Objective To observe the effect of electroacupuncture（EA） on vascular endothelial growth factor-C（VEGF-C）

vascular endothelial growth factor receptor-3（VEGFR-3）

proinflammatory factors and apoptosis in myocardial tissue in mice with acute myocardial ischemia（AMI）

and to explore the mechanism of EA for AMI. Methods Fifty male C57BL/6 mice were randomly divided into a sham operation group

a model group

an EA group

an inhibitor group and an inhibitor+EA group

10 mice in each group. Except for the sham operation group

the mice in the remaining groups were intervented with ligation at the left anterior descending（LAD） coronary artery to establish AMI model. The mice in the sham operation group were intervented without ligation after thoracotomy. The mice in the EA group were intervented with EA at "Shenmen"（HT 7） and "Tongli"（HT 5）

disperse-dense wave

2 Hz/15 Hz in frequency

1 m A in current intensity

30 min each time

once a day

for 3 d. The mice in the inhibitor group were treated with intraperitoneal injection of SAR 131675(12.5 mg·kg

-1

·d

-1

once a day for 3 d). The mice in the inhibitor+EA group were injected intraperitoneally with SAR 131675 30 min before EA. The ECG before modeling

30 min after modeling and 3 d after intervention was detected

and the ST segment displacement was recorded; after the intervention

the ELISA method was applied to measure the contents of serum creatine kinase isoenzyme（CK-MB）

aspartate aminotransferase（AST） as well as tumor necrosis factor-α（TNF-α） and interleukin-23（IL-23） in myocardial tissue; the HE staining method was used to observe the morphological changes of myocardial tissue; the immunofluorescence double labeling method was applied to measure the number of co-expression positive cells of VEGF-C/VEGFR-3 in myocardial tissue; the TUNEL method was used to detect the level of cardiomyocyte apoptosis; the Western blot method was applied to measure the protein expressions of VEGF-C

VEGFR-3

b-lymphoma-2（Bcl-2）

activated caspase-3（Cleaved Caspase-3） and activated poly adenosine diphosphate ribose polymerase-1（Cleaved PARP-1）. Results Compared with the sham operation group

in the model group the ST segment displacement was increased（P

<

0.01）; the contents of CK-MB

AST

TNF-α and IL-23 were increased（P

<

0.01）; the arrangement of myocardial fibers was disordered

and interstitial inflammatory cell infiltration was obvious; the number of co-expression positive cells of VEGF-C/VEGFR-3 was decreased（P

<

0.01）; the number of cardiomyocyte apoptosis was increased（P

<

0.01）; the expressions of VEGF-C

VEGFR-3 and Bcl-2 were decreased（P

<

0.01）; the expressions of Cleaved Caspase-3 and Cleaved PARP-1 were increased（P

<

0.01）. Compared with the model group

in the EA group the ST segment displacement was decreased（P

<

0.01）; the contents of CK-MB

AST

TNF-α

IL-23 were decreased（P

<

0.01）; the severity of myocardial pathological injury was reduced; the number of co-expression positive cells of VEGF-C/VEGFR-3 was increased（P

<

0.01）; the number of cardiomyocyte apoptosis was reduced（P

<

0.01）; the expressions of VEGF-C

VEGFR-3 and Bcl-2 were increased（P

<

0.01）; the expressions of Cleaved Caspase-3 and Cleaved PARP-1 were reduced（P

<

0.01）. There was no significant difference in all the indexes between the model group and the inhibitor group（P

>

0.05）. Compared with the model group

the protein expression of VEGF-C was increased in the inhibitor+EA group（P

<

0.01）. Compared with the inhibitor group

in the EA group the ST segment displacement was decreased（P

<

0.01）; the contents of CK-MB

AST

TNF-α

IL-23 were decreased（P

<

0.01）; the severity of myocardial pathological injury was reduced; the number of co-expression positive cells of VEGF-C/VEGFR-3 was increased（P

<

0.05）; the number of cardiomyocyte apoptosis was reduced（P

<

0.01）; the expressions of VEGF-C

VEGFR-3 and Bcl-2 were increased（P

<

0.01）; the expressions of Cleaved Caspase-3 and Cleaved PARP-1 were reduced（P

<

0.01）. Compared with the inhibitor+EA group

all the indexes in the EA group were improved except the protein expression of VEGF-C（P

<

0.01）. Conclusion EA could relieve the inflammatory reaction and apoptosis in AMI mice

and its mechanism may be related to activating VEGF-C/VEGFR-3 pathway and promoting lymphangion genesis.