Prolonged treatment with N-acetylcystine delays liver recovery from acetaminophen hepatotoxicity 英文参考文献.docVIP
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Prolonged treatment with N-acetylcystine delays liver recovery from acetaminophen hepatotoxicity 英文参考文献
Available online /content/13/2/R55
Research
Open Access
Vol 13 No 2
Prolonged treatment with N-acetylcystine delays liver recovery
from acetaminophen hepatotoxicity
Runkuan Yang1, Keita Miki1, Xin He2, Meaghan E Killeen1 and Mitchell P Fink1
1Department of Critical Care Medicine, University of Pittsburgh Medical School, 3550 Terrace Street, Pittsburgh, PA 15261, USA
2Department of Pathology, University of Pittsburgh Medical School, 3550 Terrace Street, Pittsburgh, PA 15261, USA
Corresponding author: Runkuan Yang, Yangr@
Received: 3 Jan 2009 Revisions requested: 21 Feb 2009 Revisions received: 23 Mar 2009 Accepted: 9 Apr 2009 Published: 9 Apr 2009
Critical Care 2009, 13:R55 (doi:10.1186/cc7782)
This article is online at: /content/13/2/R55
? 2009 Yang et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License /licenses/by/2.0,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introduction Acetaminophen (APAP) toxicity is the most
common cause of acute liver failure in the US and Europe.
Massive hepatocyte necrosis is the predominant feature of
APAP-induced acute liver injury (ALI). Liver regeneration is a vital
process for survival after a toxic insult, it occurs at a relative late
time point after the injurious phase. Currently, N-acetylcysteine
hours of APAP challenge, the mice were given 100 mg/kg NAC
dissolved in 0.6 mL saline, or saline treatment every 12 hours for
a total of 72 hours.
Results Seventy-two hours after APAP challenge, compared
(NAC),
a
glutathione
precursor,
is
the
antidote
for
with saline treatment, NAC treatment significantly increased
transaminase/aspartate
aminotransferase), induced evident hepatocyte vacuolation in
the periportal area and delayed liver regeneration seen in
histopathology. This detrimental effect was asso
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