Ischemia/reperfusion (I/R) injury is a main cause of acute kidney injury (AKI), and currently lacks effective therapies. This study is to investigate the level of Neutrophil gelatinase-associated lipocalin (NGAL) and autophagy status during renal I/R injury, so as to determine whether the exogenous NGAL protein could exert a protective effect for I/R injury and explore the potential mechanisms. Forty male Wistar rats were randomly divided into the following four groups: Sham, I/R, pre-treated with NGAL before I/R (I/R + pre-N), treated with NGAL after I/R (I/R + post-N). All rats were subjected to clamping the left renal pedicle for 45 min after right nephrectomy, followed by 24 h of reperfusion. Serum creatinine (SCr) and blood urea nitrogen (BUN) were used for renal function, tubular cell apoptosis and autophagy were measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method, histological examination and electron microscope, respectively. The tubular cell proliferation was assessed by the protein expression of proliferating cell nuclear antigen (PCNA). Western blotting was used to quantitate the levels of LC3, Beclin-1, Bcl-2 and Bax in kidney tissues. Exogenous NGAL protein intervention significantly improved renal function, reduced tubular cell apoptosis, increased tubular cell proliferation and promoted autophagy activation after renal I/R injury. Further, the efficacy in pre-N was significantly better than post-N. The mechanisms were involved in the regulation of several autophagy and apoptosis-related genes. Our study demonstrated that exogenous NGAL protein play a protective role during I/R injury, which may offer a novel may for prevention and treatment of renal I/R injury.

缺血/再灌注（I / R）损伤是急性肾损伤（AKI）的主要原因，目前缺乏有效的疗法。这项研究旨在研究中性粒细胞明胶酶相关脂钙蛋白（NGAL）的水平和肾脏I / R损伤过程中的自噬状态，从而确定外源性NGAL蛋白是否对I / R损伤具有保护作用，并探讨其潜在机制。40只雄性Wistar大鼠随机分为以下四组：Sham，I / R，在I / R之前用NGAL预处理（I / R + pre-N），在I / R之后用NGAL处理（I / R +） N后）。右肾切除后，所有大鼠均接受左肾蒂钳夹45分钟，然后再灌注24 h。血清肌酐（SCr）和血液尿素氮（BUN）用于肾功能，分别用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL），组织学检查和电子显微镜检测肾小管细胞的凋亡和自噬。通过增殖细胞核抗原（PCNA）的蛋白质表达来评估肾小管细胞的增殖。Western印迹法用于定量肾脏组织中LC3，Beclin-1，Bcl-2和Bax的水平。肾脏I / R损伤后，外源性NGAL蛋白干预可显着改善肾脏功能，减少肾小管细胞凋亡，增加肾小管细胞增殖并促进自噬激活。此外，N前的疗效显着优于N后。该机制参与了几种自噬和凋亡相关基因的调控。