摘要
目的探讨静脉移植脂肪组织基质血管组分(SVF)对心力衰竭大鼠心肌重构的影响及可能机制。方法体外分离培养并标记SD大鼠SVF,24只SD大鼠随机分为对照组、心力衰竭组、SVF治疗组(n=8),每周2次连续4周阿霉素腹腔注射15mg/kg建立大鼠心力衰竭模型;SVF治疗组阴茎静脉注射(移植)SVF(0.5mL,107 L-1细胞),其他2组注射等量PBS液。移植4周后,多导生理仪测大鼠心功能,心肌冰冻切片荧光显微镜检测SVF归巢;苦味酸天狼星红染色检测心肌胶原含量,计算心肌胶原容积分数(CVF);ELISA法测定血浆Ⅰ型前胶原羧基端肽(PICP)、Ⅲ型前胶原氨基端肽(PⅢNP)水平。结果与对照组比较,心力衰竭组和SVF治疗组左心室收缩末期压力(LVSP)、左心室收缩压力最大上升速度(+dp/dtmax)、左心室舒张压力最大下降速度(-dp/dtmax)降低(P<0.05或P<0.01),CVF、血浆PICP和PⅢNP升高(P<0.05或P<0.01);与心力衰竭组比较,SVF治疗组LVSP、+dp/dtmax、-dp/dtmax升高(P<0.05),CVF、血浆PICP和PⅢNP降低(P<0.05)。结论 SVF移植可降低阿霉素诱导的心力衰竭大鼠体内胶原合成,减少心肌组织基质胶原沉积,抑制心肌重构,改善心功能。
Objective To investigate the effects and possible mechanism of transplantation of adi-pose stromal vascular fraction （SVF） on myocardial remodeling of heart failure induced by Adriamycin in rat . Method SVF were isolated from Sprague-Dawley （SD） rat adipose tissue and marked with green fluorescent protein （GFP） in vitro . 24 SD rats were randomized into 3 groups （n=8）：Normal Control , Heart Failure and SVF Treated . Adriamycin 15 mg/kg was intraperitoneally injected twice a week for 4 weeks to induce heart failure rat models . SVF cells （0 .5 mL ,107 L -1 ） was injected via penis vein of SVF Treated group rats ,and PBS vehicle was injected in the same way in the contral groups . Rat cardiac function was determined by poly physiography via cardiac catheterization 4 weeks later . SVF were dem-onstrated in the myocardium by frozen section fluorescence microscope . Then ,histopathological with picrosirius stains and procollagen typeⅠ carboxylpropetide （PICP）/procollagentypeⅢ N-terminalpropetide （PⅢ NP） ELISA examination were also performed . Results Compared with Normal Contral group , both Heart Failure group and SVF Treated group LVSP ,＋dp/dtmax and -dp/dtmax decreased（P〈0 .05~0 .01） ,while CVF ,PICP and PⅢNP（P〈0 .05~0 .01）increased in blood plasma ;Compared with Heart Failure group ,SVF transplantation increased LVSP ,＋dp/dtmax ,-dp/dtmax（P〈0 .05） ,but decreased CVF ,PICP ,and PⅢNP（P〈0 .05） in blood plasma . Conclusions The transplantation of SVF inhibited myocardial remodeling by decreasing myocardial collagen synthesis and deposition in the rat models of adri-amycin-induced heart failure ,and improved the cardiac function .
出处
《福建医科大学学报》
2013年第5期284-287,共4页
Journal of Fujian Medical University
基金
福建省卫生厅青年科研基金(2009-2-14)
福建医科大学苗圃科研基金(2010MP008)
