Abstract # 2058 Repairing effects of curcumin in the rat central nervous system after gliotoxic damage

Abstract

Ethidium bromide (EB) injection into the brain is known to induce focal oligodendrocyte and astrocyte loss, leading to primary demyelination, neuroinflammation and peripheral astrogliosis, with increased immunoreactivity to glial fibrillary acidic protein (GFAP). As curcumin (Cur) exhibits antioxidant and anti-inflammatory effects, this study aimed to evaluate the effects of Cur administration on remyelination and astrocytic response following EB gliotoxic injury. Wistar rats were injected with 10 microlitres of 0.1% EB into the cisterna pontis and treated or not with Cur (100 mg/kg/day, intraperitoneal route). Brainstem sections were collected from 15 to 31 days after EB injection for ultrastructural and GFAP immunohistochemical investigation. Astrocytic reactivity and remyelination status were assessed by morphometry. By 15 days after EB injection the center of the lesion was filled with myelin debris, foamy macrophages and demyelinated axons. No astrocytic processes were found in this site and an initial association between naked axons and remyelinating cells was seen at peripheral locations. Oligodendroglial remyelination was observed near astrocyte processes, while invasive Schwann cells began to produce thicker myelin sheaths around axons in astrocyte-free areas. By 21–31 days, it was noted that Cur-treated rats presented increased oligodendroglial remyelination. GFAP-stained area around lesion was significantly smaller in Cur-treated rats in all periods when compared to untreated animals. Results show that Cur has beneficial effects on remyelination and reduces glial scar development following gliotoxic injury.