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Titolo:
Role of ERK and p38 mitogen-activated protein kinase cascades in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide
Autore:
Slomiany, BL; Slomiany, A;
Indirizzi:
Univ Med & Dent New Jersey, New Jersey Dent Sch, Res Ctr, Newark, NJ 07103USA Univ Med & Dent New Jersey Newark NJ USA 07103 s Ctr, Newark, NJ 07103USA
Titolo Testata:
IUBMB LIFE
fascicolo: 5, volume: 51, anno: 2001,
pagine: 315 - 320
SICI:
1521-6543(200105)51:5<315:ROEAPM>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; SIGNAL-TRANSDUCTION; UP-REGULATION; TNF-ALPHA; ENDOTHELIN-1; PATHWAY; INVOLVEMENT; EXPRESSION; APOPTOSIS;
Keywords:
acute gastritis; ERK and p38 MAPK inhibition; Helicobacter pylori; lipopolysaccharide; TNF-alpha; ET-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Slomiany, BL Univ Med & Dent New Jersey, New Jersey Dent Sch, Res Ctr, 110Bergen St, Newark, NJ 07103 USA Univ Med & Dent New Jersey 110 Bergen St Newark NJ USA 07103
Citazione:
B.L. Slomiany e A. Slomiany, "Role of ERK and p38 mitogen-activated protein kinase cascades in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide", IUBMB LIFE, 51(5), 2001, pp. 315-320

Abstract

The animal model of H. pylori lipopolysaccharide (LPS)-induced gastritis was used to study the role of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) in the mucosal release of tumor necrosis factor-alpha (TNF-alpha) and endothelin-1 (ET-1) in response toH. pylori infection. Rats, pretreated with specific inhibitors of p38 and ERK pathways, SB203580 and PD98059, were submitted to intragastric application of H. pylori LPS and maintained on the daily regimen of the inhibitors for 4 days. In the absence of inhibitors, the LPS elicited a pattern of mucosal inflammatory responses resembling that of acute gastritis, and reflected in a massive increase in the mucosal level of ET-1 and TNF-alpha. Administration of SB203580 led to a 63.4% reduction in the extent of inflammatoryinvolvement, the level of ET-1 fell by a 42% and TNF-alpha declined by a 52.3%, whereas PD98059 elicited a 21.2% reduction in the extent of inflammatory involvement and a 22.7% decrease in TNF-alpha, but had no effect on theLPS-induced increase in ET-1. A combination of both inhibitors, while exerting additive effect on TNF-alpha. produced no additional reduction in ET-1and the extent of inflammatory involvement achieved with SB203580 alone. The findings suggest that the p38 MAPK signaling pathway plays a key role inthe mediation of gastric mucosal inflammatory reaction to H. pylori infection.

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Documento generato il 09/04/20 alle ore 20:10:52