Cited by 322Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

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Inflammation induces mitochondrial dysfunction and dopaminergic neurodegeneration in the nigrostriatal system

Hunter, Randy L., Dragicevic, Natasa, Seifert, Kristen, Choi, Dong Young, Liu, Mei, Kim, Hyoung‐Chun, Cass, Wayne A., Sullivan, Patrick G., Bing, Guoying·2007·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2006.04327.x

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Abstract

Evidence suggests that chronic inflammation, mitochondrial dysfunction, and oxidative stress play significant and perhaps synergistic roles in Parkinson’s disease (PD), where the primary pathology is significant loss of the dopaminergic neurons in the substantia nigra. The use of anti‐inflammatory drugs for PD treatment has been proposed, and inhibition of cyclo‐oxygenase‐2 (COX‐2) or activation of peroxisome proliferator‐activated receptor gamma (PPAR‐γ) yields neuroprotection in MPTP‐induced PD. Lipopolysaccharide (LPS) induces inflammation‐driven dopaminergic neurodegeneration. We tested the hypothesis that celecoxib (Celebrex, COX‐2 inhibitor) or pioglitazone (Actos, PPAR‐γ agonist) will reduce the LPS‐induced inflammatory response, spare mitochondrial bioenergetics, and improve nigral dopaminergic neuronal survival. Rats were treated with vehicle, celecoxib, or pioglitazone and were intrastriatally injected with LPS. Inflammation, mitochondrial dysfunction, oxidative stress, decreased dopamine, and nigral dopaminergic neuronal loss were observed post‐LPS. Celecoxib and pioglitazone provided neuroprotective properties by decreasing inflammation and restoring mitochondrial function. Pioglitazone also attenuated oxidative stress and partially restored striatal dopamine as well as demonstrated dopaminergic neuroprotection and reduced nigral microglial activation. In summary, intrastriatal LPS served as a model for inflammation‐induced dopaminergic neurodegeneration, anti‐inflammatory drugs provided protective properties, and pioglitazone or celecoxib may have therapeutic potential for the treatment of neuro‐inflammation and PD.

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Authors: Hunter, R. L., Dragicevic, N., Seifert, K., Choi, D. Y., Liu, M., Kim, H., Cass, W. A., Sullivan, P. G., & Bing, G.
Affiliations: University of Kentucky (US)
Kangwon National University (KR)
Corresponding author: Bing, Guoying
ORCID: Liu, Mei
Kim, Hyoung‐Chun
Cass, Wayne A.
Sullivan, Patrick G.
Bing, Guoying
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2006-11-20
Volume: 100
Issue: 5
Pages: 1375-1386
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/j.1471-4159.2006.04327.x
OpenAlex: W1629697287
Cited by: 322
References: 56
Citations by year: 2026: 7 · 2025: 7 · 2024: 11 · 2023: 13 · 2022: 18 · 2021: 21 · 2020: 13 · 2019: 20 · 2018: 7 · 2017: 20 · 2016: 23 · 2015: 17 · 2014: 17 · 2013: 17 · 2012: 26
FWCI: 11.34
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG017963, R01AG017963)
National Institute of Neurological Disorders and Stroke (NS 044157, R01NS048191, NS 046426, NS 048191, R01NS044157, R21NS046426)
Topics: Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
Keywords: Parkinson's disease, neuroinflammation, dopaminergic neuron loss, substantia nigra, mitochondrial dysfunction, oxidative stress, lipopolysaccharide, celecoxib, pioglitazone, COX-2 inhibition, PPARγ agonism, neuroprotection, microglial activation, striatal dopamine, MPTP model
MeSH terms: Celecoxib, Pioglitazone, Animals, Corpus Striatum, Dopamine, Inflammation, Lipopolysaccharides, Male, Mitochondria, Nerve Degeneration, Neurons, Pyrazoles, Receptor, Insulin, Substantia Nigra, Sulfonamides, Cell Death, Rats, Sprague-Dawley, Microglia, Thiazolidinediones, PPAR gamma, Rats, Cyclooxygenase 2 Inhibitors, In Vitro Techniques

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Inflammation induces mitochondrial dysfunction and dopaminergic neurodegeneration in the nigrostriatal system

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