Neuroprotective effects of taurine in a rodent model of parkinson's disease involve modulating astrocyte-mediated inflammation
- PMID: 40751776
- DOI: 10.1007/s12272-025-01563-z
Neuroprotective effects of taurine in a rodent model of parkinson's disease involve modulating astrocyte-mediated inflammation
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons due to oxidative stress and inflammation. Targeting inflammation and oxidative stress offers a promising means of slowing PD progression. Taurine, a naturally occurring amino sulfonic acid, has demonstrated potent antioxidant properties, thereby preventing cell death. While taurine has been studied for its potential to restrain the progression of Alzheimer's disease and mitigate microglial activation, its impact on astrocyte activation in PD models remains underexplored. Here, we found that taurine significantly reduces astroglial activation in MPP+-induced primary astrocytes by inhibiting the NF-κB pathway. Additionally, in vivo experiments in MPTP-induced PD models using male C57BL/6 mice showed that taurine improved motor function, protected against dopaminergic neuronal loss, and reduced glial activation in the striatum and substantia nigra. These findings highlight that the anti-inflammatory effects of taurine involve the inhibition of astroglial activation, suggesting that taurine has therapeutic potential in PD.
Keywords: Astrocyte; MPTP(1, Methyl, 4, Phenyl, 1,2,3,6, Tetrahydropyridine); Mitochondria; Neuroinflammation; Parkinson’s Disease; Taurine.
© 2025. The Pharmaceutical Society of Korea.
Conflict of interest statement
Declarations. Conflict of interest: Jaewon Lee is an Editor of Archives of Pharmacal Research, but this position did not influence the editorial decision or the peer review process of this manuscript. The others have no conflict of interest.
References
-
- Allaman I, Bélanger M, Magistretti PJ (2011) Astrocyte-neuron metabolic relationships: for better and for worse. Trends Neurosci 34(2):76–87. https://doi.org/10.1016/j.tins.2010.12.001 - DOI - PubMed
-
- Antzoulatos E, Jakowec MW, Petzinger GM, Wood RI (2010) Sex differences in motor behavior in the MPTP mouse model of Parkinson’s disease. Pharmacol Biochem Behav 95(4):466–472. https://doi.org/10.1016/j.pbb.2010.03.009 - DOI - PubMed - PMC
-
- Bej E, Cesare P, Volpe AR, d’Angelo M, Castelli V (2024) Oxidative stress and neurodegeneration: insights and therapeutic strategies for Parkinson’s disease. Neurol Int 16(3):502–517. https://doi.org/10.3390/neurolint16030037 - DOI - PubMed - PMC
-
- Booth HDE, Hirst WD, Wade-Martins R (2017) The role of astrocyte dysfunction in Parkinson’s disease pathogenesis. Trends Neurosci 40(6):358–370. https://doi.org/10.1016/j.tins.2017.04.001 - DOI - PubMed - PMC
-
- Borlongan CV, Koutouzis TK, Freeman TB, Cahill DW, Sanberg PR (1995) Behavioral pathology induced by repeated systemic injections of 3-nitropropionic acid mimics the motoric symptoms of Huntington’s disease. Brain Res 697(1–2):254–257. https://doi.org/10.1016/0006-8993(95)00901-2 - DOI - PubMed
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