DENEYSEL SİYATİK SİNİR HASARINDA SELENYUMUN AKSON VE MİYELİN İYİLEŞMESİ ÜZERİNE ETKİLERİ

Amaç: Selenyumun nöroprotektif etkileri bilinmesine rağmen, periferik sinir yaralanmasında etkisi açık değildir. Bu çalışmada amacımız, deneysel siyatik sinir hasarında selenyumun akson ve miyelin yaralanmasına koruyucu etkisi olup olmadığını araştırmaktı.Gereç ve Yöntem: Yirmi sekiz adet wistar albino cinsi rat her grupta 7 rat olacak şekilde 4 eşit gruba rastlantısal olarak ayrıldı. Gruplar kontrol, selenyum, yaralanma ve selenyum ile tedavi edilen yaralanma gruplarından oluşturuldu. Yaralanma Yaşargil anevrizma klibi ile 30 saniye süreyle siyatik sinire bası oluşturularak yaralanma ve selenyumla tedavi edilen yaralanma gruplarına uygulandı. Selenyum, 1,5 mg/kg’dan oral olarak selenyum ve selenyumla tedavi edilen gruplara cerrahiden sonra birinci, yirmi dördüncü, kırk sekizinci ve yetmiş ikinci saatte verildi. Deneysel prosedüre göre dördüncü günün bitiminde elektrofizyolojik, histolojik ve biyokimyasal testler yapıldı.Bulgular: Birleşik aksiyon potansiyeli amplitüdü, sinir ileti hızı, ortalama akson çapı, miyelin kalınlığı, miyelinli ve miyelinsiz akson sayısı ve eritrositlerdeki SOD aktivitesi yaralanma grubunda kontrol, selenyum ve selenyumla tedavi edilen gruplardan belirgin olarak düşük olmasına karşın serum MDA düzeyi yaralanma grubunda diğer gruplara nazaran daha yüksekti. Sonuç: Çalışmanın bu bulguları, selenyumun siyatik sinir yaralanmasından sonra akson ve miyelin hasarını azalttığını göstermiştir. Selenyumun bu nöroprotektif etkisine en azından kısmi olarak oksidan/antioksidan mekanizmalar aracılık etmiştir.

EFFECTS OF SELENIUM ON AXON AND MYELIN HEALING IN AN EXPERIMENTAL SCIATIC NERVE INJURY MODEL

Objective: Although, the neuroprotective effects of selenium are known, its effect on peripheral nerve injury is not clear. The study was aimed to investigate whether selenium prevents axonal and myelin damage in experimental sciatic nerve injury. Materials and Methods: Twenty-eight male Wistar albino rats were divided into four groups (n=7 in each): control (C), selenium (S), injury (I), and selenium-treated injury (SI). Injury was generated by 30 second of compression via Yasargil aneurysm clip on the sciatic nerve of rats in the I and SI groups. Then, selenium was given to the S and SI groups as 1.5 mg/kg by oral gavage at 1st, 24th, 48th and 72nd hour after surgery. According to the experimental protocol, electrophysiological, histological, and biochemical tests were performed end of the day 4. Results: Whereas the amplitude of compound action potential, nerve conduction velocity, average axon diameter, myelin thickness, myelinated/unmyelinated axons and SOD activity in red blood cells of the I group were significantly lower than those of the C, S and SI groups, the serum MDA levels of the I group were significantly higher than those of the C, S and SI groups.  Conclusion: The findings of this study show that selenium decreases axonal and myelin damage after sciatic nerve injury and that this neuroprotective effect of selenium is at least partially mediated by oxidant/antioxidant mechanisms.  

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