Role of NF-κB in the progression of aldosterone-induced renal injury and its associated mechanisms
10.3760/cma.j.issn.1001-7097.2011.09.010
- VernacularTitle:NF-κB在醛固酮所致大鼠肾损伤中的作用及相关机制
- Author:
Lei YANG
;
Wei DING
;
Minmin ZHANG
;
Yong GU
- Publication Type:Journal Article
- Keywords:
Aldosterone;
NF-kappa B;
Intercellular adhesion molecule- 1;
Connective tissue growth factor
- From:
Chinese Journal of Nephrology
2011;27(9):673-677
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of NF-κB in aldosterone-1％NaCl-induced renal injury in uninephrectimized SD rats and the potential mechanisms.Methods Thirty-teo male SD rats were uninephrectomized and treated for 4 weeks.Rats were divided into four groups randomly:control group (n=8),1％NaCl group (1％NaCl in chow,n=8),aldosterone group (1％NaCl in chow,0.75 μg/h aldosterone delayed relase by osmotic mini-pump,SC,n=8),PDTC group (1％NaCl in chow,0.75 μg/h aldosterone,SC,100 mg/kg PDTC,IG,n=8).Systolic blood pressure (SBP),urinary protein,renal function and renal morphologic were observed.The expression of intercellular cell adhesion molecule 1 (ICAM-1) and connective tissue growth factor (CTGF) were measured respectively by Western blotting and real-time PCR.The activity and location of NF-κB in renal cortex were detected by electrophoretic mobility shift assay (EMSA) and immunohistochemisty.Results Rats of aldosterone group exhibited higher blood pressure and more serious renal injury characterized by proteinuria,glomerular sclerosis compared with rats of the 1％ NaCl group.Protein and mRNA levels of ICAM-1 and CTGF were significantly increased inaldosterone group rats than those in 1％NaCl group (all P＜0.05).Moreover,all these changes were associated with an increase in NF-κB activity.Treatment with PDTC which is a specific inhibitor of NF-κB notably alleviated SBP,proteinuria and renal injury in aldosterone-infused rats.Furthermore,PDTC markedly reduced the expression of ICAM-1 and CTGF (all P＜0.05).Conclusion PDTC can alleviate aldosterone-1％NaCl-induced renal injury in uninephrectimized SD rats by preventing the expression of ICAM-1 and CTGF.
