Objective　　　To determine the rol

e of paracrine mechanism in adipose-derived stem cells (ADSC) transplantation-mediated treatment for myocardial infarction (MI).　　　 Methods　　　Primarily cultured human ADSC (passage 3 to 5) were characterized and used in the experiments. A total of 36 male C57B/L mice

at an age of 8 to 10 weeks

with a weight 20 to 24 g were randomly and equally divided into sham operation group

MI+DMEM/F12 and MI+ADSC conditioned medium (ADSC-CM) groups. Mouse model of MI were subjected to MI injury by left descending artery ligation. DMEM/F12 and ADSC-CM were intra-myocardially injected into the infarct border zone after MI injury. To determine the therapeutic effect

the animal survival rate was observed

myocardial infarct size was measured by TTC staining

cardiac function was evaluated by echocardiography

and cardiomyocyte apoptosis was determined by TUNEL staining. An in vitro cell injury model was established by using neonatal rat ventricular myocytes (NRVMs) with H

2

O

2

treatment

and the cardioprotective effect of ADSC-CM was examined.　　　 Results　　　Compared with DMEM/F12

ADSC-CM significantly reduced the infarct size [(35.3±0.5)% 

vs

(41.7±1.9)%

P

0.05

]

improved cardiac function [ejection fraction: (60.4±4.8)% 

vs

(47.2±3.7)%

P

0.05

]

and decreased cardiomyocyte apoptosis in infarct border zone (TUNEL positive cardiomyocytes/10

6

neuclei: 677.4±64.2 

vs

867.3±67.9

P

0.05). Compared with DMEM/F12

ADSC-CM significantly reduced NRVM apoptosis subjected to H

2

O

2

injury [reduced expression of caspase-3 protein; TUNEL positive rate: (58.84±2.19) % vs (71.65±0.86)%

P0.05

]

.　　　 Conclusion　　　ADSC-CM exerts therapeutic effect on MI through reducing cardiomyocyte apoptosis. Paracrine effect is an important mechanism for ADSC transplantation-mediated treatment for MI.