骨髓间充质干细胞通过旁分泌作用治疗大鼠心肌梗死

目的 研究骨髓间充质干细胞（BMSC）旁分泌作用对大鼠心肌梗死模型的治疗效果.方法 将15只雄性成年SD大鼠随机分为3组,每组5只.实验组和对照组行冠状动脉结扎后再灌注,取心肌梗死区域3个点作为注射靶点,实验组注射BMSC培养基100 μL,对照组注射等量生理盐水;假手术组只进行开胸操作,不予冠状动脉结扎、注射及再灌注.于术后第10天行心脏彩色多普勒超声检查,测量各组大鼠左室舒张末期内径（LVEDd）、左室舒张末期容积（LVEDV）、左室收缩末期容积（LVESV）和左室射血分数（LVEF）.之后处死大鼠取心肌组织,采用TUNEL染色检测心肌细胞凋亡.结果 3组大鼠LVEDd、LVESV和LVEF差异有统计学意义（F=24.469,20.585,24.767;均P〈0.001）;与对照组相比,实验组大鼠LVEDd增幅较小（P=0.017）.TUNEL染色结果显示,3组大鼠凋亡心肌细胞数量差异有统计学意义（F=107.329,P〈0.001）;其中实验组凋亡心肌细胞为（12.6±2.6）个/视野,对照组为（18.4±4.1）个/视野,两组间差异有统计学意义（P〈0.001）.结论 BMSC可能通过旁分泌作用改善大鼠心肌梗死后心肌重构,减少心肌细胞凋亡.

Paracrine effects of bone marrow mesenchymal stem cells on myocardial infarction in rats

Objective To study paracrine effects of bone marrow mesenchymal stem cells （BMSC） on the rat model of myocardial infarction. Methods Fifteen male adult SD rats were divided into 3 groups： experimental group, control group and sham group （5 rats in each group ）. The experimental and control groups underwent coronary artery ligation, and then reperfusion. The experimental group was injected with 100 ~L BMSC culture medium, and the control group was injected with saline of the same volume. The sham group only underwent thoracotomy operation in the absence of coronary ligation, reperfusion and drug injection. Within 10 d after the operation, echocardiography data was recorded including left ventricular end diastolic diameter （LVEDd）, left ventricular end diastolic volume （LVEDV）, left ventricular end systolic volume （LVESV）, and left ventricular ejection fraction （LVEF）. TUNEL staining was used to calculate myocardial apoptosis. Results LVEDd, LVESV and EF of 3 groups were significantly different （ F = 24. 469,20. 585,24. 767, all P 〈0.001 ）. Compared with the control group, the experimental group had significantly smaller LVEDd （P =0.017）. Apoptotic cells was （ 12.6 ＋ 2.6）/vision in the experimental group, while the control group was （18.4 ＋ 4. 1 ）/vision. Compared with the control group, less myocardial apoptosis was observed in the experimental group （P 〈 0. 001 ）. Conclusion BMSC as the potential to reverse myocardial remodeling and reduce myocardial apoptosis after myocardial infarction through paracrine mechanism.