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Hydrogen sulfide attenuates lipopolysaccharide-induced inflammation by inhibition of p38 mitogen-activated protein kinase in microglia.
J Neurochem. 2007 Feb; 100(4):1121-8.JN

Abstract

The present study attempts to investigate the effect of H(2)S on lipopolysaccharide (LPS)-induced inflammation in both primary cultured microglia and immortalized murine BV-2 microglial cells. We found that exogenous application of sodium hydrosulfide (NaHS) (a H(2)S donor, 10-300 micro mol/L) attenuated LPS-stimulated nitric oxide (NO) in a concentration-dependent manner. Stimulating endogenous H(2)S production decreased LPS-stimulated NO production, whereas lowering endogenous H(2)S level increased basal NO production. Western blot analysis showed that both exogenous and endogenous H(2)S significantly attenuated the stimulatory effect of LPS on inducible nitric oxide synthase expression, which is mimicked by SB 203580, a specific p38 mitogen-activated protein kinase (MAPK) inhibitor. Exogenously applied NaHS significantly attenuated LPS-induced p38 MAPK phosphorylation in BV-2 microglial cells. Moreover, both NaHS (300 micro mol/L) and SB 203580 (1 micro mol/L) significantly attenuated LPS-induced tumor necrosis factor-alpha secretion, another inflammatory indicator. In addition, NaHS (10-300 micro mol/L) dose-dependently decreased LPS-stimulated NO production in primary cultured astrocytes, suggesting that the anti-neuroinflammatory effect of H(2)S is not specific to microglial cells alone. Taken together, H(2)S produced an anti-inflammatory effect in LPS-stimulated microglia and astrocytes, which may be due to inhibition of inducible nitric oxide synthase and p38 MAPK signaling pathways. These findings may have important implications in the treatment of neuroinflammation-related diseases.

Authors+Show Affiliations

Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17212697

Citation

Hu, Li-Fang, et al. "Hydrogen Sulfide Attenuates Lipopolysaccharide-induced Inflammation By Inhibition of P38 Mitogen-activated Protein Kinase in Microglia." Journal of Neurochemistry, vol. 100, no. 4, 2007, pp. 1121-8.
Hu LF, Wong PT, Moore PK, et al. Hydrogen sulfide attenuates lipopolysaccharide-induced inflammation by inhibition of p38 mitogen-activated protein kinase in microglia. J Neurochem. 2007;100(4):1121-8.
Hu, L. F., Wong, P. T., Moore, P. K., & Bian, J. S. (2007). Hydrogen sulfide attenuates lipopolysaccharide-induced inflammation by inhibition of p38 mitogen-activated protein kinase in microglia. Journal of Neurochemistry, 100(4), 1121-8.
Hu LF, et al. Hydrogen Sulfide Attenuates Lipopolysaccharide-induced Inflammation By Inhibition of P38 Mitogen-activated Protein Kinase in Microglia. J Neurochem. 2007;100(4):1121-8. PubMed PMID: 17212697.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen sulfide attenuates lipopolysaccharide-induced inflammation by inhibition of p38 mitogen-activated protein kinase in microglia. AU - Hu,Li-Fang, AU - Wong,Peter T-H, AU - Moore,Philip K, AU - Bian,Jin-Song, Y1 - 2006/12/22/ PY - 2007/1/11/pubmed PY - 2007/4/11/medline PY - 2007/1/11/entrez SP - 1121 EP - 8 JF - Journal of neurochemistry JO - J Neurochem VL - 100 IS - 4 N2 - The present study attempts to investigate the effect of H(2)S on lipopolysaccharide (LPS)-induced inflammation in both primary cultured microglia and immortalized murine BV-2 microglial cells. We found that exogenous application of sodium hydrosulfide (NaHS) (a H(2)S donor, 10-300 micro mol/L) attenuated LPS-stimulated nitric oxide (NO) in a concentration-dependent manner. Stimulating endogenous H(2)S production decreased LPS-stimulated NO production, whereas lowering endogenous H(2)S level increased basal NO production. Western blot analysis showed that both exogenous and endogenous H(2)S significantly attenuated the stimulatory effect of LPS on inducible nitric oxide synthase expression, which is mimicked by SB 203580, a specific p38 mitogen-activated protein kinase (MAPK) inhibitor. Exogenously applied NaHS significantly attenuated LPS-induced p38 MAPK phosphorylation in BV-2 microglial cells. Moreover, both NaHS (300 micro mol/L) and SB 203580 (1 micro mol/L) significantly attenuated LPS-induced tumor necrosis factor-alpha secretion, another inflammatory indicator. In addition, NaHS (10-300 micro mol/L) dose-dependently decreased LPS-stimulated NO production in primary cultured astrocytes, suggesting that the anti-neuroinflammatory effect of H(2)S is not specific to microglial cells alone. Taken together, H(2)S produced an anti-inflammatory effect in LPS-stimulated microglia and astrocytes, which may be due to inhibition of inducible nitric oxide synthase and p38 MAPK signaling pathways. These findings may have important implications in the treatment of neuroinflammation-related diseases. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/17212697/Hydrogen_sulfide_attenuates_lipopolysaccharide_induced_inflammation_by_inhibition_of_p38_mitogen_activated_protein_kinase_in_microglia_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04283.x DB - PRIME DP - Unbound Medicine ER -