NLRP3 inflammasome regulates astrocyte transformation in brain injury induced by chronic intermittent hypoxia
Open accessAbstract
BACKGROUND: Obstructive sleep apnea (OSA) is mainly characterized by sleep fragmentation and chronic intermittent hypoxia (CIH), the latter one being associated with multiple organ injury. Recently, OSA-induced cognition dysfunction has received extensive attention from scholars. Astrocytes are essential in neurocognitive deficits via A1/A2 phenotypic changes. Nucleotide oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is considered the most important factor inducing and maintaining neuroinflammation. However, whether the NLRP3 regulates the A1/A2 transformation of astrocytes in CIH-related brain injury remains unclear. METHODS: We constructed an OSA-related CIH animal model and assessed the rats' learning ability in the Morris water maze; the histopathological assessment was performed by HE and Nissl staining. The expression of GFAP (astrocyte marker), C3d (A1-type astrocyte marker), and S100a10 (A2-type astrocyte marker) were detected by immunohistochemistry and immunofluorescence. Western blotting and RT-qPCR were used to evaluate the changes of A1/A2 astrocyte-related protein and NLRP3/Caspase-1/ASC/IL-1β. RESULTS: The learning ability of rats decreased under CIH. Further pathological examination revealed that the neurocyte in the hippocampus were damaged. The cell nuclei were fragmented and dissolved, and Nissl bodies were reduced. Immunohistochemistry showed that astrocytes were activated, and morphology and number of astrocytes changed. Immunofluorescence, Western blotting and RT-qPCR showed that the expression of C3d was increased while S100a10 was decreased. Also, the expression of the inflammasome (NLRP3/Caspase-1/ASC/IL-1β) was increased. After treatment of MCC950 (a small molecule inhibitor of NLRP3), the damage of nerve cells was alleviated, the Nissl bodies increased, the activation of astrocytes was reduced, and the expression of A2-type astrocytes was increased. In contrast, A1-type astrocytes decreased, and the expression of inflammasome NLRP3/Caspase-1/ASC/IL-1β pathway-related proteins decreased. CONCLUSION: The NLRP3 inflammasome could regulate the A1/A2 transformation of astrocytes in brain injury induced by CIH.
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NLRP3 inflammasome activation and subsequent secretion of IL-18 and IL-1β from microglia drives astrocytes into the neurotoxic reactive state, which induces upregulation of the secretion of complement protein C3 and results in lower synapse numbers.
“Currently, published studies suggest that NLRP3 inflammasome activation and subsequent secretion of IL-18 and IL-1β from microglia drives astrocytes into the neurotoxic reactive state, which induces upregulation of the secretion of the complement protein C3 and results in lower synapse numbers [180, 189–191].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [190]
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- Authors
- She, N., Shi, Y., Feng, Y., Ma, L., Yuan, Y., Zhang, Y., Cao, Z., Chen, X., Zhao, B., Liu, H., & Ren, X.
- Affiliations
- Second Affiliated Hospital of Xi'an Jiaotong University (CN)
- Corresponding author
- Liu, Haiqin
- Ren, Xiaoyong
- Venue
- BMC Neuroscience
- Published
- 2022-11-27
- Volume
- 23
- Issue
- 1
- Pages
- 70-70
- ISSN
- 1471-2202 (ISSN-L)
- PMC
- PMC9703760
- OpenAlex
- W4310272726
- Cited by
- 32
- References
- 39
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 8 · 2023: 6
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- BMC Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Key Research and Development Program in Social Development Field of Shaanxi (2021SF-286, 2020GXLH-Y005)
- National Natural Science Foundation of China (62076198)
- Topics
- Health Sciences › Medicine › Physiology › Obstructive Sleep Apnea Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- NLRP3 inflammasome, astrocyte transformation, chronic intermittent hypoxia, obstructive sleep apnea, neuroinflammation, hippocampal neurodegeneration, learning disabilities, caspase-1, IL-1β, S100A10, C3d, MCC950
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Hypoxia, Astrocytes, Brain Injuries, Hypoxia, Brain, Caspases, Sleep Apnea, Obstructive, Rats, Inflammasomes
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