Neuroprotective Effect of Ghrelin in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Mouse Model of Parkinson’s Disease by Blocking Microglial Activation
Abstract
Ghrelin is an endogenous ligand for growth hormone (GH) secretagogue receptor 1a (GHS-R1a) and is produced and released mainly from the stomach. It was recently demonstrated that ghrelin can function as a neuroprotective factor by inhibiting apoptotic pathways. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic neurotoxicity in rodents; previous studies suggest that activated microglia actively participate in the pathogenesis of Parkinson's disease (PD) neurodegeneration. However, the role of microglia in the neuroprotective properties of ghrelin is still unknown. Here we show that, in the mouse MPTP PD model generated by an acute regimen of MPTP administration, systemic administration of ghrelin significantly attenuates the loss of substantia nigra pars compacta (SNpc) neurons and the striatal dopaminergic fibers through the activation of GHS-R1a. We also found that ghrelin reduced nitrotyrosine levels and improved the impairment of rota-rod performance. Ghrelin prevents MPTP-induced microglial activation in the SNpc and striatum, the expression of pro-inflammatory molecules tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta), and the activation of inducible nitric oxide synthase. The inhibitory effect of ghrelin on the activation of microglia appears to be indirect by suppressing matrix metalloproteinase-3 (MMP-3) expression in stressed dopaminergic neurons because GHS-R1a is not expressed in SNpc microglial cells. Finally, in vitro administration of ghrelin prevented 1-methyl-4-phenylpyridinium-induced dopaminergic cell loss, MMP-3 expression, microglial activation, and the subsequent release of TNF-alpha, IL-1beta, and nitrite in mesencephalic cultures. Our data indicate that ghrelin may act as a survival factor for dopaminergic neurons by functioning as a microglia-deactivating factor and suggest that ghrelin may be a valuable therapeutic agent for neurodegenerative diseases such as PD.
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Ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express GHSR, such as neurons and astrocytes.
“Hence, ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express the GHSR, such as neurons [53, 54, 57] and astrocytes [58].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [54]
Microglia lack GHSR, the primary receptor for ghrelin.
“Moreover, microglia lack the GHSR, the primary receptor for ghrelin [53–55].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [54]
Ghrelin treatment suppresses inflammatory response and reduces reactive oxygen species production in microglial cells.
“Yet, ghrelin treatment has been shown to suppress inflammatory response and reduce reactive oxygen species production in microglial cells [53, 54].”
From Protective PLCG2 variants associate with a delayed onset of Alzheimer’s disease among heterozygous APOE ε4 carriers (2026) · cites this paper as [54]
The beneficial effects of ghrelin in PD models are attributed to its ability to promote autophagy, enhance mitochondrial biogenesis and bioenergetics, mitigate neuroinflammation, and inhibit apoptosis.
“These beneficial effects are attributed to its ability to promote autophagy, enhance mitochondrial biogenesis and bioenergetics, mitigate neuroinflammation, and inhibit apoptosis.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [567]
Ghrelin has neuroprotective effects in multiple rodent models of PD, including MPTP-induced PD mice, 6-OHDA-induced PD rats, and A53T α-synuclein transgenic mice.
“accumulating evidence has demonstrated the neuroprotective effects of ghrelin in multiple rodent models of PD, including MPTP-induced PD mice”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [567]
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“Hence, ghrelin could affect microglia functions indirectly by modulating other brain cell types that do express the GHSR, such as neurons [53, 54, 57] and astrocytes [58].”
- Authors
- Moon, M., Kim, H. G., Hwang, L., Seo, J.-H., Kim, S., Hwang, S., Kim, S., Lee, D., Chung, H., Oh, M. S., Lee, K.-T., & Park, S.
- Affiliations
- Kyung Hee University (KR)
- Corresponding author
- Park, Seungjoon
- ORCID
- Venue
- Neurotoxicity Research
- Published
- 2009-03-17
- Volume
- 15
- Issue
- 4
- Pages
- 332-347
- ISSN
- 1029-8428 (ISSN-L)
- 1476-3524
- OpenAlex
- W2090644845
- Cited by
- 203
- References
- 66
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 11 · 2023: 4 · 2022: 14 · 2021: 14 · 2020: 9 · 2019: 11 · 2018: 11 · 2017: 21 · 2016: 13 · 2015: 15 · 2014: 14 · 2013: 19 · 2012: 12
- FWCI
- 21.09
- Type
- book chapter
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neurotoxicity Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- ghrelin, Parkinson's disease, MPTP, microglial activation, GHS-R1a, neuroprotection, dopaminergic neurons, substantia nigra pars compacta, nitrotyrosine, inducible nitric oxide synthase, MMP-3, TNF-α, IL-1β, neuroinflammation, neurodegeneration
- MeSH terms
- Analysis of Variance, Animals, Animals, Newborn, Cells, Cultured, Corpus Striatum, Disease Models, Animal, Dopamine, Dose-Response Relationship, Drug, Embryo, Mammalian, Gene Expression Regulation, Gliosis, Male, Mesencephalon, Mice, Inbred C57BL, Motor Activity, Nerve Degeneration, Neurons, Nitrites, Tumor Necrosis Factor-alpha, Tyrosine 3-Monooxygenase, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Microglia, Neuroprotective Agents, Matrix Metalloproteinase 3, MPTP Poisoning, Mice, Rats, Interleukin-1beta, Tandem Mass Spectrometry, Ghrelin, Receptors, Ghrelin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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