Study on acute kidney injury model induced by renal ischemia-reperfusion in rats.
10.19540/j.cnki.cjcmm.20181218.001
- Author:
Qin GONG
1
;
Mu-Lan WANG
2
;
Sha-Sha ZUO
3
;
Yuan-Li ZHANG
2
;
Xi XU
2
;
Lu-Ling HE
2
;
Yu-Lin FENG
1
;
Li-Jun DU
4
;
Jun LI
1
Author Information
1. Jiangxi University of Traditional Chinese Medicine Nanchang 330006,China State Key Laboratory of Innovative Drugs and Efficient Energy-saving Pharmaceutical Equipment,Jiangxi University of Traditional Chinese Medicine Nanchang 330006,China.
2. State Key Laboratory of Innovative Drugs and Efficient Energy-saving Pharmaceutical Equipment,Jiangxi University of Traditional Chinese Medicine Nanchang 330006,China.
3. Jiangxi University of Traditional Chinese Medicine Nanchang 330006,China.
4. State Key Laboratory of Innovative Drugs and Efficient Energy-saving Pharmaceutical Equipment,Jiangxi University of Traditional Chinese Medicine Nanchang 330006,China School of Life Sciences,Tsinghua University Beijing 100084,China.
- Publication Type:Journal Article
- Keywords:
acute kidney injury;
arteriovenous ligation;
inflammatory reaction;
rats;
renal ischemia reperfusion
- MeSH:
Acute Kidney Injury;
pathology;
Animals;
Blood Urea Nitrogen;
Creatinine;
blood;
Disease Models, Animal;
Kidney;
pathology;
Kidney Tubules;
pathology;
Ligation;
Male;
Rats;
Rats, Sprague-Dawley;
Renal Artery;
Reperfusion Injury
- From:
China Journal of Chinese Materia Medica
2019;44(5):996-1003
- CountryChina
- Language:Chinese
-
Abstract:
In this study,in-depth systematic evaluation of rat of acute kidney injury(AKI) caused by renal arteriovenous ligation was conducted to better master and apply this model for drug research. Male SD rats of 2-3 months old were employed in this study.The left kidney was removed,and the right kidney received ligation for 40 min and reperfusion for 24 h. Serum creatinine(Crea),urea nitrogen(BUN) and the renal tissue sections were assayed as the basic indicators to evaluate their renal function. The mRNA expression of inflammatory necrosis factors and apoptotic factors was used to evaluate the mechanism of molecular pathophysiological changes. The results showed that the serum Crea and BUN caused by ligation of both renal arteries and veins were significantly higher than those of rats with renal artery ligation. After renal arteriovenous ligation for 40 min and reperfusion for 24 h in rats,the serum Crea of the rats varied from less than 100 μmol·L-1 to more than 430 μmol·L-1. Among them,5 rats showed less than 100 μmol·L-1 serum Crea,20 rats with 100-200 μmol·L-1 serum Crea and 12 rats with more than 430 μmol·L-1. Rats with serum Crea between 300-430 μmol·L-1 accounted for 66.3%(122/184) of the total number of the experiment rats. After 72 h reperfusion,serum Crea in the group of Crea 370-430 μmol·L-1 continued to increase,while the serum Crea in the group of Crea 200-300 μmol·L-1 and the group of Crea 300-370 μmol·L-1 recovered quickly. No matter serum Crea was elevated or decreased,the renal tubules showed pathological changes such as vacuolar degeneration or even necrosis. The mRNA expression levels of Toll-like receptor(TLR4),tumor necrosis factor(TNF-α) and interleukin(IL-6) in renal tissueswere significantly up-regulated,and the effect was most obvious in the group of serum Crea 370-430 μmol·L-1. The study indicated that the model for AKI caused by renal arteriovenous ligation and reperfusion is easy to operate,and the serum Crea and BUN have the characteristics of continuous increase,beneficial to the observation of drug effects. This acute kidney injury is mainly related to the pathophysiological response of inflammatory necrosis.
