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Curcumin supplementation improves motor dysfunction in lipopolysaccharide induced Parkinon’s disease model: Possible biochemical, neurochemical and immunohistochemical alterations in rats

N. Sharma, B. Nehru (Chandigarh, India)

Meeting: 2016 International Congress

Abstract Number: 1828

Keywords: Apoptosis, Behavioral abnormalities, Dopaminergic neurons, Microglial activation

Session Information

Date: Thursday, June 23, 2016

Session Title: Neuropharmacology

Session Time: 12:00pm-1:30pm

Location: Exhibit Hall located in Hall B, Level 2

Objective: In the present study potential neuroprotective effects of curcumin were tested to determine if they could help to minimize microglia–mediated damage in single intranigral lipopolysaccharide induced model of PD.

Background: With the identification of microglia as a target for pharmacological inhibition to halt or prevent slowly progressing neurodegenerative diseases, drugs with anti-inflammatory properties are gaining importance. This would have great clinical impact on diseases which involve neuroinflammation as a causative factor including Alzheimer’s disease (AD), Huntington’s chorea (HD) and Parkinson’s disease (PD) etc. Curcumin, which is a natural dietary pigment is one such drug with well-known antioxidant and anti-inflammatory properties.

Methods: LPS (5ug/5ul PBS) was injected stereotaxically into the Substantia Nigra (SN) of rats. Curcumin [40mg/kg b.wt (i.p)] was administered daily for a period of 21 days following LPS injection.

Results: LPS induced an inflammatory response characterized by glial activation [Iba-1 and glial fibrillary acidic protein (GFAP)] and pro-inflammatory cytokine production (TNF-α and IL-1β) leading to extensive dopaminergic loss in rats. The behavioral observations, biochemical markers, quantification of dopamine and its metabolites using HPLC followed by IHC of TH were evaluated after 21 days of LPS injection. Supplementation with curcumin 40mg/kg b.wt (i.p) showed significant protection against neuronal degeneration when compared to LPS treated animals by normalizing the altered level of biomarkers. Same order of effectiveness was observed in the TH level and behavioral abnormality as depicted from (actophotometer, rotarod, beam and grid walking tests) in rats.

Conclusions: Curcumin shielded dopaminergic neurons against LPS induced inflammatory response which is associated with suppression of NFKB and NADPH oxidase activation. Therefore, treatment with curcumin might be a potential therapeutic strategy for inflammation driven PD as well other neurodegenerative disorders. Its neuroprotective role should be explored further.

To cite this abstract in AMA style:

N. Sharma, B. Nehru. Curcumin supplementation improves motor dysfunction in lipopolysaccharide induced Parkinon’s disease model: Possible biochemical, neurochemical and immunohistochemical alterations in rats [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/curcumin-supplementation-improves-motor-dysfunction-in-lipopolysaccharide-induced-parkinons-disease-model-possible-biochemical-neurochemical-and-immunohistochemical-alterations-in-rats/. Accessed June 14, 2025.
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