中文摘要：

目的探讨旁分泌机制在脂肪间允质干细胞（adiopose—derivedstemcells，ADSC）移植治疗心肌梗死中的作用。方法原代分离和培养人ADSC，将经鉴定的第3～5代的ADSC用于实验。①用8—10周龄（20～24g）的雄性C57B／L小鼠，结扎左前降支建赢心肌梗北（myocardialinfarction，MI）损伤模型，实验分假手术组，MI±DMEM／F12组和MI±ADSC—CM（conditionedmedium，条件培养液）组（n=12）。在MI处理的小鼠心肌梗死边缘区分别注射DMEM／F12和ADSC—CM，观察动物生存率、TTC染色测量心肌梗死面积、超声评价心功能变化、TUNEL染色检测心肌细胞凋亡等方法评价心肌梗死的治疗效果。②用H202建立乳鼠心肌细胞（neonatalratventricularmyoeytes，NRVM）体外损伤模型，观察ADSC—CM对心肌细胞的保护作用。实验分埘照组，H202±DMEM／F12组和H202±ADSC—CM组（n=5）。分别用caspase-3蛋白定鞋和TUNEL染色检测心肌细胞凋亡。结果①相较于DMEM／F12，ADSC—CM显著减少心肌梗死面积[（35．3±0．5％）vs（41．7±1．9％）P〈0．05]、提高心功能[EF：（60．4±4．8）％椰（47．2±3．7）％，P〈0．05]、减少梗死边缘区心肌细胞凋亡[TUNEL±心肌细胞／10。细胞核：（677．4±64．2）掷（867．3±67．9），P〈0．05]；②相对于DMEM／F12，ADSC-CM明显减少H2O2诱导的心肌细胞凋亡[caspase-3蛋白表达下降；TUNEL阳性率：（58．84±2．19）％掷（71．65±0．86）％，P〈0．05]。结论ADSC—CM通过减少心肌细胞凋亡发挥对心肌梗死的治疗作用；旁分泌作用是ADSC移植治疗心肌梗死的重要机制，

英文摘要：

Objective To determine the role 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 lO weeks, with a weight 20 to 24 g were randomly and equally divided into sham opera- tion 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-myoeardi- ally 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 TrC 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 H2 02 treatment, and the cardioprotective effect of ADSC-CM was examined. Results Compared with DMEM/F12, ADSC-CM signifi- cantly 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/106 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 H2O2 injury [reduced expression of caspase-3 protein; TUNEL positive rate： （58.84 ±2.19） % vs （71.65 ±0.86）%, P 〈 0.05 ]. Conclusion ADSC-CM exerts therapeutic effect on MI through reducing cardiomyocyte al6optosis. Paracrine effect is an important mechanism for ADSC transplantation-mediated treatment for MI.