ArticleCurrent issues in molecular biology2026
Boiogito Ameliorates Inflammation-Associated Adipocyte Dysfunction and Restores Adipogenesis in Association with Suppression of NF-κB Signaling.
Article in Current issues in molecular biology, 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
Boiogito (BOT), a traditional Kampo herbal medicine, has been reported to exhibit anti-inflammatory and anti-obesity properties. However, its potential role in protecting adipocyte function under inflammatory conditions at different stages of adipocyte development remains unclear. This study investigated the effects of BOT on adipogenesis and tumor necrosis factor-α (TNF-α)-induced inflammatory responses in differentiating and mature 3T3-L1 adipocytes. In this study, 3T3-L1 preadipocytes were induced to differentiate and exposed to TNF-α in the presence or absence of BOT during differentiation or after full adipocyte maturation. Lipid accumulation was assessed by Oil Red O staining, while adipokine secretion and inflammatory cytokine production were evaluated by ELISA. The expression of adipogenic markers and inflammatory signaling molecules was analyzed using quantitative PCR and Western blotting. TNF-α significantly inhibited the expression of adipogenesis-related factors at the transcriptional level in adipocytes, reduced lipid accumulation and adiponectin expression, and enhanced inflammatory cytokine production. BOT treatment dose-dependently attenuated these effects, restoring adipogenic capacity and suppressing inflammatory responses in both differentiating and mature adipocytes. Mechanistically, BOT reduced TNF-α-induced activation of the NF-κB pathway, as evidenced by decreased phosphorylation of NF-κB p65 and IκB. These findings demonstrate that BOT preserves adipocyte function and mitigates inflammation-associated adipocyte dysfunction throughout adipocyte development. The protective effects of BOT may contribute to the regulation of obesity-associated metabolic inflammation, partly through modulation of NF-κB signaling.
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