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GW24-e2367 Tirofiban improves renal outcome in a rat model of ischaemia/reperfusion injury by modulating NO synthases
  1. Guan Weiwei1,2,
  2. Chunyu Zeng1,2
  1. 1Department of Cardiology, Daping Hospital, The Third Military Medical University
  2. 2Chongqing Institute of Cardiology

Abstract

Objectives Renal ischaemia/reperfusion (I/R) injury is a common clinical disease. We have known that NO-signal transduction has an important effect on renal I/R injury. NO is produced by NO synthases. Endothelial NO synthase (eNOS) plays a protective role while inducible NO synthase (iNOS) induces impairment. There is evidence that tirofiban may cause alteration of NO production by affecting eNOS/iNOS. So in present study, we investigated whether tirofiban can affect NO Synthases and improve renal outcome in a rat model of I/R injury.

Methods Tirofiban (100 µg/kg) was intraperitoneally administered to Sprague-Dawley rats, which were divided into four groups: sham operated control group (N = 3); sham operated plus tirofiban (100 µg/kg) group (N = 3); I/R group (N = 3); I/R plus tirofiban group (N = 3). After 24 h reperfusion, kidney and blood were collected to estimate renal function, oxidative stress, apoptosis of renal tissues and plasma NOx-production. In I/R group, the level of serum urea, Scr, and AST was much higher compared with control. Pathological damage score was also much higher in I/R group. Tirofiban improves renal function damaged by I/R injury and reduce histopathological changes. Besides, tirofiban also decrease oxidative stress, apoptosis and the level of plasm.

Results Tirofiban (100 µg/kg) was intraperitoneally administered to Sprague-Dawley rats, which were divided into four groups: sham operated control group (N = 3); sham operated plus tirofiban (100 µg/kg) group (N = 3); I/R group (N = 3); I/R plus tirofiban group (N = 3). After 24 h reperfusion, kidney and blood were collected to estimate renal function, oxidative stress, apoptosis of renal tissues and plasma NOx-production. In I/R group, the level of serum urea, Scr, and AST was much higher compared with control. Pathological damage score was also much higher in I/R group. Tirofiban improves renal function damaged by I/R injury and reduce histopathological changes. Besides, tirofiban also decrease oxidative stress, apoptosis and the level of plasma NOx.

Conclusions Tirofiban plays a protective role in renal I/R injury. And the alterations of NO-transduction related to eNOS/iNOS may participate in the mechanism of tirofiban protection.

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