Experimental study on attenuation of contrast-induced acute kidney injury by enhancing autophagy in rats

Abstract

Objective To evaluate the effects of autophagy on contrast-induced acute kidney injury (CI-AKI) in rat models. Methods Eighteen male rats were divided into control group (Con), CI-AKI group (CI-AKI) and rapamycin-pretreated group (Rapa). In the CI-AKI group, CI-AKI was induced by intraperitoneal injection of iohexol (12.25 g/kg I). In the Rapa group, rapamycin was given by intraperitoneal injection with a dose of 5 mg/(kg·d) for consecutive 7 days, and then injected with iohexol (12.25 g/kg I). Rats in the Con group were injected by the same dose of saline. The renal function, renal histopathology, and the levels of LC3 Ⅱ/Ⅰ and Beclin-1 as well as catalase (CAT) in the kidneys of rats were evaluated one day after the injection. Results Compared with the Con group, serum creatinine in the CI-AKI group was significantly increased ((239.93±27.00) μmol/L) vs (51.70±10.59) μmol/L, P<0.05), and the content of CAT was significantly decreased ((14.86 ± 0.32) U/mg vs (18.72±1.46) U/mg, P<0.05). In the CI-AKI group, renal tubules were severely injured, and the expression of autophagy-related proteins LC3 Ⅱ/Ⅰ and Beclin-1 in renal tissue was increased. Compared with the CI-AKI group, the pretreatment of rapamycin (Rapa group) increased the expression of LC3 Ⅱ/Ⅰ and Beclin-1 as well as the content of CAT in renal tissue ((17.62±1.86) U/mg vs (14.86±0.32) U/mg, P<0.05), and inhibited the increase of contrast-induced serum creatinine ((187.62±47.76) μmol/L vs (239.93±27.00) μmol/L, P<0.05) and renal tubule injury. Conclusions The results showed that contrast administration can induce autophagy activation in kidneys, while enhancing autophagy can attenuate contrast-induced oxidative stress injury and related renal injury. Key words: Contrast-induced acute kidney injury; Autophagy; Oxidative stress