PMID- 23341905
OWN - NLM
STAT- MEDLINE
DCOM- 20130709
LR  - 20211117
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 1
DP  - 2013
TI  - Protective effect of gadolinium chloride on early warm ischemia/reperfusion 
      injury in rat bile duct during liver transplantation.
PG  - e52743
LID - 10.1371/journal.pone.0052743 [doi]
LID - e52743
AB  - BACKGROUND: Activation of Kupffer cell (KC) is acknowledged as a key event in the 
      initiation and perpetuation of bile duct warm ischemia/reperfusion injury. The 
      inhibitory effect of gadolinium chloride (GdCl(3)) on KC activation shows 
      potential as a protective intervention in liver injury, but there is less 
      research with regard to bile duct injury. METHODS: Sixty-five male Sprague-Dawley 
      rats (200-250 g) were randomly divided into three experimental groups: a sham 
      group (n = 15), a control group (n = 25), and a GdCl(3) group (n = 25). Specimen 
      was collected at 0.5, 2, 6, 12 and 24 h after operation. Alanine aminotransferase 
      (ALT), alkaline phosphatase (ALP) and total bilirubin (TBIL) of serum were 
      measured. Tumor necrosis factor-alpha (TNF-alpha), Capase-3 activity and soluble Fas 
      (sFas) were detected. The pathologic changes of bile duct were observed. 
      Immunochemistry for bile duct Fas was performed. Apoptosis of bile duct cells was 
      evaluated by the terminal UDP nick end labeling assay. RESULTS: GdCl(3) 
      significantly decreased the levels of ALT, ALP and TBIL at 2, 6, 12, and 24 h, 
      and increased serum sFas at 2, 6 and 12 h (P<0.05). TNF-alpha was lower in the 
      GdCl(3) group than in the control group at 2, 6, 12 and 24 h (P<0.05). 
      Preadministration of GdCl(3) significantly reduced the Caspase-3 activity and 
      bile duct cell apoptosis at 2, 6, 12 and 24 h. After operation for 2, 6 and 12 h, 
      the expression of Fas protein was lower in the GdCl(3) group than in the control 
      group (P<0.05). CONCLUSIONS: GdCl(3) plays an important role in suppressing bile 
      duct cell apoptosis, including decreasing ALT, ALP, TBIL and TNF-alpha; suppressing 
      Fas-FasL-Caspase signal transduction during transplantation.
FAU - Wang, Biao
AU  - Wang B
AD  - Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical 
      University, Guangzhou, People's Republic of China.
FAU - Zhang, Qi
AU  - Zhang Q
FAU - Zhu, Bili
AU  - Zhu B
FAU - Cui, Zhonglin
AU  - Cui Z
FAU - Zhou, Jie
AU  - Zhou J
LA  - eng
PT  - Journal Article
DEP - 20130114
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Fas protein, rat)
RN  - 0 (Protective Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (fas Receptor)
RN  - AU0V1LM3JT (Gadolinium)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - EC 3.4.22.- (Caspase 3)
RN  - P7082WY76D (gadolinium chloride)
SB  - IM
MH  - Alanine Transaminase/blood
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Aspartate Aminotransferases/blood
MH  - Bile Ducts/*blood supply/drug effects/enzymology/*pathology
MH  - Caspase 3/metabolism
MH  - Gadolinium/pharmacology/*therapeutic use
MH  - Immunohistochemistry
MH  - *Liver Transplantation
MH  - Male
MH  - Protective Agents/pharmacology/*therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/blood/*drug therapy/enzymology/pathology
MH  - Solubility
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/blood
MH  - *Warm Ischemia
MH  - fas Receptor/blood
PMC - PMC3544894
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/01/24 06:00
MHDA- 2013/07/10 06:00
PMCR- 2013/01/14
CRDT- 2013/01/24 06:00
PHST- 2012/08/07 00:00 [received]
PHST- 2012/11/21 00:00 [accepted]
PHST- 2013/01/24 06:00 [entrez]
PHST- 2013/01/24 06:00 [pubmed]
PHST- 2013/07/10 06:00 [medline]
PHST- 2013/01/14 00:00 [pmc-release]
AID - PONE-D-12-23394 [pii]
AID - 10.1371/journal.pone.0052743 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(1):e52743. doi: 10.1371/journal.pone.0052743. Epub 2013 Jan 14.