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Hydrogen sulfide acts as a mediator of inflammation in acute pancreatitis: in vitro studies using isolated mouse pancreatic acinar cells.

Tamizhselvi R, Moore PK, Bhatia M - J. Cell. Mol. Med. (2007 Mar-Apr)

Bottom Line: Caerulein increased the levels of H(2)S and CSE mRNA expression while CBS mRNA expression was decreased.Inhibition of endogenous production of H(2)S by PAG significantly suppressed SP concentration, PPT-A expression and NK1-R expression in the acini.To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and NK1-R in acinar cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, National University of Singapore, Yong Loo Lin School of Medicine, Centre for the Sciences, 28 Medical Drive, Singapore 117456.

ABSTRACT
Hydrogen sulphide (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS). We have earlier shown that H(2)S acts as a mediator of inflammation. However the mechanism remains unclear. In this study, we investigated the presence of H(2)S and the expression of H(2)S synthesizing enzymes, CSE and CBS, in isolated mouse pancreatic acini. Pancreatic acinar cells from mice were incubated with or without caerulein (10(-7) M for 30 and 60 min). Caerulein increased the levels of H(2)S and CSE mRNA expression while CBS mRNA expression was decreased. In addition, cells pre-treated with DL-propargylglycine (PAG, 3 mM), a CSE inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that CSE may be the main enzyme involved in H(2)S formation in mouse acinar cells. Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue caerulein-treated acinar cells. Inhibition of endogenous production of H(2)S by PAG significantly suppressed SP concentration, PPT-A expression and NK1-R expression in the acini. To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and NK1-R in acinar cells. These results suggest that the pro-inflammatory effect of H(2)S may be mediated by SP-NK-1R related pathway in mouse pancreatic acinar cells.

Show MeSH
Effect of H2S donor, sodium hydro-sulphide (NaHS), on SP level in pancreatic acinar cells. Freshly prepared pancreatic acinar cells were treated with NaHS (10, 50 and 100 μM) for 30 min. Substance P level was measured as described in Materials and Methods. Results shown are the mean ± S.E.M. of at least six separate determinations. **P < 0.01 between control and NaHS-induced cells.
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fig06: Effect of H2S donor, sodium hydro-sulphide (NaHS), on SP level in pancreatic acinar cells. Freshly prepared pancreatic acinar cells were treated with NaHS (10, 50 and 100 μM) for 30 min. Substance P level was measured as described in Materials and Methods. Results shown are the mean ± S.E.M. of at least six separate determinations. **P < 0.01 between control and NaHS-induced cells.

Mentions: These experiments suggest that the inhibition of endogenous H2S biosynthesis results in an anti-inflammatory effect in caerulein-induced pancreatic acinar cells and thereby provides indirect evidence that H2S exerts pro-inflammatory activity in acinar cells. To investigate a possible direct role of H2S in acinar cells, we treated the cells with the H2S donor drug, NaHS (10 and 100 μM) and evaluated its effect on SP level. As shown in Fig. 6 (P < 0.01) 100 μM of NaHS significantly increased SP level in pancreatic acinar cells after 30 min treatment. In addition, PPT-A (P < 0.05; Fig 7A) and NK-1R expression were markedly increased 30 min after treatment with NaHS (P < 0.01; Fig 7B).


Hydrogen sulfide acts as a mediator of inflammation in acute pancreatitis: in vitro studies using isolated mouse pancreatic acinar cells.

Tamizhselvi R, Moore PK, Bhatia M - J. Cell. Mol. Med. (2007 Mar-Apr)

Effect of H2S donor, sodium hydro-sulphide (NaHS), on SP level in pancreatic acinar cells. Freshly prepared pancreatic acinar cells were treated with NaHS (10, 50 and 100 μM) for 30 min. Substance P level was measured as described in Materials and Methods. Results shown are the mean ± S.E.M. of at least six separate determinations. **P < 0.01 between control and NaHS-induced cells.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822830&req=5

fig06: Effect of H2S donor, sodium hydro-sulphide (NaHS), on SP level in pancreatic acinar cells. Freshly prepared pancreatic acinar cells were treated with NaHS (10, 50 and 100 μM) for 30 min. Substance P level was measured as described in Materials and Methods. Results shown are the mean ± S.E.M. of at least six separate determinations. **P < 0.01 between control and NaHS-induced cells.
Mentions: These experiments suggest that the inhibition of endogenous H2S biosynthesis results in an anti-inflammatory effect in caerulein-induced pancreatic acinar cells and thereby provides indirect evidence that H2S exerts pro-inflammatory activity in acinar cells. To investigate a possible direct role of H2S in acinar cells, we treated the cells with the H2S donor drug, NaHS (10 and 100 μM) and evaluated its effect on SP level. As shown in Fig. 6 (P < 0.01) 100 μM of NaHS significantly increased SP level in pancreatic acinar cells after 30 min treatment. In addition, PPT-A (P < 0.05; Fig 7A) and NK-1R expression were markedly increased 30 min after treatment with NaHS (P < 0.01; Fig 7B).

Bottom Line: Caerulein increased the levels of H(2)S and CSE mRNA expression while CBS mRNA expression was decreased.Inhibition of endogenous production of H(2)S by PAG significantly suppressed SP concentration, PPT-A expression and NK1-R expression in the acini.To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and NK1-R in acinar cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, National University of Singapore, Yong Loo Lin School of Medicine, Centre for the Sciences, 28 Medical Drive, Singapore 117456.

ABSTRACT
Hydrogen sulphide (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS). We have earlier shown that H(2)S acts as a mediator of inflammation. However the mechanism remains unclear. In this study, we investigated the presence of H(2)S and the expression of H(2)S synthesizing enzymes, CSE and CBS, in isolated mouse pancreatic acini. Pancreatic acinar cells from mice were incubated with or without caerulein (10(-7) M for 30 and 60 min). Caerulein increased the levels of H(2)S and CSE mRNA expression while CBS mRNA expression was decreased. In addition, cells pre-treated with DL-propargylglycine (PAG, 3 mM), a CSE inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that CSE may be the main enzyme involved in H(2)S formation in mouse acinar cells. Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue caerulein-treated acinar cells. Inhibition of endogenous production of H(2)S by PAG significantly suppressed SP concentration, PPT-A expression and NK1-R expression in the acini. To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and NK1-R in acinar cells. These results suggest that the pro-inflammatory effect of H(2)S may be mediated by SP-NK-1R related pathway in mouse pancreatic acinar cells.

Show MeSH