Regulation of the autophagy plays an important role in acute kidney injury induced acute lung injury

Abstract

Aim This study aimed to investigate the regulatory role of autophagy in acute kidney injury (AKI) induced acute lung injury (ALI). Methods The male Sprague–Dawley rats were divided into four groups: normal saline-treated sham rats (sham group), normal saline-treated ischemia-reperfusion injury rats (IRI group), 3-methyladenine-treated IRI rats (3-MA group), and rapamycin-treated IRI rats (RA group). The rats in the IRI rat model received the nephrectomy of the right kidney and was subjected to 60 mins of left renal pedicle occlusion, followed by 12, 24, 48, and 72 h of reperfusion. The levels of Scr, BUN, wet-to-dry ratio of lung, inflammatory cytokines, and oxidative stress were determined. The damage to tissues was detected by histological examinations. The western blot and immunohistochemistry methods were conducted to determine the expression of indicated proteins. Results Renal IRI could induce the pulmonary injury after AKI, which caused significant increases in the function index of pulmonary and renal, the levels of inflammatory cytokines, and biomarkers of oxidative stress. In comparison to the IRI group, the RA group showed significantly decreased P62 and Caspase-3 expression and increased LC-II/LC3-I, Beclin-1, Bcl-2, and unc-51-like autophagy activating kinase 1 expression. Meanwhile, by suppressing the inflammation and oxidative stress, as well as inhibiting the pathological lesions in kidney and lung tissues, the autophagy could effectively ameliorate IRI-induced AKI and ALI. Conclusions Autophagy plays an important role in AKI-induced ALI, which could be used as a new target for AKI therapy and reduce the mortality caused by the complication.