| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Pharmacology, National University of Singapore, Singapore, Singapore
* To whom correspondence should be addressed. E-mail: mbhatia{at}nus.edu.sg.
Endogenous hydrogen sulfide (H2S) is naturally synthesized in various types of mammalian cells from L-cysteine in a reaction catalyzed by two enzymes, cystathionine-
-lyase (CSE) and/or cystathionine-
-synthase (CBS). Latest studies have implied that H2S functions as vasodilator and neurotransmitter. However, so far there is little information about the role played by H2S in systemic inflammation such as sepsis. Thus, the aim of this study was to investigate the potential role of endogenous H2S in cecal ligation and puncture (CLP) induced sepsis. Male Swiss mice were subjected to CLP induced sepsis and treated with saline (i.p.), DL-propargylglycine (PAG, 50 mg/kg i.p.), a CSE inhibitor or NaHS (10mg/kg, i.p.). PAG was administered either 1 hour before or 1 hour after the induction of sepsis while NaHS was given at the same time of CLP. CLP induced sepsis significantly increased the plasma H2S level and the liver H2S synthesis 8 hours after CLP as compared with sham operation. Induction of sepsis also resulted in a significant up-regulation of CSE mRNA in liver. On the other hand, prophylactic as well as therapeutic administration of PAG, significantly reduced sepsis associated systemic inflammation as evidenced by myeloperoxidase activity and histological changes in lung and liver, and attenuated the mortality of CLP induced sepsis. Injection of NaHS significantly aggravated sepsis associated systemic inflammation. Therefore, the effect of inhibition of H2S formation and administration of NaHS suggests that H2S plays a pro-inflammatory role in regulating the severity of sepsis and associated organ injury.
This article has been cited by other articles:
|
|
 |
|
  B. Vollmar and M. D. Menger The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair Physiol Rev, October 1, 2009; 89(4): 1269 - 1339. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Zoccali, C. Catalano, and S. Rastelli Blood pressure control: hydrogen sulfide, a new gasotransmitter, takes stage Nephrol. Dial. Transplant., May 1, 2009; 24(5): 1394 - 1396. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Zhang, L. Zhi, S. M. Moochhala, P. K. Moore, and M. Bhatia Endogenous hydrogen sulfide regulates leukocyte trafficking in cecal ligation and puncture-induced sepsis J. Leukoc. Biol., October 1, 2007; 82(4): 894 - 905. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Zhi, A. D. Ang, H. Zhang, P. K. Moore, and M. Bhatia Hydrogen sulfide induces the synthesis of proinflammatory cytokines in human monocyte cell line U937 via the ERK-NF-{kappa}B pathway J. Leukoc. Biol., May 1, 2007; 81(5): 1322 - 1332. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. He, R. Horuk, S. M. Moochhala, and M. Bhatia Treatment with BX471, a CC chemokine receptor 1 antagonist, attenuates systemic inflammatory response during sepsis Am J Physiol Gastrointest Liver Physiol, April 1, 2007; 292(4): G1173 - G1180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Zhang, L. Zhi, S. Moochhala, P. K. Moore, and M. Bhatia Hydrogen sulfide acts as an inflammatory mediator in cecal ligation and puncture-induced sepsis in mice by upregulating the production of cytokines and chemokines via NF-{kappa}B Am J Physiol Lung Cell Mol Physiol, April 1, 2007; 292(4): L960 - L971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Bhatia, L. Zhi, H. Zhang, S.-W. Ng, and P. K. Moore Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice Am J Physiol Lung Cell Mol Physiol, November 1, 2006; 291(5): L896 - L904. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
