ArticleNeurochemical research2025
SAM Alleviates Neuroinflammation by Regulating M1/M2 Polarization of Microglia Through α7nAChR/Nrf2/HO-1 Signaling Pathway.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Curcumin regulates ferroptosis by activating α7 nicotinic acetylcholine receptor to improve sepsis-induced acute kidney injury.Renal failure · 2026Article
- The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.Molecular neurobiology · 2026Review
- Microglia-derived neuroinflammatory pathways in neuropathic pain.The Korean journal of pain · 2026Review
- The nitrate-nitrite-nitric oxide pathway of neuroinflammation and cognitive impairment in ischemic stroke.Frontiers in immunology · 2026Review
- Disruption of Circadian NRF2 Expression and Its Impact on Pain Sensitivity in Diabetes Peripheral Neuropathy.Pain research & management · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Microglia are the drivers of neuroinflammation. Microglia activation plays a critical role in the pathogenesis of aging. However, the mechanisms underlying microglial activation during aging are still not fully understood. Here, we investigated the role of S-adenosylmethionine (SAM) and its interplay with microglial activation in aging. In this study, we investigated the effect of SAM on BV2 cells treated with D-galactose (D-gal) and its molecular mechanism by Cell Counting Kit-8 (CCK8) assay, Senescence-associated β-Galactosidase (SA-β-gal) staining, western blot and immunofluorescence. We found that D-gal could induce microglia senescence. SAM intervention induced a significant decrease in the levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and increased arginase-1 (Arg1), α7 nicotinic acetylcholine receptor (α7nAChR), nuclear factor erythrocyte 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) expression. Moreover, after administration of α7nAChR selective antagonist methyllycaconitine citrate (MLA), our results showed that SAM enhanced expression of α7nAChR, Nrf2 and HO-1, promoted the transformation of microglia from M1 to M2 subtype, and decreased the proinflammatory cytokines compared with MLA + D-gal group. These results suggest that SAM attenuates neuroinflammation by inhibiting microglia polarization through the α7nAChR/Nrf2/HO-1 pathway.
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Registered trials
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