Background: Since apoptosis of renal tubular cells is the basis of the damage caused by ischaemia-reperfusion, the antiapoptotic effect on kidney tubular epithelial cells of the monoamino oxidase-B (MAO-B) inhibitor (-) deprenyl (selegiline), known neuroprotective agent, with antiapoptotic properties, was studied in a rat model. Material/Methods: Warm renal ischaemia was caused by clamping the left renal artery of rats for 30 minutes. With the start of reperfusion 0.015 mg/kg, 0.15 mg/kg and 1.5 mg/kg of (-)-deprenyl was injected simultaneously into the carotid artery of the animals, respectively. Five rats served as control, in which renal artery clamping was performed, but the rats were only treated with the solvent (physiological saline). After 6 hours of reperfusion the rats were exsanguinated and the kidneys were histologically examined. Results: Severe tubular damage characterised by apoptosis was found in the kidneys of the untreated rats. Apoptosis was verified on the basis of morphological features, methylgreen-pyronin staining and TUNEL reaction. (-)-Deprenyl diminished dose-dependently the apoptotic damage, 0.15 mg/kg being the most effective dose. The same dose of (-)-Deprenyl is used in the therapy of human Parkinson's disease. Conclusion: Our findings suggest, that (-)-deprenyl might have an impact on decreasing renal injury also in case of human cadaveric renal transplantation.
|Journal||Medical Science Monitor|
|Publication status||Published - márc. 23 2002|
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