The mechanism of ischemic preconditioning renal tubular cell-derived exosomes in the repair of renal ischemia-reperfusion injury in rats
10.3760/cma.j.cn431274-20210129-00135
- VernacularTitle:缺血预处理肾小管细胞来源外泌体修复大鼠肾缺血再灌注损伤的作用机制
- Author:
Lixiang LI
1
;
Yanzi ZHANG
;
Yunpeng XU
;
Zibin XU
;
Xiaolu SUI
;
Qicheng ZENG
;
Jiefeng ZOU
;
Shuzhen YUAN
;
Tingfei XIE
;
Jihong CHEN
Author Information
1. 广东医科大学深圳宝安临床医学院(深圳市宝安区人民医院)肾内科，深圳 518000
- Keywords:
Ischemic preconditioning;
Exosomes;
Kidney tubules;
Reperfusion injury;
Kidney
- From:
Journal of Chinese Physician
2022;24(2):260-265
- CountryChina
- Language:Chinese
-
Abstract:
Objective:Clamping bilateral renal arteries with refined surgical methods to establish the rat renal ischemia-reperfusion injury (RIRI) model, and study the protective mechanism of ischemic preconditioning renal (IPC) tubular cell-derived exosomes in RIRI.Methods:25 female Sprague Dawley (SD) rats were divided into sham group, model group, inactivated group, normoxic group, IPC group. In the sham operation group, after bilateral renal arteries were dissociated, the back incision was disinfected and closed. The model group established RIRI model; RIRI models were established in inactivated group, normoxia group and IPC group, and then 200 μg of inactivated exosomes, normal exosomes and IPC exosomes were injected into the caudal vein 24 hours after operation. Serum creatinine (Scr) and urea nitrogen (BUN) levels were detected. The pathological changes of renal tissue were observed under light microscope. Transmission electron microscopy (TEM) was used to observe the shape and size of renal tubular exosomes. Nanoparticle tracking analysis (NTA)was used to detect the concentration and size of renal tubular exosomes.Results:Compared with the sham group, the Scr and BUN levels in the model group were significantly elevated ( P<0.01). Renal pathological changes in the model group showed damaged of the tubular structure, necrosis and shedding of tubular epithelial cells, and a large number of inflammatory cells accumulated in the renal interstitial tissue with varying degrees of edema. Compared with the inactivated group, the Scr and BUN levels significantly decreased in the normoxic group and IPC group ( P<0.01). Renal pathological changes in the normoxic group and IPC group showed that the renal tubular cell necrosis alleviated, inflammatory was reduced, the improved edema. Compared with the normoxic group, the Scr and BUN levels in the IPC group were further reduced ( P<0.01). Renal pathological changes in the IPC group showed that the inflammatory cells were significantly reduced, the cell edema was significantly improved, and the cell apoptosis was significantly reduced. Conclusions:Clamping bilateral renal arteries with refined surgical methods is the main and optimal way to build a rat model of RIRI. IPC tubular cell-derived exosomes have protective and repair effects on RIRI.
