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Abrogation of neuroinflammation and behavioural deficit by Chlorogenic acid and Tinosporia cordiofolia in MPTP-Induced Parkinsonian mice model via suppressing NF-κB pathway

D. Singh, M. Singh (Allahabad, India)

Meeting: MDS Virtual Congress 2020

Abstract Number: 105

Keywords: 1-Methyl-4-phenylpyridinium (MPP+), Catalase, Drug-induced parkinsonism(DIP)

Category: Drug-Induced Movement Disorders

Objective: The current study was designed with the aim to investigate the anti-neuroinflammatory activity of chlorogenic acid (CGA) and ethanolic extract of Tinospora cordifolia (TPE) in MPTP induced Parkinson’s disease (PD) in the mice model along with its possible mechanism of action.

Background: Parkinson’s disease is most common occurring age-related chronic movement disorder that displays impaired dopaminergic (DA) neurons and α-synuclein protein aggregates within the compacta substantia nigra pars (SNpc). Literature documented the degeneration of  DA nigrostriatal pathway takes place because of pro-inflammatory cytokine production. Various reports are available in the literature on the efficacy of  Chlorogenic acid and Tinosporia cordifolia for its application in neurological disorder and scrutinized  in vitro and invivo studies.

Method: Animals were categorized into 5 groups and exposed to MPTP for 21 days.  Behavioural impediments (rota-rod, narrow beam walking test and hanging test) were performed to determine the motor impairment. Brain tissue of mice was utilized to analysis the inflammatory markers expression via immunochemical staining.  Mitochondrial enzyme activity and oxidative stress were also estimated.

Results: There was alteration in the motor impairment (Behavioural paradigms) after supplementation of CGA and TPE.  Reduced activation of NF-κB suggested upregulation in the Anti-inflammatory cytokines production (IL-10) and downregulation in the pro-inflammatory cytokine production i.e. IL-1β which was proved by Immunohistochemical studies. Reduction in the pro-inflammatory markers gene expression and enhancement in the TH immunoreactivity were observed after the administration of the CGA and TPE.

Conclusion: The outcomes reveals that the synergistic effects CGA and TPE exerts its anti-neuroinflammatory property via regulating the activation of NF-κB in MPTP induced Parkinson’s Disease in mice model and prevents the degeneration of DA neurons in substantia nigra pars compacta.

To cite this abstract in AMA style:

D. Singh, M. Singh. Abrogation of neuroinflammation and behavioural deficit by Chlorogenic acid and Tinosporia cordiofolia in MPTP-Induced Parkinsonian mice model via suppressing NF-κB pathway [abstract]. Mov Disord. 2020; 35 (suppl 1). https://www.mdsabstracts.org/abstract/abrogation-of-neuroinflammation-and-behavioural-deficit-by-chlorogenic-acid-and-tinosporia-cordiofolia-in-mptp-induced-parkinsonian-mice-model-via-suppressing-nf-%ce%bab-pathway/. Accessed June 15, 2025.
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