Ameliorating effects of curcumin on 6-OHDA-induced dopaminergic denervation, glial response, and SOD1 reduction in the striatum of hemiparkinsonian mice.

BACKGROUND: Inflammation and oxidative stress are believed to contribute to neuronal degeneration of the nigrostriatal dopaminergic (DA) pathway in Parkinson's disease. Curcumin, a component of the yellow curry spice, has been reported possessing anti-inflammatory and anti-oxidative effects. AIM: The present study investigated the effects of curcumin on the extent of DA innervation, glial response, and Cu/Zn superoxide dismutase (SOD1) expression in the striatum of 6-hydroxydopamine (6-OHDA)-lesioned mice.
MATERIALS AND METHODS: 6-OHDA was unilaterally injected into the right striatum of ICR male mice. Curcumin (200 mg/kg) was administered daily for 7 days starting instantaneously after 6-OHDA injection. Seven days after 6-OHDA insult, mice were euthanized and striatal sections were collected, immunohistochemically stained, and quantitated for tyrosine hydroxylase (TH), glial fibrillary acidic protein (GFAP), ionized calcium binding adapter molecule 1 (Iba1), and SOD1 immunoreactivity.
RESULTS: 6-OHDA injection triggered a significant loss of TH-immunoreactive (-IR) axons, induced reaction of GFAP-IR astrocytes and Iba1-IR microglia, and decreased SOD1 expression in the 6-OHDA-lesioned striatum. Curcumin attenuated loss of TH-IR fibers, diminished activation of astrocytes and microglia, and sustained SOD1 level in the lesioned striatum.
CONCLUSIONS: These results suggest that curcumin counteracts the neurotoxicity of 6-OHDA through its anti-inflammatory properties (inhibition of glial response) and preservation of SOD1 expression.