期刊
NATURE MEDICINE
卷 6, 期 4, 页码 422-428出版社
NATURE AMERICA INC
DOI: 10.1038/74680
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资金
- NHLBI NIH HHS [HL55330, HL60234] Funding Source: Medline
- NIAID NIH HHS [AI42365] Funding Source: Medline
The stress-inducible protein heme oxygenase-1 provides protection against oxidative stress. The antiinflammatory properties of heme oxygenase-1 may serve as a basis for this cytoprotection. We demonstrate here that carbon monoxide, a by-product of heme catabolism by heme oxygenase, mediates potent anti-inflammatory effects. Both in vivo and in vitro, carbon monoxide at low concentrations differentially and selectively inhibited the expression of lipopolysaccharide-induced pro-inflammatory cytokines tumor necrosis factor-alpha, interleukin-1 beta, and macrophage inflammatory protein-lp and increased the lipopolysaccharide-induced expression of the anti-inflammatory cytokine interleukin-10. Carbon monoxide mediated these anti-inflammatory effects not through a guanylyl cyclase-cGMP or nitric oxide pathway, but instead through a pathway involving the mitogen-activated protein kinases. These data indicate the possibility that carbon monoxide may have an important protective function in inflammatory disease states and thus has potential therapeutic uses.
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