ArticleBMC research notes2025
Piperine suppresses M1 phenotype and induces indoleamine 2,3-dioxygenase gene in LPS-stimulated murine macrophage cell line.
Article in BMC research notes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
Abstract
objectiveActivated macrophages play important roles during immune responses by polarizing into M1 and M2 subsets and overproducing several mediators such as nitric oxide (NO), pro- and anti-inflammatory cytokines, and indoleamine 2,3-dioxygenase (IDO). This study aims to investigate the possible effects of piperine, a major component of the pepper plant, on the expression of M1 and M2 macrophage markers.
resultsPiperine dose-dependently decreased iNOS gene expression and NO level in LPS-stimulated macrophages. Additionally, at concentrations of 1-20 µg/ml, it significantly suppressed the production and/or gene expression levels of proinflammatory M1-related cytokines. Its effects on cytokine genes were dose-dependent, and reduced IL-1β, TNF-α, and IFN-γ expression (17 ± 11.8, 1.33 ± 0.76, and 25.4 ± 5.2 fold, respectively, compared with LPS-stimulated cells). Piperine at 1 µg/ml didn't affect the IL-10 gene but significantly increased IDO1 (from 8.4 ± 0.24-fold in LPS-treated cells to 28.3 ± 5.3-fold in piperine-treated cells), and decreased IL-4 gene expressions at the higher concentrations. Dexamethasone (a glucocorticoid anti-inflammatory drug) reduced most mediators but did not affect the IDO gene. Our data demonstrate that piperine dose-dependently inhibits M1-macrophages and upregulates IDO1 at low concentration, a unique mechanism of action, positioning it as a multifaceted therapeutic candidate for inflammatory conditions.
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