Objective: The objective of this study was to investigate the anti-neuroinflammatory effect of chlorogenic acid (CGA) in the 1-methyl-4-phenyl-1,2, 3, 6- tetrahydropyridine (MPTP) model of Parkinson’s disease (PD).

Background: Parkinson’s disease, a second most wide-spread age-related chronic movement disorder, which shows damaged dopaminergic (DA) neurons and aggregates of α-synuclein protein within the substantia nigra pars compacta (SNpc). Studies in animals and human from last few years have suggested that the degeneration of DA nigrostriatal pathway is mainly influenced by inflammation-induced oxidative stress and neurotoxicity due to pro-inflammatory cytokine production.

Methods: 30 mice were divided into 5 different groups, viz., control, MPTP-treated group and rest three groups were given 25 mg/kg, 50 mg/kg and 100mg/kg body weight (wt.) of CGA, respectively after MPTP intoxication. After completion of treatment, experimental mice were subjected to behavioral analysis to check motor impairment and further their brains were isolated and used to check the expression of inflammatory markers by Immunohistochemical staining and real-time PCR analysis.

Results: Immunohistochemical studies have shown the reduced activation of NF-κB, leading to decline in the production of pro-inflammatory cytokines such as IL-1β and enhanced production of anti-inflammatory cytokines such as IL-10 in CGA medicated parkinsonian mice model. Real-time PCR analysis has shown the reduced gene expression of pro-inflammatory markers (TNF-α, IL-1β) due to CGA treatment after MPTP intoxication. Enhanced TH immunoreactivity was seen after CGA treatment in MPTP-intoxicated mice. Motor deficits were also found to be upgraded through rota-rod, narrow beam walking test and hanging test. Supplementation of CGA has protected the DA neurons from degeneration in SNpc and nerve terminals in the striatum from the MPTP insult.

Conclusions: Altogether, our study indicates CGA attributed to its anti-neuroinflammatory effect against MPTP-induced DA neurodegeneration by down regulating NF-κB activity and thus can be used as a therapeutic drug for the prevention and management of PD, in which 50mg/kg body wt. CGA was seen to have most prominent effect.

References: 1. Shih R-H, Wang C-Y and Yang C-M (2015) NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review. Front. Mol. Neurosci. 8:77. doi: 10.3389/fnmol.2015.00077. 2. Hwang SJ, Kim YW, Park Y, Lee HJ, Kim KW. (2014). Anti-inflammatory effects of chlorogenic acid in lipopolysaccharide-stimulated RAW 264.7 cells. Inflamm Res. 63:81-90. doi: 10.1007/s00011-013-0674-4.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/chlorogenic-acid-exerts-anti-neuroinflammatory-effect-by-suppressing-nf-%ce%bab-pathway-in-parkinsonian-mice-model/