Suppression of the lipid peroxidation process in the CNS reduces neurological expression of experimentally induced autoimmune encephalomyelitis.

OBJECTIVE Here we report the influence of malondialdehyde (MDA) as a measure of the lipid peroxidation process (LP), on multiple sclerosis (MS) pathogenesis and its neurological signs, during the treatment with aminoguanidine (AG) - a selective inducible nitric oxide synthase inhibitor and N-Acetyl cysteine (NAC) - an oxidative scavenger, in the experimental autoimmune encephalomyelitis (EAE), an animal model for studying MS. MATERIAL AND METHODS Encephalomyelitis induction by the subcutaneous injection of myelin basic protein of bovine type, dissolved in phosphate buffered saline (PBS) emulsified in equal volume of the complete Freund's adjuvant (CFA), was described in detail in our earlier published papers. Each of animals was randomly assigned to seven groups - control (PBS), EAE, CFA, EAE + AG, AG, EAE + NAC and NAC group. In each animal, the development of neurological signs of EAE was scored, these results were published earlier. MDA was evaluated in the central nervous system (CNS) structure - cerebellums and spinal cords. RESULTS The obtained results show that the AG and NAC treatment significantly reduces the MDA level in both examined tissues (p < 0.05) ameliorating at the same time EAE clinical signs (p < 0.05). CONCLUSIONS Taking together our present and earlier findings we conclude that LP may provoke and promote MS, while blocking of this process results in amelioration of the clinical onset and disease activity. These results may be useful as a new insight into mechanisms and potential targets for therapeutic strategies in MS.