Limb ischemic preconditioning reduces rabbit hepatic ischemia-reperfusion injury through inhibition the phosphorylation of proteins in the MAPK signal pathway in the late phase.
10.3969/j.issn.1672-7347.2012.06.009
- Author:
Lijun CAO
1
;
Guixiu YUAN
;
Yaping WANG
;
Yetian CHANG
;
Junmei XU
;
Dingquan ZOU
;
Lai WEI
Author Information
1. Department of Anesthesiology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Extremities;
blood supply;
Ischemic Preconditioning;
methods;
Liver;
blood supply;
MAP Kinase Signaling System;
Male;
Phosphorylation;
Rabbits;
Reperfusion Injury;
prevention & control;
p38 Mitogen-Activated Protein Kinases;
chemistry;
physiology
- From:
Journal of Central South University(Medical Sciences)
2012;37(6):591-597
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the liver protection mechanisms of MAPK signaling pathway of limb ischemia preconditioning in the late phase.
METHODS:Thirty-six adult male New Zealand white rabbits, weighing 1.8-2.0 kg, were randomly divided equally into 3 groups: group C (sham operation), group L (liver ischemia-reperfusion 24 h after limb ischemia preconditioning), group IR (liver ischemia-reperfusion without limb ischemia preconditioning). Serum alanine transaminase (ALT) was measured during ischemia reperfusion. The tissue and cell injury of liver were examined by optical and electron microscopy. Activation of P38MAPK, P44/P42MAPK, and JNK in hepatic tissue was assessed by western blot after 30 min of reperfusion.
RESULTS:Serum ALT and cell injury in the liver as examined by optical and electron microscopy was decreased in group L as compared with the group IR. Phosphorylation of P38MAPK, P44/ P42MAPK, and JNK were all increased significantly after 30 min of reperfusion. Phosphorylation of P38MAPK and JNK was reduced by limb ischemia pre-treatment.
CONCLUSION:Limb ischemia pre-treatment can induce the late phase of preconditioning in rabbit liver through the inhibition of the phosphorylation of P38MAPK and JNK.
