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If one has plenty of DHEA, one has plenty of androstenediol
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James Michael Howard
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Joined: 30 Apr 2005
Posts: 78

PostPosted: Fri Jun 02, 2006 9:53 am    Post subject: If one has plenty of DHEA, one has plenty of androstenediol Reply with quote

Cytokine. 2006 May 29; [Epub ahead of print]


Androstenediol ameliorates alterations in immune cells cytokine production
capacity in a two-hit model of trauma-hemorrhage and sepsis.

Suzuki T, Shimizu T, Szalay L, Choudhry MA, Rue LW 3rd, Bland KI, Chaudry
IH.

Center for Surgical Research and Department of Surgery, University of
Alabama at Birmingham, Birmingham, AL 35294, USA.

Although administration of androstenediol (a metabolite of
dehydroepiandrosterone) following trauma-hemorrhage (T-H) produces
beneficial effects on inflammatory cytokines and organ function, it remains
unknown whether this metabolite has any salutary effects in preventing
alterations in immune cell cytokine production following a combined insult
of T-H and sepsis. To examine this, male rats underwent laparotomy,
hemorrhagic shock (mean BP 40mmHg for 90min) and resuscitation or sham
operation. Androstenediol (1mg/kg BW i.v.) or vehicle was administered at
the end of resuscitation. Twenty hrs after T-H or sham operation, sepsis
was induced by cecal ligation and puncture (CLP). Five hours thereafter,
plasma cytokine levels and cytokine production of various immune cells were
determined. In a separate set of experiments, survival was monitored for 10
days after the induction of sepsis. Administration of androstenediol
markedly decreased plasma IL-6 and TNF-alpha levels following T-H and CLP.
Furthermore, it prevented the increased production of IL-6 and TNF-alpha by
Kupffer cells and alveolar macrophages and attenuated the decrease in IL-6
and TNF-alpha production by splenic macrophages; however, it had no
significant effects on the depressed IL-6 and TNF-alpha production by PBMC
following T-H and CLP. The depressed IL-2 and IFN-gamma production by
splenocytes under those conditions was attenuated by the administration of
androstenediol. Furthermore, survival rate following T-H and subsequent
sepsis was improved by androstenediol treatment. Since androstenediol
administration following T-H attenuated cytokine production and reduced
mortality in a double-hit model of T-H and sepsis, this agent appears to be
a novel and useful adjunct for maintaining the immune cell functions
following T-H and for decreasing the mortality rate from subsequent
susceptibility to sepsis.
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