Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/16027
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dc.titleThe role of hydrogen sulfide in cecal ligation and puncture induced sepsis in the mouse
dc.contributor.authorZHANG HUILI
dc.date.accessioned2010-04-08T11:00:11Z
dc.date.available2010-04-08T11:00:11Z
dc.date.issued2008-07-23
dc.identifier.citationZHANG HUILI (2008-07-23). The role of hydrogen sulfide in cecal ligation and puncture induced sepsis in the mouse. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/16027
dc.description.abstractThe present study was aimed to investigate the potential role of endogenous H2S in cecal ligation and puncture induced sepsis and associated multiple organ damage. An overproduction of endogenous H2S was observed 8 hours after onset of sepsis. Blockage of H2S formation significantly reduced sepsis associated systemic inflammation and organ injuries. In contrast, injection of NaHS significantly aggravated sepsis associated systemic inflammation. Furthermore, H2S may provoke the inflammatory events at the leukocyte-endothelial interface in sepsis via regulating the expression of adhesion molecules. The pro-inflammatory role of H2S in sepsis may be mediated by the activation of ERK-NF-kappa B pathway. In addition, it was revealed that overproduced endogenous H2S in sepsis could up-regulate the expression of substance P, thereby contributing to lung injury. In conclusion, our findings suggest that endogenous H2S plays an important role in modulating systemic inflammation and severity of sepsis and associated organ damage.
dc.language.isoen
dc.subjectHydrogen sulfide; sepsis; inflammation; multiple organ damage; inflammatory mediator; substance P
dc.typeThesis
dc.contributor.departmentPHARMACOLOGY
dc.contributor.supervisorMADHAV BHATIA
dc.contributor.supervisorMOORE, PHILIP KEITH
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
dc.identifier.isiutNOT_IN_WOS
Appears in Collections:Ph.D Theses (Open)

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