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Titolo:
FR167653 attenuates ischemia and reperfusion injury of the rat lung with suppressing p38 mitogen-activated protein kinase
Autore:
Kawashima, Y; Takeyoshi, I; Otani, Y; Koibuchi, Y; Yoshinari, D; Koyama, T; Kobayashi, M; Matsumoto, K; Morishita, Y;
Indirizzi:
Gunma Univ, Sch Med, Dept Surg 2, Maebashi, Gumma 3718511, Japan Gunma Univ Maebashi Gumma Japan 3718511 2, Maebashi, Gumma 3718511, Japan Nippon Med Sch, Dept Pathol, Kawasaki, Kanagawa, Japan Nippon Med Sch Kawasaki Kanagawa Japan Pathol, Kawasaki, Kanagawa, Japan
Titolo Testata:
JOURNAL OF HEART AND LUNG TRANSPLANTATION
fascicolo: 5, volume: 20, anno: 2001,
pagine: 568 - 574
SICI:
1053-2498(200105)20:5<568:FAIARI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; MAP KINASE; CELLULAR STRESSES; HEPATIC ISCHEMIA; INTERLEUKIN-1; DOGS; INHIBITOR; APOPTOSIS; CYTOKINES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Kawashima, Y Gunma Univ, Sch Med, Dept Surg 2, 3-39-15 Showa Machi, Maebashi, Gumma 3718511, Japan Gunma Univ 3-39-15 Showa Machi Maebashi Gumma Japan 3718511 n
Citazione:
Y. Kawashima et al., "FR167653 attenuates ischemia and reperfusion injury of the rat lung with suppressing p38 mitogen-activated protein kinase", J HEART LUN, 20(5), 2001, pp. 568-574

Abstract

Background: FR167653 is a potent suppressant of tumor necrosis factor (TNF)-alpha and interleukin-1 (IL-1) production, and was shown to attenuate ischemia and reperfusion (IIR) organ injury in our previous experiment. Because p38 mitogen-activated protein (MAP) kinase has been reported to regulate the production of TNF-alpha and IL-1, we examined the effects of FR167653 in the rat lung I/R model and determined the expression and activation of p38 MAP kinase. Methods: Experiment 1: After 1 hour of ischemia, p38 MAP kinase, phosphorylated p38 MAP kinase (active form), histologic changes of the lung, and serum levels of TNF-alpha: and IL-1 beta were examined. Experiment 2: After 2 hours of reperfusion, arterial oxygen content (Pao(2)) and saturation (Sao(2)), serum TNF-alpha and IL-1 beta levels, and histologic changes in the lung were examined. Rats were divided into three groups in Experiment 1. In the control group, a saline solution was administered and, in the FR group, 0.1 mg/kg per hour of FR167653 was administered, intravenously throughout the experiment, beginning 30 minutes before ischemia. In the non-ischemic group, samples were taken soon after thoracotomy. The rats were divided into control and FR groups in Experiment 2. Results: Experiment 1: One hour of ischemia induced almost no changes in the lung or serum cytokine levels. Meanwhile, FR167653 markedly attenuated the expression of phosphorylated p38 MAP kinase, Experiment 2: Sao(2) and Pao(2) were improved, serum cytokines were lower, and lung damage was less extensive in the FR group than in the control group. Conclusion: FR167653 attenuates I/R injury of the lung and this attenuation is associated with suppression of p38 MAP kinase activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 04:40:49