Neuroprotective Effects of Sodium Meta Silicate on Motoneurons of Spinal Cord Ventral Horn In Rats Underwent to Compressived Injury of Sciatic Nerve

Purpose: It has been shown that sodium meta silicate has an antioxidant effects and suppress the production of oxidative enzymes. Since the inflammation phenomena and increase the level of free radicals mostly take part in post-injury neuronal degeneration, the purpose of the present research was to examine weather the antioxidant property of sodium meta silicate can prevent the central degeneration of spinal motoneurons of rats underwent to compressived injury of sciatic nerve. Materials and Methods: Thirty male Wistar rats were divided into control, sham and 3 experimental groups (n=6). The control rats were remained intact while the sciatic nerve of sham and experimental rats were highly compressed in the gluteal region. The experimental groups 1, 2 and 3 received 3, 6 and 9 injection of 6 mg/kg sodium meta-silicate (i.p.) respectively by 72 hours interval. At the end of experimental period (1 month) all rats were cardialy perfused by 10% formaldehyde and their L4-L6 lumbar segments of spinal cord were sampled, post fixed by the same fixator and processed for histological examination. The paraffin blocks were serially cut (7mm) and stained and then the numerical density (Nv) of motoneurons and all neurons in spinal ventral horn were estimated stereologicaly by applying the 'dissector' technique. The results were then analysed statistically by JMP softwear. Results: In comparison with control group the Nv of motoneurons in sham group was significantly reduced (p<0.001) while there was no significant difference between control and experimental groups. Furthermore the Nv of motoneurons was significantly increased in experimental groups when compared with sham (p<0.05). There was no significant difference between the Nv of all neurons (gamma and interneurons). Conclusion: The results obtained from the present study indicate that sodium meta-silicate may have a beneficial effect in neural regeneration and probably insert this property by delay in central degeneration and in acceleration of regeneration in injured fibers. By this mean the nerve fibers reach their target cells before the central degeneration occur.