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Titolo:
The role of Kupffer cell alpha(2)-adrenoceptors in norepinephrine-induced TNF-alpha production
Autore:
Zhou, M; Yang, SL; Koo, DJ; Ornan, DA; Chaudry, IH; Wang, P;
Indirizzi:
Univ Alabama, Sch Med, Surg Res Ctr, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 rg Res Ctr, Birmingham, AL 35294 USA Univ Alabama, Sch Med, Dept Surg, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 Dept Surg, Birmingham, AL 35294 USA
Titolo Testata:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
fascicolo: 1, volume: 1537, anno: 2001,
pagine: 49 - 57
SICI:
0925-4439(20010727)1537:1<49:TROKCA>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; SYSTEMIC INFLAMMATORY RESPONSE; HEPATOCELLULAR DYSFUNCTION; EARLY SEPSIS; EXPERIMENTAL ENDOTOXEMIA; GENE-EXPRESSION; CECAL LIGATION; RAT-LIVER; INTERLEUKIN-1; MACROPHAGES;
Keywords:
isolated perfused liver preparation; catecholamine; clonidine; yohimbine; proinflammatory cytokine; endotoxin; sepsis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, P Univ Alabama, Sch Med, Surg Res Ctr, 1670 Univ Blvd,Volker Hall,Room G094P, Birmingham, AL 35294 USA Univ Alabama 1670 Univ Blvd,Volker Hall,Room G094P Birmingham AL USA 35294
Citazione:
M. Zhou et al., "The role of Kupffer cell alpha(2)-adrenoceptors in norepinephrine-induced TNF-alpha production", BBA-MOL BAS, 1537(1), 2001, pp. 49-57

Abstract

Although previous studies have demonstrated that plasma levels of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) increase during early sepsis, the precise mechanism responsible for its upregulation remains to be elucidated. Since recent studies have shown that the gut is an important source of norepinephrine (NE) release during early sepsis and enterectomy prior to the onset of sepsis attenuates TNF-alpha production, we hypothesized that gut-derived NE plays a major role in upregulating TNF-alpha via the activation of alpha (2)-adrenoceptors on Kupffer cells. To confirm that NE increases TNF-alpha synthesis and release, Kupffer cells were isolated from normal rats and incubated with NE (20 or 50 nM) or another alpha (2)-adrenergic agonist clonidine (50 nM) without addition of Escherichia coli endotoxin. Supernatant levels of TNF-alpha were then measured. In additional animals, intraportal infusion of NE (20 muM) with or without the specific alpha (2)-adrenergic antagonist yohimbine (1 mM) at a rate of 13 mul/minwas carried out for 2 h. Plasma and Kupffer cell levels of TNF-alpha, wereassayed thereafter. Moreover, the effects of NE and yohimbine on TNF-alphaproduction was further examined using an isolated perfused liver preparation. The results indicate that both NE and clonidine increased TNF-alpha release by approximately 4-7-fold in the isolated cultured Kupffer cells. Similarly, intraportal infusion of NE in vivo or in isolated livers increased TNF-alpha synthesis and release which was inhibited by co-infusion of yohimbine. Furthermore, the increased cellular levels of TNF-alpha in Kupffer cells after in vivo administration of NE was also blocked by yohimbine. These results, taken together, suggest that gut-derived NE upregulates TNF-alpha production in Kupffer cells through an alpha (2)-adrenergic pathway, which appears to be responsible at least in part for the increased levels of circulating TNF-alpha observed during early sepsis as well as other pathophysiologic conditions such as trauma, hemorrhagic shock, or gut ischemia/reperfusion. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 00:42:23