scholarly journals Rosiglitazone Affects Nitric Oxide Synthases and Improves Renal Outcome in a Rat Model of Severe Ischemia/Reperfusion Injury

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Boris Betz ◽  
Reinhard Schneider ◽  
Tobias Kress ◽  
Martin Alexander Schick ◽  
Christoph Wanner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
No Synthase ◽  
Renal Ischemia ◽  
Renal Outcome ◽  
Inos Mrna ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Morphological Alterations

Background.Nitric oxide (NO)-signal transduction plays an important role in renal ischemia/reperfusion (I/R) injury. NO produced by endothelial NO-synthase (eNOS) has protective functions whereas NO from inducible NO-synthase (iNOS) induces impairment. Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor (PPAR)-γagonist exerted beneficial effects after renal I/R injury, so we investigated whether this might be causally linked with NOS imbalance.Methods.RGZ (5 mg/kg) was administered i.p. to SD-rats (f) subjected to bilateral renal ischemia (60 min). Following 24 h of reperfusion, inulin- and PAH-clearance as well as PAH-net secretion were determined. Morphological alterations were graded by histopathological scoring. Plasma NOx-production was measured. eNOS and iNOS expression was analyzed by qPCR. Cleaved caspase 3 (CC3) was determined as an apoptosis indicator and ED1 as a marker of macrophage infiltration in renal tissue.Results.RGZ improves renal function after renal I/R injury (PAH-/inulin-clearance, PAH-net secretion) and reduces histomorphological injury. Additionally, RGZ reduces NOxplasma levels, ED-1 positive cell infiltration and CC3 expression. iNOS-mRNA is reduced whereas eNOS-mRNA is increased by RGZ.Conclusion.RGZ has protective properties after severe renal I/R injury. Alterations of the NO pathway regarding eNOS and iNOS could be an explanation of the underlying mechanism of RGZ protection in renal I/R injury.

scholarly journals Agonists of Peroxisome-Proliferator Activated Receptor-Gamma Reduce Renal Ischemia/Reperfusion Injury

2003 ◽  
Vol 23 (4) ◽  
pp. 267-276 ◽  
Author(s):  
Ahila Sivarajah ◽  
Prabal K. Chatterjee ◽  
Nimesh S.A. Patel ◽  
Zoran Todorovic ◽  
Yoshiyuki Hattori ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Renal Ischemia Reperfusion Injury

Protective Effect of Nitric Oxide Pathway in L-Citrulline Renal Ischemia-Reperfusion Injury in Rats

2013 ◽  
Vol 634-638 ◽  
pp. 1357-1361
Author(s):  
Xin Ling ◽  
Xiao Bin Fu ◽  
Li Liu ◽  
Xia Tian ◽  
Ling Yan Sun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Cortex ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Protective Effects ◽  
Significant Protection ◽  
Renal Ischemia Reperfusion Injury ◽  
Reperfusion Period ◽  
Oxide Synthase

To observe the protective effects of L-citrulline on the renal ischemia-reperfusion (I/R) injury and elucidate the mechanisms involved. Forty-eight rats were randomized into eight groups. At the end of the reperfusion period, serum was collected and the kidneys were removed for histological and biochemical examinations. Our results showed that pretreatment with L-citrulline significantly ameliorated the renal injury caused by I/R. Moreover, L-citrulline increased the levels of NO. The I/R-induced decreases in total nitric oxide synthase (NOS) activity, inducible NOS activity and constitutive NOS activity in the renal cortex were significantly prevented. These results suggested that L-citrulline administration exhibited significant protection on renal I/R injury.

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