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Titolo:
Effects of a dual inhibitor of tumor necrosis factor-alpha and interleukin-1 on lipopolysaccharide-induced lung injury in rats: Involvement of the p38 mitogen-activated protein kinase pathway
Autore:
Yoshinari, D; Takeyoshi, I; Koibuchi, Y; Matsumoto, K; Kawashima, Y; Koyama, T; Ohwada, S; Morishita, Y;
Indirizzi:
Gunma Univ, Sch Med, Dept Surg 2, Maebashi, Gumma 371, Japan Gunma Univ Maebashi Gumma Japan 371 pt Surg 2, Maebashi, Gumma 371, Japan Nippon Med Sch Second Hosp, Div Pathol, Kawasaki, Kanagawa, Japan Nippon Med Sch Second Hosp Kawasaki Kanagawa Japan saki, Kanagawa, Japan
Titolo Testata:
CRITICAL CARE MEDICINE
fascicolo: 3, volume: 29, anno: 2001,
pagine: 628 - 634
SICI:
0090-3493(200103)29:3<628:EOADIO>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-DISTRESS SYNDROME; ISCHEMIA-REPERFUSION INJURY; INDUCED PULMONARY-EDEMA; MAP KINASE; ENDOTOXIN; FR167653; NEUTROPHILS; SHOCK; PROSTAGLANDINS; PERMEABILITY;
Keywords:
lipopolysaccharide; lung; rat; FR167653; p38; mitogen-activated protein kinase; kinase interleukin-1; tumor necrosis factor-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Takeyoshi, I 3-39-15 Showa Machi, Maebashi, Gumma 3718511, Japan 3-39-15 Showa Machi Maebashi Gumma Japan 3718511 8511, Japan
Citazione:
D. Yoshinari et al., "Effects of a dual inhibitor of tumor necrosis factor-alpha and interleukin-1 on lipopolysaccharide-induced lung injury in rats: Involvement of the p38 mitogen-activated protein kinase pathway", CRIT CARE M, 29(3), 2001, pp. 628-634

Abstract

Objective: Sepsis is a major cause of adult respiratory distress syndrome. In this study, we evaluated the effect of FR167653, which is a potent suppressant of tumor necrosis factor (TNF)-alpha. and interleukin (IL)-1 production, on lipopolysaccharide (LPS)induced lung injury and lethality in rats,and we examined the involvement of p38 mitogen-activated protein (MAP) kinase in the action of FR167653. Design: Prospective, randomized study. Setting: Animal research facility in a university. Subjects: Male Sprague-Dawley rats weighing 200-270 g. Interventions: All the animals were assigned to one of the following four groups: control group, FR-only group, LPS-only group, and LPS/FR group. Animals in the LPS-only and LPS/FR groups received 6 mg/kg of LPS intravenously. The animals in the FR-only and LPS/FR groups also received an infusion of FR167653 at 0.2 mg kg(-1) hr(-1), commencing 30 mins before the LPS (or vehicle) injection and continuing for 5.5 hrs. Measurements and Main Results: LPS significantly induced the accumulation of pulmonary neutrophils and lung edema, both of which were significantly attenuated by treatment with FR167653. FR167653 also significantly decreasedthe LPS-induced lethality. Histologically, tissue damage was milder in theLPS/FR group than in the LPS-only group, Serum concentrations of TNF-alpha. and IL-1 beta and plasma concentrations of thromboxane B-2 were all suppressed in the LPS/FR group compared with the LPS-only group. Western blot analysis revealed that FR167653 inhibited the phosphorylation of p38 MAP kinase in lung tissues. Conclusions: FR167653 administration decreased serum TNF-alpha and IL-1 beta concentrations, which was associated with decreased lung injury and lethality. The mechanism responsible for the decreased TNF-alpha and IL-1 may be related to the inhibitory effect of FR167653 on p38 MAP kinase activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 03:58:12