Inhibitory effect of SIN-1 on ICAM-1 expression in rat kidney after ischemia/reperfusion injury
- VernacularTitle:SIN-1抑制缺血再灌注肾脏ICAM-1表达
- Author:
Hong LIU
;
Xiongfei WU
;
Xiyu JIN
;
Lian LI
;
- Publication Type:Journal Article
- Keywords:
nitric oxide;
ischemia reperfusion;
ICAM 1
- From:Journal of Third Military Medical University
2003;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the therapeutic mechanisms of nitric oxide donor (SIN 1) in ischemic acute renal failure (IARF). Methods The effects of SIN 1 on intercellular adhesion molecule 1 (ICAM 1) expression and inflammatory cell infiltration in rat kidney after ischemia/reperfusion (I/R) injury were examined using ICAM 1, ?2 integrin polyclonal antibody, and immunohistochemistry. The renal functions were measured simultaneously. Results Progressive increased expression of ICAM 1 was found in kidneys, especially in vasa recta, after IR injury. ?2 integrin positive cells increased simultaneously in the outer medulla. The two indexes reached the peak values at 24 h after I/R injury. SIN 1 infusion at the beginning of reperfusion could remarkably inhibit the enhanced ICAM 1 expression, reduce the local infiltration of inflammatory cells, and ameliorate the renal functions. Conclusion NO donor can inhibit the renal expression of ICAM 1 and the infiltration of leukocytes after ischemia reperfusion injury, which may play an important role in the treatment of ischemic acute renal failure.
