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2015 ; 8
(7
): 8655-62
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gab.com Text
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N-acetylcysteine protects against liver injure induced by carbon tetrachloride
via activation of the Nrf2/HO-1 pathway
#MMPMID26339453
Cai Z
; Lou Q
; Wang F
; Li E
; Sun J
; Fang H
; Xi J
; Ju L
Int J Clin Exp Pathol
2015[]; 8
(7
): 8655-62
PMID26339453
show ga
Chronic liver injury is an important clinical problem which eventually leads to
cirrhosis, hepatocellular carcinoma and end-stage liver failure. It is well known
that cell damage induced by reactive oxygen species (ROS) is an important
mechanism of hepatocyte injure. N-acetylcysteine (NAC), a precursor of
glutathione (GSH), is well-known role as the antidote to acetaminophen toxicity
in clinic. NAC is now being utilized more widely in the clinical setting for
non-acetaminophen (APAP) related causes of liver injure. However, the mechanisms
underlying its beneficial effects are poorly defined. Thus, Aim of the present
study was to investigate potential hepatic protective role of NAC and to
delineate its mechanism of action against carbon tetrachloride (CCl4)-induced
liver injury in models of rat. Our results showed that the alanine
aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as
malondialdehyde (MDA) contents decreased significantly in CCl4-induced rats with
NAC treatment. GSH content and superoxide dismutase (SOD) activities remarkably
increased in the NAC groups compared with those in CCl4-induced group. Treatment
with NAC had been shown to an increase in nuclear factor erythroid 2-related
factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels. In conclusion, these
results suggested that NAC upregulated HO-1 through the activation of Nrf2
pathway and protected rat against CCl4-induced liver injure. The results of this
study provided pharmacological evidence to support the clinical application of
NAC.
|Acetylcysteine/*pharmacology
[MESH]
|Animals
[MESH]
|Antioxidants/*pharmacology
[MESH]
|Biomarkers/metabolism
[MESH]
|Carbon Tetrachloride
[MESH]
|Chemical and Drug Induced Liver Injury/enzymology/genetics/pathology/*prevention
& control
[MESH]