Propofol ameliorates rat liver ischemia-reperfusion injury possibly by inhibiting nuclear factor-kappaB expression.
- Author:
Jing HE
1
;
Kai-Zhi LU
;
Guo-Cai TAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Down-Regulation; drug effects; Liver; blood supply; Male; NF-kappa B; biosynthesis; genetics; Propofol; pharmacology; RNA, Messenger; biosynthesis; genetics; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; prevention & control; Reverse Transcriptase Polymerase Chain Reaction
- From: Journal of Southern Medical University 2008;28(6):1064-1066
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the role of nuclear factor-kappaB (NF-kappaB) in the protective effects of propofol against liver ischemia-reperfusion (IR) injury.
METHODSForty male rats were randomized into 4 equal groups, namely the sham operation (N) group, IR group with hepatic IR injury (induced by ischemia of the left, right and median hepatic lobes for 1 h followed by reperfusion for 2 h), propofol (P) group with sham operation and propofol perfusion at 10 mg kg(-1) h(-1), and propofol treatment (PIR) group with IR injury and propofol perfusion. RT-PCR was used to detect the transcription level of NF-kappaB, and Western blotting was used for assaying NF-kappaB protein expression in the liver.
RESULTSCompared with either the N or the P group, the IR group showed obvious swelling, fatty degeneration and scatter focal necrosis of the hepatocytes as well as mild congestion in the hepatic sinusoid, with significantly increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and NF-kappaB expressions at both mRNA and protein levels (P<0.05). In the PIR group, the histopathological changes of the liver was lessened as compared with the IR group, and ALT and AST elevation was significantly inhibited (P<0.05) as was the protein expression of NF-kappaB (P<0.05), but NF-kappaB transcription level was further enhanced (P<0.05).
CONCLUSIONPropofol can protect the liver from IR injury possibly by inhibiting NF-kappaB expression.