Potencial terapéutico del derivado de 1,3,4-oxadiazol en la neuritis óptica inducida por EAE

Optic neuritis is a debilitating inflammatory condition of the optic nerve and is often an early manifestation of multiple sclerosis (MS). Optic nerve damage in MS causes visual impairment due to oxidative stress, inflammation, and demyelination. This study explores the effect of a potential oxadiazole derivative, 2-{[5-(2-chlorophenyl)-1, 3, 4-oxadiazol-2-yl] sulfanyl} ethan-1-ol (abbreviated as OX-2), on optic neuritis induced by using an experimental autoimmune encephalomyelitis model. The impact of the compound was analyzed through various methods, including clinical scoring, weight evaluation, and histopathological analysis, utilizing staining techniques like H&E, Nissl, trichrome, and Oil Red O. Polymerase chain reaction was used to examine the expression of inflammatory cytokines, including TLR4, NF-κB, IL-1β, and TNF-α, as well as antioxidant pathways like Nrf2 and HO-1. Additionally, DNA damage in the optic nerve was analyzed using a comet assay. Oxidative stress was assessed by measuring antioxidant enzymes (GSH, GST, and CAT) and stress markers (MDA, NO). The results indicated that OX-2 plays a significant role in alleviating clinical symptoms of EAE-induced optic neuritis. The compound appears to enhance the antioxidant defense system, thereby reducing oxidative stress. Furthermore, it decreased inflammation and cytokine production by downregulating the TLR-4/NF-κB pathway. In conclusion, OX-2 demonstrated notable neuroprotective, anti-inflammatory, and antioxidant properties.