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目的探讨骨髓间充质干细胞(M SC s)移植治疗肺动脉高压(PAH)致右心室损伤的作用效果及其机制,观察M SC s移植后存活及转化情况。方法取SD大鼠骨髓,经贴壁筛选法体外培养并纯化M SC s,CM-D iI荧光染料标记后备用。将实验动物随机分为M SC s移植治疗组(M SC s组)、肺动脉高压模型组(PAH组)和生理盐水阴性对照组(对照组),每组10只。M SC s组和PAH组大鼠皮下注射野百合碱(MCT)建立肺动脉高压模型,对照组皮下注射等量0.9%生理盐水代替MCT;1周后M SC s组大鼠经舌下静脉注射M SC s细胞悬液1mL,对照组及PAH组注射等量低糖DM EM液。移植3周后荧光显微镜下观察M SC s体内存活及转化情况,并对右心室(RV)肥厚和右心室收缩压(RVSP)升高情况进行评价。结果 M SC s在大鼠体内能存活至少3周,荧光显微镜可见M SC s转化为血管平滑肌细胞,与PAH组相比,M SC s组RVSP及RV质量与体质量比值明显降低。结论静脉移植M SC s可明显减轻甚至逆转MCT诱导的肺动脉高压的进程,改善心功能及血流动力学指标,其机制可能是通过旁分泌作用实现的。
Objective To investigate the effects and mechanisms of bone marrow mesenchymal stem cells (M SCs) transplantation on right ventricular injury induced by pulmonary hypertension (PAH) and to observe the survival and transformation of M SCs after transplantation. Methods The bone marrow of SD rats was taken and cultured in vitro and purified by M SCs and CM-D il fluorescent dye. The experimental animals were randomly divided into M SCs transplantation group (M SCs group), pulmonary hypertensive model group (PAH group) and normal saline negative control group (control group), 10 rats in each group. Rats in M SC s group and PAH group were injected subcutaneously with monocrotaline (MCT) to establish a model of pulmonary hypertension, and the control group was injected subcutaneously with 0.9% normal saline instead of MCT. After 1 week, M SCs rats were injected sublingually with M SC s cell suspension 1mL, the control group and PAH group were injected with the same amount of low-glucose DM EM solution. Three weeks after transplantation, the survival and transformation of M SCs in vivo were observed under a fluorescence microscope, and the right ventricular (RV) hypertrophy and right ventricular systolic pressure (RVSP) were evaluated. Results M SC s could survive for at least 3 weeks in rats. M SC s was converted to vascular smooth muscle cells by fluorescence microscopy. Compared with PAH group, the ratio of RVSP and RV mass to body mass in M SCs group was significantly lower. Conclusion Intravenous transplantation of SCCs can significantly reduce or even reverse the process of MCT-induced pulmonary hypertension and improve cardiac function and hemodynamic parameters. The mechanism may be through paracrine effect.