Vitamin E and 5-amino salicylic acid ameliorates acrylamide-induced peripheral neuropathy by inhibiting caspase-3 and inducible nitric oxide synthase immunoexpression

Acrylamide is a fundamental cause of accidental toxicity in humans. This study aimed to investigate the neuroprotective effect of vitamin E (Vit. E), 5-amino salicylic acid (5-ASA), and their combination against acrylamide-induced sciatic nerve toxicity. For this purpose, 25 male Wister rats were divided into 5 groups: control, acrylamide, acrylamide + Vit. E, acrylamide + 5-ASA, and acrylamide + Vit. E + 5-ASA. Food intake and body weight were assessed after 7 days. Furthermore, the gait score was also evaluated for each rat. The sciatic nerve was dissected, fixed, and processed for routine light and electron microscopic examination. Haematoxylin and eosin, osmium tetroxide for myelin sheath, and toluidine blue for semithin section were used. In addition, immunohistochemistry for caspase-3 and inducible nitric oxide synthase (iNOS) were performed. The results showed reduced food intake and body weight in acrylamide rats. Abnormal gait score was also recorded in acrylamide rats with significant improvement in Vit. E, and Vit. E + 5-ASA groups. Histologically, Vit. E and 5ASA provided potential protection against decreased sciatic nerve axon density, disrupted myelination, and the alteration in the immunohistochemistry induced by acrylamide. Vit. E and its combination with 5-ASA provided more evident protection compared to 5-ASA alone. 5-ASA significantly decreased apoptotic cell death (caspase-3 immunoexpression) while Vit. E failed. Both Vit. E and 5-ASA significantly decreased iNOS immunoexpression in the sciatic nerve, where 5-ASA was superior to Vit. E. These findings concluded that both Vit. E and 5-ASA protect against acrylamide-induced peripheral neuropathy through downregulation of both caspase-3 and iNOS immunoexpression.

Automated summary

Vitamin E and 5-aminosalicylic acid provide protection against acrylamide-induced peripheral neuropathy by downregulating expression of both caspase-3 and iNOS.