ArticleScientific reports2026
Gnetum montanum extract attenuates lipopolysaccharide induced acute lung inflammation through Nrf2 and heme oxygenase 1 mediated redox modulation in macrophages.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The Nrf2/HO-1 pathway is a promising therapeutic target for inflammatory disease management. Stilbene derivatives can activate this pathway and exert potent anti-inflammatory effects. Gnetum montanum Markgr., a stilbene-rich medicinal plant traditionally used in Vietnam, China, and other Asian countries for the treatment of inflammatory disorders, has not been systematically investigated for its anti-inflammatory properties or underlying mechanisms. Our study evaluated the protective effects of a stilbene-rich G. montanum extract (SGME) against inflammatory responses in vitro and in vivo. In lipopolysaccharide (LPS)-activated raw 264.7 macrophages, SGME significantly suppressed the expression and production of pro-inflammatory mediators by inhibiting NF-κB activation. In bone marrow-derived macrophages, SGME effectively prevented polarization toward the pro-inflammatory M1 phenotype. Mechanistically, SGME promoted Nrf2 nuclear translocation, leading to the upregulation of HO-1 and other Nrf2 target genes, attenuating LPS-induced oxidative stress in macrophages. Both Nrf2 knockdown and pharmacological inhibition significantly diminished these protective effects, confirming Nrf2’s pivotal role. Notably, in an oropharyngeal LPS-induced acute lung inflammation model, SGME reduced leukocyte infiltration, suppressed excessive cytokine production, and alleviated oxidative stress, accompanied by increased expression of Nrf2-dependent antioxidant genes, including Cat, Sod2, and Hmox1. These findings demonstrate that SGME exerts potent anti-inflammatory effects via Nrf2 pathway activation, warranting further studies to evaluate its therapeutic potential in inflammation-related diseases.
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