Sporoderm-removed ganoderma lucidum spore powder (S-GLSP) alleviates neuroinflammation injury by regulating microglial polarization through inhibition of NLRP3 inflammasome activation Article Swipe
Wenli Li
,
Wei Huang
,
Peng Zhou
,
Peng Zhou
,
Peng Zhou
,
Yongchuan Yao
,
Biao Cai
,
Biao Cai
,
Biao Cai
,
Shu Ye
,
Shu Ye
,
Shu Ye
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.3389/fphar.2025.1690192
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.3389/fphar.2025.1690192
Introduction Sporoderm-Removed Ganoderma lucidum Spore Powder (S-GLSP), derived from the spores of the medically valued fungus Ganoderma lucidum, exhibits diverse pharmacological activities and shows considerable potential in the treatment of Alzheimer’s disease (AD). However, its underlying mechanisms of action remain incompletely elucidated. This study aims to investigate the protective effects of S-GLSP against AD and to explore the molecular mechanisms involved. Materials and Methods The chemical profile of S-GLSP extract was characterized using LC-MS/MS. Alzheimer’s disease models were established both in vivo and in vitro : a rat model was induced by D-galactose combined with intracerebroventricular injection of Aβ, while a cellular model was stimulated with LPS. The neuroprotective effects of S-GLSP were assessed through behavioral tests and hematoxylin-eosin (HE) staining. Immunofluorescence staining, Western blot (WB), RT-qPCR, and ELISA were employed to evaluate microglial polarization and NLRP3 inflammasome activation. Cell viability was measured using MTT and EdU assays. Finally, NLRP3 knockdown was performed to verify whether S-GLSP modulates microglial polarization via regulation of the NLRP3 inflammasome. Results A total of 42 chemical compounds were identified in S-GLSP, including flavonoids, alkaloids, terpenoids, saccharides, phenolics, fatty acids, nucleosides, amino acids, and other. S-GLSP treatment alleviated neuronal damage, improved learning and memory deficits, and reduced the expression of phosphorylated tau (p-tau) in AD model rats. Further experiments in vitro and in vivo showed that S-GLSP downregulated M1 phenotypic markers (CD86, iNOS, TNF-α) and upregulated M2 markers (CD206, Arg-1, IL-10). Moreover, S-GLSP inhibited NLRP3 inflammasome activation and regulated the secretion of IL-1β and IL-18, effects that were consistent with those observed following NLRP3 knockdown. Conclusion Our findings demonstrate that S-GLSP alleviates Alzheimer’s disease pathology by inhibiting NLRP3 inflammasome activation, promoting a shift in microglial polarization from the M1 to the M2 phenotype, and modulating the release of inflammatory cytokines. This study provides novel mechanistic insights into the therapeutic potential of S-GLSP for AD.
Related Topics
Concepts
Inflammasome
Neuroinflammation
Western blot
Chemistry
Neuroprotection
Gene knockdown
Viability assay
Microglia
Ganoderma lucidum
Secretion
Pharmacology
Downregulation and upregulation
Cell biology
Lipopolysaccharide
Macrophage polarization
MTT assay
Blot
Cancer research
Cell
Innate immune system
Mechanism of action
Biochemistry
Mode of action
Microbiology
Pathogenesis
Signal transduction
Molecular biology
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.3389/fphar.2025.1690192
- https://public-pages-files-2025.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1690192/pdf
- OA Status
- gold
- References
- 49
- OpenAlex ID
- https://openalex.org/W7106499539
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W7106499539Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.3389/fphar.2025.1690192Digital Object Identifier
- Title
-
Sporoderm-removed ganoderma lucidum spore powder (S-GLSP) alleviates neuroinflammation injury by regulating microglial polarization through inhibition of NLRP3 inflammasome activationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-11-25Full publication date if available
- Authors
-
Wenli Li, Wei Huang, Peng Zhou, Peng Zhou, Peng Zhou, Yongchuan Yao, Biao Cai, Biao Cai, Biao Cai, Shu Ye, Shu Ye, Shu YeList of authors in order
- Landing page
-
https://doi.org/10.3389/fphar.2025.1690192Publisher landing page
- PDF URL
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https://public-pages-files-2025.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1690192/pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://public-pages-files-2025.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1690192/pdfDirect OA link when available
- Concepts
-
Inflammasome, Neuroinflammation, Western blot, Chemistry, Neuroprotection, Gene knockdown, Viability assay, Microglia, Ganoderma lucidum, Secretion, Pharmacology, Downregulation and upregulation, Cell biology, Lipopolysaccharide, Macrophage polarization, MTT assay, Blot, Cancer research, Cell, Innate immune system, Mechanism of action, Biochemistry, Mode of action, Microbiology, Pathogenesis, Signal transduction, Molecular biologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
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49Number of works referenced by this work
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