Effect of anakinra, an interleukin one beta antagonist, on oxidative testicular damage induced in rats with ischemia reperfusion

2017 
Abstract Background It has been reported in the literature that proinflammatory interleukin-1 beta (IL-1β) is increased in cases of testicular ischemia reperfusion (I/R) damage. This information suggests that anakinra, an IL-1β antagonist, may be effective in testicular I/R damage. Objective In our study, we investigated the effect of anakinra on testicular I/R damage induced in rats with torsion/detorsion. Methods The 50 mg/kg anakinra + testicular torsion/detorsion (KTD-50) and 100 mg/kg anakinra + testicular torsion/detorsion (KTD-100) groups received an intraperitoneal (i.p.) injection of 50 mg/kg and 100 mg/kg of anakinra, respectively. In turn, the testicular torsion/detorsion (TTD) and sham operation (SOG) groups received a single dose of distilled water as a solvent 1 h before ketamine anaesthesia. After the testes of the TTD, KTD-50 and KTD-100 groups were subjected to torsion and detorsion for 4 h each, the rats were killed with a high-dose anaesthesia, and their testicles were removed and evaluated through biochemical, gene expression and histopathological examinations. The results were evaluated in comparison with those of the SOG group. Results The levels of malondialdehyde (MDA), myeloperoxidase (MPO) and IL-1β showed significant increases in the TTD group, which underwent torsion/detorsion, compared to the KTD-50, KTD-100 and SOG groups. Conversely, the levels of glutathione (tGSH), glutathione peroxidase (GPO) and glutathione s-transferase (GST) were found to be significantly higher in the KTD-50, KTD-100 and SOG groups than in the TTD group. Conclusion Anakinra at a 100 mg/kg dose histologically suppressed better oxidative stress and tunica albuginea, germ cell, seminiferous tubule and interstitial damage in the testicular tissue compared to a 50 mg/kg dose. Experimental results indicate that anakinra might be beneficial in the attenuation of testicular I/R damage.
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