Influence of rhBMP-2 on the renal tissue of rat with renal ischemia reperfusion injury and its molecular mechanism.
- Author:
Shun YANG
1
;
Ling PEI
Author Information
1. Department of Anesthesiology, Liaoning Cancer Hospital and Institute, Shenyang 110042, China. mafuu@163.com
- Publication Type:Journal Article
- MeSH:
Adrenal Cortex;
pathology;
ultrastructure;
Animals;
Blood Urea Nitrogen;
Bone Morphogenetic Protein 2;
pharmacology;
Creatine;
blood;
Interleukin-6;
metabolism;
Interleukin-8;
metabolism;
Kidney;
blood supply;
metabolism;
Male;
Malondialdehyde;
metabolism;
Random Allocation;
Rats;
Rats, Wistar;
Recombinant Proteins;
pharmacology;
Reperfusion Injury;
metabolism;
pathology;
Superoxide Dismutase;
metabolism;
Transforming Growth Factor beta;
pharmacology;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Acta Pharmaceutica Sinica
2009;44(10):1089-1094
- CountryChina
- Language:Chinese
-
Abstract:
The objective of this research is to investigate the influence of rhBMP-2 on the renal tissue of rat with renal ischemia reperfusion injury. In this program the ischemia reperfusion rat model was established and Wistar rats were divided into six groups: sham operation group (S group), renal ischemia reperfusion injury group (R group), rhBMP-2 treatment group (B1, B2, B3 and B4 group). In the rhBMP treatment groups, rhBMP-2 was intravenously administered with different doses before reperfusion. The contents of TNF-alpha, IL-6, IL-8, MDA and SOD in kidney tissue were observed. At the same time, renal function (blood creatine (Scr) and urea nitrogen (BUN)) were measured. As a result, compared with renal ischemia reperfusion group, administration of rhBMP-2 significantly reduced the content of IL-6 and IL-8 (P < 0.05) and ameliorated renal dysfunction cellular damages (P < 0.05). Higher dose of rhBMP-2 may reduce the content of TNF-alpha (P < 0.05) in kidney tissue. rhBMP-2 also increased activity of SOD and reduced the level of MDA, BUN and Scr. So, we can draw a conclusion that rhBMP-2 treatment attenuates renal ischemia reperfusion injury through inhibition of pro-inflammatory cytokines production and anti-oxidation activity.
