Abstract
Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)1β, IL-3, IL-6, IL-10, IL-12p40, IL-23], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)] and the activation and expression of CD29 as judged by cell-cell adhesion and surface staining experiments. The inhibition was due to the induction of heme oxygenase (HO)-1 in LPS-activated macrophages, since blocking HO-1 activity with ZnPP, an HO-1 specific inhibitor, abolished hydroquinone's NO inhibitory activity. In addition, hydroquinone and inhibitors (wortmannin and LY294002) of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway had very similar inhibitory effects on LPS-induced and CD29-mediated macrophage responses, including the phoshorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanism.
Original language | English |
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Pages (from-to) | 198-206 |
Number of pages | 9 |
Journal | Molecules and cells |
Volume | 23 |
Issue number | 2 |
Publication status | Published - 2007 Apr 30 |
Keywords
- Akt
- Cell-cell adhesion
- Cytokines
- Cytotoxic molecules
- Heme oxygenase-1
- Hydroquinone
- Macrophages
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology