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SAM Alleviates Neuroinflammation by Regulating M1/M2 Polarization of Microglia Through α7nAChR/Nrf2/HO-1 Signaling

Kang Ma1, Jiandong Niu2, Liang Zeng2

  • 1School of Basic Medicine, Qingdao University, 308 Ningxia Road, Qingdao, Shandong Province, 266071, China.

Neurochemical Research
|March 29, 2025
PubMed

Insights

S-adenosylmethionine (SAM) reduces aging-related neuroinflammation by preventing microglia activation. SAM promotes a shift from pro-inflammatory M1 to anti-inflammatory M2 microglia via the α7nAChR/Nrf2/HO-1 pathway.

Area of Science:

  • Neuroscience
  • Immunology
  • Aging Research

Background:

  • Microglia are key drivers of neuroinflammation and play a critical role in aging pathogenesis.
  • The precise mechanisms of microglial activation during aging remain incompletely understood.
  • Investigating the role of S-adenosylmethionine (SAM) in modulating microglial activation during aging is crucial.

Purpose of the Study:

  • To investigate the effect of SAM on D-galactose-induced microglia senescence and activation.
  • To elucidate the molecular mechanisms underlying SAM's action on microglia.
  • To determine if SAM attenuates neuroinflammation by inhibiting microglial polarization.

Main Methods:

  • Utilized BV2 cells treated with D-galactose (D-gal) to model aging-related microglia activation.
  • Employed Cell Counting Kit-8 (CCK8) assay, Senescence-associated β-Galactosidase (SA-β-gal) staining, western blot, and immunofluorescence.
  • Investigated the role of the α7 nicotinic acetylcholine receptor (α7nAChR) pathway using a selective antagonist (methyllycaconitine citrate, MLA).

Main Results:

  • D-galactose induced microglia senescence.
  • SAM intervention decreased pro-inflammatory markers (iNOS, TNF-α, IL-1β) and increased anti-inflammatory markers (Arg1, α7nAChR, Nrf2, HO-1).
  • SAM promoted M1 to M2 microglia polarization, suppressed pro-inflammatory cytokines, and upregulated α7nAChR, Nrf2, and HO-1, an effect partially dependent on α7nAChR signaling.

Conclusions:

  • SAM effectively attenuates D-galactose-induced microglia senescence and neuroinflammation.
  • SAM inhibits microglia polarization towards a pro-inflammatory M1 phenotype.
  • The neuroprotective effects of SAM are mediated through the α7nAChR/Nrf2/HO-1 signaling pathway, highlighting its therapeutic potential in aging-related neuroinflammation.
Keywords:
AgingMicroglia polarizationNeuroinflammationSAM

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