and Beclin-1) was significantly higher in IH group than that in NC group (P<0.05). Conclusions: IH can not only cause renal tubular injury, but also induce increased autophagy in renal tubular epithelial cells. Autophagy activation might participate in renal tubular epithelial cell injury induced by IH.