Articles: hydrogen-sulfide-metabolism.
-
Hydrogen sulfide (H(2)S) up-regulates inflammatory response in several inflammatory diseases. However, to date, little is known about the molecular mechanism by which H(2)S provokes the inflammatory response in sepsis. Thus, the aim of this study was to investigate the signaling pathway underlying the proinflammatory role of H(2)S in cecal ligation and puncture (CLP)-induced sepsis. ⋯ As a result, pretreatment with PAG significantly reduced the production of cytokines and chemokines in sepsis, whereas exogenous H(2)S greatly increased it. In addition, pretreatment with PD98059, an inhibitor of ERK kinase (MEK-1), significantly prevented NaHS from aggravating systemic inflammation in sepsis. In conclusion, the present study shows for the first time that H(2)S may regulate systemic inflammatory response in sepsis via ERK pathway.
-
Zhonghua yi xue za zhi · Aug 2008
[The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide].
To explore the role of hydrogen sulfide (H2S) in acute lung injury (ALI) during endotoxic shock (ES) and its relationship with nitric oxide (NO) and carbon monoxide (CO). ⋯ The increase of H(2)S generation participates in the lung tissue injury during ES and this event is related to eNOS activity decrease, iNOS activity increase that causes the production of large amount of NO. H2S up-regulates the HO-1/CO system in the lung tissues during ES, which may be the endogenous compensatory response against the injury.
-
Am. J. Physiol. Regul. Integr. Comp. Physiol. · Aug 2008
Hydrogen sulfide as an oxygen sensor in trout gill chemoreceptors.
O2 chemoreceptors elicit cardiorespiratory reflexes in all vertebrates, but consensus on O2-sensing signal transduction mechanism(s) is lacking. We recently proposed that hydrogen sulfide (H2S) metabolism is involved in O2 sensing in vascular smooth muscle. Here, we examined the possibility that H2S is an O2 sensor in trout chemoreceptors where the first pair of gills is a primary site of aquatic O2 sensing and the homolog of the mammalian carotid body. ⋯ In isolated zebrafish neuroepithelial cells, the putative chemoreceptive cells of fish, both hypoxia and H2S, produced a similar approximately 10-mV depolarization. These studies are consistent with H2S involvement in O2 sensing/signal transduction pathway(s) in chemoreceptive cells, as previously demonstrated in vascular smooth muscle. This novel mechanism, whereby H2S concentration ([H2S]) is governed by the balance between constitutive production and oxidation, tightly couples tissue [H2S] to PO2 and may provide an exquisitely sensitive, yet simple, O2 sensor in a variety of tissues.
-
The present study aimed to examine the regulatory effect of hydrogen sulfide (H2S) on vascular collagen remodeling in hypertensive rats. After 5 weeks of H2S donor treatment, tail blood pressure, the endogenous H2S production rate, levels of hydroxyproline and collagen type I, collagen type I protein expression in the thoracic aorta, [3H]thymidine ([3H]TdR) incorporation, [3H]proline incorporation, and [3H]hydroxyproline secretion in cultured vascular smooth muscle cells (VSMCs) were measured. We also examined the effects of NaHS on angiotensin II-induced mitogen-activated protein kinase (MAPK) activation and angiotensin II type 1 (AT1) receptor binding affinity. ⋯ Moreover, NaHS could dose-dependently decrease angiotensin II-induced MAPK activation. NaHS also decreased AT1 receptor binding as well as the binding affinity of the AT1 receptor. Thus, in SHRs, which demonstrated vascular remodeling and collagen accumulation, the endogenous H2S pathway is involved in the regulation of excess vascular collagen.
-
Acta Pharmacol. Sin. · Dec 2006
Interaction between hydrogen sulfide/cystathionine gamma-lyase and carbon monoxide/heme oxygenase pathways in aortic smooth muscle cells.
To investigate the interaction between hydrogen sulfide (H2S)/cystathionine gamma-lyase (CSE) and carbon monoxide (CO)/heme oxygenase (HO) pathways in aortic smooth muscle cells (ASMC). ⋯ The results suggested that endogenous CO/HO and H2S/CSE pathways inhibited each other in ASMC under physiological conditions.