期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 67, 期 7, 页码 1119-1132出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-009-0250-9
关键词
Glucocorticoids; Hydrogen sulfide; Cystathionine gamma-lyase; Lipopolysaccharide; Macrophages
资金
- National Natural Science Foundation of China [30670815, 30770846]
- Science and Technology Commission of Shanghai Municipals [09XD1405600]
Hydrogen sulfide (H2S) plays an important role in inflammation. We showed that macrophages expressed the H2S-forming enzyme cystathionine gamma-lyase (CSE) and produced H2S. Lipopolysaccharide (LPS) stimulated the CSE expression and H2S production rate. l-cysteine reduced LPS-induced nitric oxide (NO) production. CSE inhibitor blocked the inhibitory effect of l-cysteine. CSE knockdown increased, whereas CSE overexpression decreased LPS-induced NO production. Dexamethasone suppressed LPS-induced CSE expression and the H2S production rate as well as NO production. l-arginine increased, whereas N-G-nitro-l-arginine methyl ester (l-NAME) decreased LPS-induced CSE expression and H2S production. Dexamethasone plus l-NAME significantly decreased LPS-induced CSE expression and H2S production compared to l-NAME. Our results suggest that macrophages are one of the H2S producing sources. H2S might exert anti-inflammatory effects by inhibiting NO production. Dexamethasone may directly inhibit CSE expression and H2S production, besides the NO-dependent way. Inhibition of H2S and NO production may be a mechanism by which glucocorticoids coordinate the balance between pro- and anti-inflammatory mediators during inflammation.
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