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Amelioration of αLPHA-synuclein aggregation and motor behavior deficits by apocyanin in intranigral lipopolysaccharide induced animal model of Parkinson’s disease

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

Meeting: 2016 International Congress

Abstract Number: 1834

Keywords: Dopaminergic neurons, Inflammation, Neurobehavioral disorders, Parkinsonism

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: The present study evaluated the therapeutic potentials of apocyanin for the treatment of neurobehavioral consequences in LPS induced PD model.

Background: Parkinson’s disease (PD), is an age-related, progressive neurodegenerative disorder that affects movement and is characterized by the loss of dopaminergic neurons in the nigrostriatal region. Although the clinical and pathological features of PD are complex, our earlier study on LPS induced PD model have indicated that microglia mediated inflammatory response and overproduction of free radicals, especially superoxide (O2-) derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase play a key role in the PD pathology. A little information is available regarding the role of apocyanin, an NADPH oxidase inhibitor, in ameliorating α-synuclein aggregation and neurobehavioral consequences of PD.

Methods: Lipopolysaccharide (LPS) was injected intranigral at a dose of (5ug/animal) once during the experiment whereas apocyanin (10mg/kg b.wt, (i.p)] was administered daily for a period of 21 days.

Results: Statistical analysis revealed that apocynin (10mg/kg) significantly ameliorated LPS induced inflammatory response characterized by NFkB, TNF-α and IL-1β upregulation as assessed by ELISA. It also prevented DA-nergic neurons from toxic insult of LPS as indicated by inhibition of apoptotic markers i.e caspase 3 and caspase 9 as depicted from RT-PCR and ELISA studies. This is further supported by TUNEL assay for DNA fragmentation. Effectiveness of apocyanin in protecting DA-nergic neuronal degeneration was further confirmed by assessment of α-synuclein deposition in DA-neurons as depicted by IHC analysis. Consequently, an improvement in the behavioral outcome was observed following apocyanin treatment as depicted from (Actophotometer, rotarod, foot print analysis, beam balance and grid walking tests).

Conclusions: Hence the data suggests that specific NADPH oxidase inhibitors, such as apocynin, may provide a new therapeutic approach to the control of neurological disabilities induced by LPS induced PD.

To cite this abstract in AMA style:

B. Nehru, N. Sharma. Amelioration of αLPHA-synuclein aggregation and motor behavior deficits by apocyanin in intranigral lipopolysaccharide induced animal model of Parkinson’s disease [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/amelioration-of-lpha-synuclein-aggregation-and-motor-behavior-deficits-by-apocyanin-in-intranigral-lipopolysaccharide-induced-animal-model-of-parkinsons-disease/. Accessed May 18, 2025.
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