Objective:To investigate the changes of the protein expression in heart tissue of rats after ischemia-reperfusion(I/R) injury and pre-treatment of carvedilol

and to elucidate the new protective mechanism of carvedilol pre-treatment to I/R heart injury. Methods:18 rats were randomly divided into sham-operation group

I/R injury group and carvedilol pre-treated group. The model of myocardial I/R injury was established by 30min ligation of the left anterior descending branch of the coronary artery and 2h reperfusion. Serum malondiadehyde (MDA) was determined

and the cytosolic fraction of myocardial tissue homogenate was separated applying two-dimensional gel electrophoresis technique. Differentially expressed protein spots were figured out with PDQuest software

while preliminary protein-identification was carried out by means of the two-dimensional gel electrophoresis database on the web. Results:Compared with the sham-operation group

after I/R injury

serum MDA was increased(P<0.05)

and 8 protein spots were differentially expressed with all of them down-regulated(P<0.05)

one of which was identified as Cu/Zn superoxide dismutase

while 1 protein spot was totally absent. Compared with the I/R injury group

serum MDA was significantly decreased(P<0.01)

5 protein spots were up-regulated with 4 protein spots down-regulated(P<0.05)

while 3 protein spots were absent and 1 new protein spot appeared in the carvedilol pre-treated group. Pre-treatment of carvedilol enabled the expression of Cu/Zn superoxide dismutase normalized

transthyretin precursor(TTRP) up-regulated

myosin heavy chain 1 fragment down-regulated significantly

while the expression of ATP synthaseαchain mito.precursor and Enoyl-CoA hydratase mito.precursor missed. Conclusion:The main characteristics of the cytosolic protein change after I/R injury is down-regulation. Among them the down-regulation of Cu/Zn superoxide dismutase is one of the molecular mechanisms inducing I/R injury. Carvedilol exerts its protection of mitochondrion

structural and contractile proteins

through not only recovering the expression of Cu/Zn superoxide dismutase but also up-regulating the TTRP expression.