Ethanol preconditioning reduces hepatic I/R injury by inhibiting the complement system activation.
BACKGROUND
Ethanol preconditioning (EtOH-PC) refers to a phenomenon in which cerebral, intestinal, and myocardial tissues are protected from the deleterious effects of ischemia/reperfusion (I/R) by prior ingestion of ethanol at low to moderate levels. Whether EtOH-PC can offer protective effects against hepatic I/R injury and whether these effects are associated with inhibition of complement activation were investigated.


METHODS
Male SD rats were divided into four groups, i.e., sham operation, ethanol control, IR, and ethanol-pretreatment I/R (EIR) groups. EtOH-PC was induced by gavaging rats with 40% ethanol at a dose of 5 g/kg body weight 24 h prior to experiment. Animal survival rate was compared. Liver function, hepatic MDA level, plasma complement C3 level, and serum hemolytic activity were determined. Histologic changes and complement C3 deposition in liver section were examined. Expression of liver complement 3 mRNA was analyzed by quantitative real-time -PCR.


RESULTS
The 14-d survival rates were remarkably higher in the EIR groups than in the corresponding IR groups when hepatic ischemia time was 110, 120, and 130 min. Serum ALT, AST, IL-1β, and liver tissue MDA were significantly lower, and histopathologic changes significantly milder in the EIR group than in the IR group (P <0.05). Compared with the IR group, both the reduction in CH50 and plasma C3 were significantly suppressed, and the staining of C3 in liver tissue significantly reduced in the EIR group. There were no significant differences of hepatic C3 mRNA among four groups.


CONCLUSIONS
Ethanol preconditioning reduces hepatic I/R injury, and the effect is associated with inhibition of complement activation.
Ma
Zheng-Wei
ZW
Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Feng
Xiao-Bin
XB
Zheng
Shu-Guo
SG
Bie
Ping
P
Wang
Shu-Guang
SG
Li
Kun
K
Zhang
Yu-Jun
YJ
Dong
Jia-Hong
JH
D000818:Animals; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology; D003167:Complement Activation / Q000187:drug effects*; D003176:Complement C3 / Q000235:genetics / Q000378:metabolism; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D006461:Hemolysis / Q000187:drug effects; D053583:Interleukin-1beta / Q000097:blood; D019194:Ischemic Preconditioning / Q000379:methods*; D015227:Lipid Peroxidation / Q000187:drug effects; D008107:Liver Diseases / Q000276:immunology / Q000401:mortality / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000276:immunology / Q000401:mortality / Q000517:prevention & control*
D002492:Central Nervous System Depressants; D003176:Complement C3; D053583:Interleukin-1beta; D012333:RNA, Messenger; D000431:Ethanol; D008315:Malondialdehyde