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• W2012162544 endingPage "484" @default.
• W2012162544 startingPage "476" @default.
• W2012162544 abstract "Septic shock is believed to be a consequence of excessive stimulation of the immune system by bacterial toxins that results in systemic overproduction of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), IL-1, and IL-6. Various studies have shown that TNF-α, a major mediator of septic shock, induces tissue injury, loss of blood pressure, organ failure, and ultimately death. Administration of the opioid antagonist naloxone has been reported to reverse opiate-mediated hypotension, promote organ perfusion and increase patient survival. In this study, we examined the mechanism by which the opioid receptor antagonist, naltrexone, modulates the septic shock response in BALB/c mice after injection with lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in combination with d-galactosamine (d-gal), or with agonistic anti-Fas antibody (Jo2) alone. Each of these treatments induced rapid-onset, acute shock, and ultimately mortality (6–9 h after injection), although different mechanisms are involved. Administration of the opioid antagonist naltrexone protected mice from shock induced by LPS + d-gal, but not SEB + d-gal or Jo2 antibody, a protective effect that was reversed by morphine. Naltrexone significantly inhibited the production of TNF-α induced by LPS, but not SEB in vivo. When bone marrow-derived, splenic or peritoneal macrophages were treated with LPS in vitro, administration of naltrexone had no direct effect on TNF-α production. These results suggest that naltrexone is capable of preventing LPS-induced septic shock mortality by indirect inhibition of TNF-α production in vivo." @default.
• W2012162544 created "2016-06-24" @default.
• W2012162544 creator A5039937464 @default.
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• W2012162544 creator A5065727282 @default.
• W2012162544 date "2004-09-01" @default.
• W2012162544 modified "2023-10-16" @default.
• W2012162544 title "The opioid antagonist naltrexone blocks acute endotoxic shock by inhibiting tumor necrosis factor-α production" @default.
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• W2012162544 doi "https://doi.org/10.1016/j.bbi.2003.12.001" @default.
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