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Titolo:
Anisodamine inhibits shiga toxin type 2-mediated tumor necrosis factor-alpha production in vitro and in vivo
Autore:
Zhang, HM; Ou, ZL; Yamamoto, T;
Indirizzi:
Niigata Univ, Sch Med, Dept Bacteriol, Niigata 9518510, Japan Niigata Univ Niigata Japan 9518510 ept Bacteriol, Niigata 9518510, Japan Int Med Ctr Japan, Inst Res, Dept Clin Pharmacol, Tokyo 1628655, Japan IntMed Ctr Japan Tokyo Japan 1628655 in Pharmacol, Tokyo 1628655, Japan
Titolo Testata:
EXPERIMENTAL BIOLOGY AND MEDICINE
fascicolo: 6, volume: 226, anno: 2001,
pagine: 597 - 604
SICI:
1535-3702(200106)226:6<597:AISTT2>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEMOLYTIC-UREMIC SYNDROME; ESCHERICHIA-COLI; CYTO-TOXICITY; FACTOR TNF; CELL LINE; INDUCTION; MECHANISM; RELEASE; COAGULATION; PROTEIN-1;
Keywords:
anisodamine; Stx2; TNF-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Yamamoto, T Niigata Univ, Grad Sch Med & Dent Sci, Dept Infect Dis Control& Int Med, Div Bacteriol, 757 Ichibanchou, Niigata, Japan Niigata Univ 757Ichibanchou Niigata Japan u, Niigata, Japan
Citazione:
H.M. Zhang et al., "Anisodamine inhibits shiga toxin type 2-mediated tumor necrosis factor-alpha production in vitro and in vivo", EXP BIOL ME, 226(6), 2001, pp. 597-604

Abstract

Cytokines, in particular tumor necrosis factor (TNF), appear to be necessary to develop the pathological process of Shiga toxin-producing Escherichiacoli(STEC) infection. In this study we examined the effect of anisodamine,a vasoactive drug, on TNF-alpha production in Shiga toxin type 2 (Stx2)-stimulated human monocytic cells in vitro and in Stx2-injected mice sera in vivo. Human monocytes and THP-1 cells were stimulated by StxP (1-100 ng/ml) with or without anisodamine addition (1-400 mug/ml). For in vivo evaluations, C57BL/6 mice were given a single intraperitoneal injection of anisodamine (6-50 mg/kg) or saline after intraperitoneal injection of StxP (50 ng/kg). The results showed that anisodamine suppressed Stx2-induced TNF-alpha production in a dose- and time-dependent manner, Anisodamine also suppressed Stx2-induced TNF-alpha mRNA expression. Further study showed that endogenousprostaglandin E2 may be involved in this inhibitory effect. In contrast toTNF-a mRNA, anisodamine at concentrations as high as 400 mug/ml did not decrease Stx2-induced IL-1 beta and IL-8 mRNA levers. In addition, anisodamine (> 50 mug/ml) increased Stx2-stimulated THP-I cell viability. Levels of TNF-alpha in anisodamine-treated mice sera were significantly lower than those in the saline-treated group 1.5 and 24 hr after Stx2 injection, Anisodamine induced a lower percentage of death in Stx2-injected mice, Taken together, our results indicate that anisodamine has an important regulatory effect on Stx2-induced TNF-alpha production in vitro and in vivo. The present study suggested that this drug should be further investigated for its effectson Stx2-mediated diseases in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 11:35:58