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Sporoderm-removed ganoderma lucidum spore powder (S-GLSP) alleviates neuroinflammation injury by regulating microglial polarization through inhibition of NLRP3 inflammasome activation

Summary

Researchers found that sporoderm-removed Ganoderma lucidum spore powder (S-GLSP) protects against Alzheimer’s disease by reducing brain inflammation. The supplement works by shifting immune cells in the brain called microglia from a harmful pro-inflammatory state to a protective anti-inflammatory state. This is accomplished by blocking the NLRP3 inflammasome, a key trigger of brain inflammation. In animal and cell studies, S-GLSP improved memory, reduced neuronal damage, and decreased harmful tau protein accumulation.

Background

Alzheimer’s disease remains a major neurodegenerative disorder with limited effective treatments. Ganoderma lucidum spore powder exhibits diverse pharmacological activities and potential therapeutic value. Microglia-mediated chronic neuroinflammation drives AD progression, making microglial polarization a promising therapeutic target.

Objective

To investigate the protective effects of sporoderm-removed Ganoderma lucidum spore powder (S-GLSP) against Alzheimer’s disease and elucidate the molecular mechanisms underlying its neuroprotective effects, particularly involving microglial polarization and NLRP3 inflammasome activation.

Results

S-GLSP contained 42 chemical compounds including flavonoids, alkaloids, and terpenoids. Treatment alleviated neuronal damage, improved memory deficits, and reduced phosphorylated tau expression. S-GLSP downregulated M1 markers and upregulated M2 markers, inhibited NLRP3 inflammasome activation, and reduced IL-1β and IL-18 secretion in both in vivo and in vitro models.

Conclusion

S-GLSP alleviates AD pathology by inhibiting NLRP3 inflammasome activation and promoting microglial polarization from M1 to M2 phenotype, thereby modulating inflammatory cytokine release and creating a neuroprotective environment. These findings support S-GLSP as a promising candidate for AD therapeutic development.
  • Published in:Frontiers in Pharmacology,
  • Study Type:Experimental Research (In vivo and In vitro Study),
  • Source: PMID: 41378217, PMCID: PMC12685938, doi: 10.3389/fphar.2025.1690192
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