Objective:To study the effect of losartan on the changes of expression of signal molecule PKC、ERK1/ERK2

and p-ERK1/ERK2 in non-infarction zone of left ventricule(LVNIZ)and left ventricular remodeling(LVRM)in rat with acute my- ocardial infarction(AMI). Methods:The 36 surviving AMI male Wistar rats were randomly divided into 2 groups:AMI group(n= 30)(subdivided into 5 groups according to the different intervals at 1

3

7

14

28 days after AMI.) and losartan group(n=6) (by gastric gavate

20mg(/kg·d)

for 4 weeks). used Sham 7d group(n=6) was used as controls. LVEDP was analyzed by ALC -MPA biological signal analysis system. LVWI was measured when the hearts were harvested. The concentration of plas- ma and non-infarcted myocardial tissue AngⅡ were measured with radioimmunoassay. The expression of PKC

ERK1/ERK2

and p -ERK1/ERK2 protein in remote non -infarcted myocardium were evaluated by Western blot. Results:Compared with Sham-operated rats

LVEDP、LVWI and the concentration of LVNIZ AngⅡ in the 28th day after MI group were all markedly increased(P<0.01). In non-infarcted myocardium

the expression of PKC

ERK1/ERK2

and p-ERK1/ERK2 protein increased at 24h after AMI

peaked at 4w(P<0.01). There was a significant positive correlation between PKC and AngⅡ(P<0.05)

and a signifi-cant positive correlation between p-ERK1 and PKC

LVEDP

and LVWI(P<0.01). PKC

ERK1/ERK2

and p-ERK1/ERK2 protein were all decreased in losartan treated group with lightened LVRM

as compared with 28 th day after MI group(P<0.01). Conclusion:Myocardial local angiotensin Ⅱ can activate PKC-ERK1/ERK2 signaling pathway. The molecular mechanisms of losartan in improving cardiac remodeling may be via blocking angiotensinⅡ adverse effect

then blocking the signal conductionof PKC-ERK1/ERK2.