Abstract
Introduction. Oxygen free radicals are involved in pathophysiology of ischemia/reperfusion (I/R) injury. This study was designed to assess the possible protective effect of pycnogenol (PYC) against I/R-induced oxidative renal damage. Materials and methods. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 3 h of reperfusion. PYC (10 mg kg−1, i.p.) or saline was administered at 15 min prior to ischemia and immediately before the reperfusion period. At the end of the 3 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN), and lactate dehydrogenase (LDH) activity were measured in the serum samples, while proinflammatory cytokines, TNF-α, IL-1β, and IL-6 levels were assayed in plasma samples. Kidney samples were taken for the determination of tissue malondialdehyde (MDA), glutathione (GSH) levels, Na+,K+-ATPase, and myeloperoxidase (MPO) activities, and the extent of tissue injury was analyzed microscopically. Results. Ischemia/reperfusion caused a significant decrease in tissue GSH level and Na+,K+-ATPase activity, which was accompanied with significant increases in the renal MDA level and MPO activity. Similarly, serum creatinine and BUN levels, as well as LDH and IL-1β, IL-6, and TNF-α levels, were elevated in the saline-treated I/R group as compared to saline-treated control group. On the other hand, PYC treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. Conclusions. Findings of the present study suggest that pycnogenol exerts renoprotective effects, via its free radical scavenging and antioxidant activities, that appear to involve the inhibition of tissue neutrophil infiltration.
ACKNOWLEDGMENTS
The authors are grateful to Mikrogen Pharmaceuticals for supplying pycnogenol. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.