Beneficial effects of MnTBAP, a broad-spectrum reactive species scavenger, in rat renal ischemia/reperfusion injury
- 26 September 2005
- journal article
- Published by Springer Nature in Clinical and Experimental Nephrology
- Vol. 9 (3) , 212-218
- https://doi.org/10.1007/s10157-005-0359-6
Abstract
In recent years, several lines of evidence have implicated reactive species as contributors to renal ischemia/reperfusion injury (I/R). This study was designed to investigate the effect of Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), a broad-spectrum reactive species scavenger, in the prevention of renal I/R injury. Experiments were performed on rats anesthetized with pentobarbital. After tracheotomy, the right femoral artery was cannulated and the mean arterial pressure and heart rate were recorded. A midline laparatomy was performed, and the renal arteries were carefully separated from surrounding tissues. After surgery and a stabilization period (60 min), the animals were randomly assigned to four groups: sham-operated; sham+MnTBAP; I/R; I/R+MnTBAP. In I/R groups, the rats were subjected to bilateral renal artery occlusion for 40 min followed by 6 h reperfusion. Other groups underwent the surgery protocol but did not undergo renal artery occlusion, and were maintained under anesthesia for the duration of the experiment. Rats were administered either MnTBAP (10 mg kg−1, i.v. bolus, 15 min prior to I/R) or saline. Renal function was assessed by plasma creatinine (Cr), blood urea nitrogen (BUN), and aspartate aminotransferase (AST) measurements. The fractional excretion of Na+ (FENa+) and urinary N-acetyl-β-D-glucosaminidase (NAG) activities were also measured. Renal section damage was evaluated by light microscopy, and oxidative stress status was evaluated by measurements of plasma and renal vitamin E levels. We found that MnTBAP significantly reduced the I/R-mediated increases in plasma Cr, BUN, AST, FENa+, and NAG and improved the renal tissue histology. Our results showed that MnTBAP was effective in preventing the development of I/R-induced renal injury.Keywords
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