Effect of S-diclofenac, a novel hydrogen sulfide releasing derivative, on carrageenan-induced hindpaw oedema formation in the rat

Sidhapuriwala, Jenab N.; Li, Ling; Sparatore, Anna; Bhatia, Madhav; Moore, Philip K.

doi:10.1016/j.ejphar.2007.05.003

Cited by 65 publications

(48 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nonetheless, as a therapeutic tool, pharmaceutical-grade Na 2 S shows great potential and has been successfully used to prevent and treat myocardial infarction, ischemia-reperfusion injury and endotoxic shock [112,113]. It is Table 2 By sharp contrast, no effect was observed with mesalamine or ADT-OH treatment alone, suggesting protective effects in addition to H 2 S release [111] Male Wistar rats: Carageenan-induced hindpaw edema The study concluded that the additional anti-inflammatory effect of S-diclofenac was due to H 2 S release [134] Male Wistar rats: Trinitrobenzene sulfonic acid-induced colitis [125] Male Swiss albino mice: Cecal ligation and puncture-induced sepsis PPT-A gene expression and substance P levels whereas NaSH increased substance P levels and lung injury [71] Balb/C mice: Acute pancreatitis and associated lung inflammation induced by cerulein…”

Section: H 2 S Donor Molecules and Inflammation: Notes Of Cautionmentioning

confidence: 97%

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Whiteman

Winyard

2011

Expert Review of Clinical Pharmacology

279

232

View full text Add to dashboard Cite

Section: H 2 S Donor Molecules and Inflammation: Notes Of Cautionmentioning

confidence: 97%

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Whiteman

Winyard

2011

Expert Review of Clinical Pharmacology

279

232

View full text Add to dashboard Cite

“…In contrast to these findings, there are additional studies showing that H 2 S has antiinflammatory effects. For instance, recent studies demonstrated that different H 2 S donors inhibit leukocyte infiltration in carrageenan-injected air pouch or hindpaw (23,41), gastric injury induced by anti-inflammatory nonsteroidal anti-inflammatory drugs (NSAID; Ref. 42), colitis induced by trinitrobenzenesulfonic acid (43) and into lung during caerulein-induced pancreatitis and systemic inflammation induced by high doses of LPS (44,45).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Augments Neutrophil Migration through Enhancement of Adhesion Molecule Expression and Prevention of CXCR2 Internalization: Role of ATP-Sensitive Potassium Channels

Dal-Secco¹,

Cunha²,

Freitas³

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

In this study, we have addressed the role of H2S in modulating neutrophil migration in either innate (LPS-challenged naive mice) or adaptive (methylated BSA (mBSA)-challenged immunized mice) immune responses. Treatment of mice with H2S synthesis inhibitors, dl-propargylglycine (PAG) or β-cyanoalanine, reduced neutrophil migration induced by LPS or methylated BSA (mBSA) into the peritoneal cavity and by mBSA into the femur/tibial joint of immunized mice. This effect was associated with decreased leukocyte rolling, adhesion, and P-selectin and ICAM-1 expression on endothelium. Predictably, treatment of animals with the H2S donors, NaHS or Lawesson’s reagent, enhanced these parameters. Moreover, the NaHS enhancement of neutrophil migration was not observed in ICAM-1-deficient mice. Neither PAG nor NaHS treatment changed LPS-induced CD18 expression on neutrophils, nor did the LPS- and mBSA-induced release of neutrophil chemoattractant mediators TNF-α, keratinocyte-derived chemokine, and LTB4. Furthermore, in vitro MIP-2-induced neutrophil chemotaxis was inhibited by PAG and enhanced by NaHS treatments. Accordingly, MIP-2-induced CXCR2 internalization was enhanced by PAG and inhibited by NaHS treatments. Moreover, NaHS prevented MIP-2-induced CXCR2 desensitization. The PAG and NaHS effects correlated, respectively, with the enhancement and inhibition of MIP-2-induced G protein-coupled receptor kinase 2 expression. The effects of NaHS on neutrophil migration both in vivo and in vitro, together with CXCR2 internalization and G protein-coupled receptor kinase 2 expression were prevented by the ATP-sensitive potassium (KATP+) channel blocker, glybenclamide. Conversely, diazoxide, a KATP+ channel opener, increased neutrophil migration in vivo. Together, our data suggest that during the inflammatory response, H2S augments neutrophil adhesion and locomotion, by a mechanism dependent on KATP+ channels.

show abstract

“…In addition, H 2 S ''scavenges'' proinflammatory oxidants such nitric oxide ( NO), peroxynitrite (ONOO -), hypochlorous acid (HOCl) (25,26), superoxide, and hydrogen peroxide (3,6,15); such effects might be expected to alleviate inflammation. Finally, S-diclofenac (an H 2 S-releasing derivative of the nonsteroidal antiinflammatory drug, diclofenac) exhibits more-pronounced antiinflammatory activity in endotoxic shock (11) and against carrageenan-induced hindpaw edema (18) in the rat than does diclofenac. In each case, evidence has been presented that the augmented antiinflammatory action of this compound is secondary to the release of H 2 S from the parent molecule.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Hydrogen Sulfide Donors on Lipopolysaccharide-Induced Formation of Inflammatory Mediators in Macrophages

Whiteman

Rose

et al. 2010

Antioxidants & Redox Signaling

Self Cite

329

302

View full text Add to dashboard Cite

The role of hydrogen sulfide (H 2 S) in inflammation is controversial, with both pro-and antiinflammatory effects documented. Many studies have used simple sulfide salts as the source of H 2 S, which give a rapid bolus of H 2 S in aqueous solutions and thus do not accurately reflect the enzymatic generation of H 2 S. We therefore compared the effects of sodium hydrosulfide and a novel slow-releasing H 2 S donor (GYY4137) on the release of pro-and antiinflammatory mediators in lipopolysaccharide (LPS)-treated murine RAW264.7 macrophages. For the first time, we show that GYY4137 significantly and concentration-dependently inhibits LPS-induced release of proinflammatory mediators such as IL-1b, IL-6, TNF-a, nitric oxide ( NO), and PGE 2 but increased the synthesis of the antiinflammatory chemokine IL-10 through NF-kB=ATF-2=HSP-27-dependent pathways. In contrast, NaHS elicited a biphasic effect on proinflammatory mediators and, at high concentrations, increased the synthesis of IL-1b, IL-6, NO, PGE 2 and TNF-a. This study clearly shows that the effects of H 2 S on the inflammatory process are complex and dependent not only on H 2 S concentration but also on the rate of H 2 S generation. This study may also explain some of the apparent discrepancies in the literature regarding the pro-versus antiinflammatory role of H 2 S.

show abstract

Effect of S-diclofenac, a novel hydrogen sulfide releasing derivative, on carrageenan-induced hindpaw oedema formation in the rat

Cited by 65 publications

References 21 publications

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Hydrogen Sulfide Augments Neutrophil Migration through Enhancement of Adhesion Molecule Expression and Prevention of CXCR2 Internalization: Role of ATP-Sensitive Potassium Channels

The Effect of Hydrogen Sulfide Donors on Lipopolysaccharide-Induced Formation of Inflammatory Mediators in Macrophages

Contact Info

Product

Resources

About