ArticleMolecular nutrition & food research2026
Daidzein Mitigates Nicotine-Induced Atherogenesis via Nrf2/ROS/TXNIP-Dependent Inhibition of Macrophage Pyroptosis and Lipid Accumulation.
Article in Molecular nutrition & food research, 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
Food-derived bioactive components play a crucial role in the prevention of cardiovascular diseases. Daidzein (DAI), a soy isoflavone, possesses notable cardioprotective potential; however, its precise role in nicotine-induced atherosclerosis (AS) and its underlying mechanisms remain unclear. This study explored whether DAI protects against AS by modulating macrophage pyroptosis and lipid metabolism via redox-sensitive signaling pathways. In human acute monocytic leukemia cell line (THP-1)-derived macrophages, DAI alleviated nicotine-induced pyroptosis, as evidenced by the downregulation of NOD-like receptor family pyrin domain-containing 3 (NLRP3), ASC, cleaved caspase-1, and gasdermin D (GSDMD)-N, accompanied by reduced secretion of interleukin (IL)-1β, IL-6, and IL-18, and decreased lactate dehydrogenase (LDH) release and caspase-1 activity. DAI also enhanced (7-nitrobenz-2-oxa-1,3-diazole)-cholesterol (NBD)-cholesterol efflux, suppressed DiI-labeled oxidized low-density lipoprotein (DiI-ox-LDL) uptake, and mitigated intracellular lipid droplet accumulation. Mechanistically, silencing nuclear factor erythroid 2-related factor 2 (Nrf2), inducing reactive oxygen species (ROS), or overexpressing thioredoxin-interacting protein (TXNIP) abolished the protective effects of DAI, confirming the involvement of the Nrf2/ROS/TXNIP pathway. In nicotine-exposed apolipoprotein E-deficient (apoE
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