中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
8期
1371-1375
,共5页
耿志敏%王珏%范鸿洋%郑哲%翁家侃%孙成超%褚茂平
耿誌敏%王玨%範鴻洋%鄭哲%翁傢侃%孫成超%褚茂平
경지민%왕각%범홍양%정철%옹가간%손성초%저무평
骨髓间充质干细胞%微粒%心肌梗死%血管新生
骨髓間充質榦細胞%微粒%心肌梗死%血管新生
골수간충질간세포%미립%심기경사%혈관신생
Bonemarrowmesenchymalstemcells%Microparticles%Myocardialinfarction%Angiogenesis
目的:观察骨髓间充质干细胞膜微粒(MSC-MPs)对大鼠心肌梗死后血管新生以及心功能的影响。方法:提取Sprague-Dawley大鼠MSCs并培养,在低氧低营养条件下培养72 h,以诱导细胞凋亡释放MSC-MPs。将培养上清液超速离心获取MSC-MPs,透射电镜下观察其大小及形态,并用流式细胞术分析其表型。建立SD大鼠心肌梗死模型,心肌梗死边缘区注射膜微粒及对照试剂。超声心动图检测心功能,Masson染色检测心梗面积,免疫组织化学染色技术检测梗死边缘区血管α-平滑肌肌动蛋白和von Willebrand因子以确定血管新生情况,real-time PCR检测心梗组织中血管内皮生长因子(VEGF)表达变化。结果:MSCs凋亡后可以释放膜微粒,MSC-MPs来自MSCs,直径为100~1000 nm。心肌梗死大鼠心肌内注射MSC-MPs后,第7天和第28天时心功能明显改善,第28 d 时心梗面积比对照组减小,新生血管密度明显增加,第7天时心梗组织VEGF的表达增加。结论:MSC-MPs可以促进大鼠心肌梗死后的血管新生,改善心功能。
目的:觀察骨髓間充質榦細胞膜微粒(MSC-MPs)對大鼠心肌梗死後血管新生以及心功能的影響。方法:提取Sprague-Dawley大鼠MSCs併培養,在低氧低營養條件下培養72 h,以誘導細胞凋亡釋放MSC-MPs。將培養上清液超速離心穫取MSC-MPs,透射電鏡下觀察其大小及形態,併用流式細胞術分析其錶型。建立SD大鼠心肌梗死模型,心肌梗死邊緣區註射膜微粒及對照試劑。超聲心動圖檢測心功能,Masson染色檢測心梗麵積,免疫組織化學染色技術檢測梗死邊緣區血管α-平滑肌肌動蛋白和von Willebrand因子以確定血管新生情況,real-time PCR檢測心梗組織中血管內皮生長因子(VEGF)錶達變化。結果:MSCs凋亡後可以釋放膜微粒,MSC-MPs來自MSCs,直徑為100~1000 nm。心肌梗死大鼠心肌內註射MSC-MPs後,第7天和第28天時心功能明顯改善,第28 d 時心梗麵積比對照組減小,新生血管密度明顯增加,第7天時心梗組織VEGF的錶達增加。結論:MSC-MPs可以促進大鼠心肌梗死後的血管新生,改善心功能。
목적:관찰골수간충질간세포막미립(MSC-MPs)대대서심기경사후혈관신생이급심공능적영향。방법:제취Sprague-Dawley대서MSCs병배양,재저양저영양조건하배양72 h,이유도세포조망석방MSC-MPs。장배양상청액초속리심획취MSC-MPs,투사전경하관찰기대소급형태,병용류식세포술분석기표형。건립SD대서심기경사모형,심기경사변연구주사막미립급대조시제。초성심동도검측심공능,Masson염색검측심경면적,면역조직화학염색기술검측경사변연구혈관α-평활기기동단백화von Willebrand인자이학정혈관신생정황,real-time PCR검측심경조직중혈관내피생장인자(VEGF)표체변화。결과:MSCs조망후가이석방막미립,MSC-MPs래자MSCs,직경위100~1000 nm。심기경사대서심기내주사MSC-MPs후,제7천화제28천시심공능명현개선,제28 d 시심경면적비대조조감소,신생혈관밀도명현증가,제7천시심경조직VEGF적표체증가。결론:MSC-MPs가이촉진대서심기경사후적혈관신생,개선심공능。
AIM:Toobservetheeffectsofmicroparticlesderivedfrombonemarrowmesenchymalstemcells ( MSC-MPs) on angiogenesis and cardiac function in a rat myocardial infarction model .METHODS:MSCs were obtained from Sprague-Dawley rats.MSCs were treated under serum-free condition in hypoxia for 72 h, and the microparticles were isolated from the supernatants .The phenotypic profile of MSC-MPs was determined by bead-based flow cytometry and the morphology was observed under a transmission electron microscope .The rat myocardial infarction model was established . The cardiac function was evaluated by echocardiography after the intramyocardial injection of MSC -MPs.The myocardial in-farct size was observed by Masson staining .The blood vessel density in the peri-infarcted area was measured using immuno-histochemical staining for von Willebrand factor and α-smooth muscle actin.The expression of vascular endothelial growth factor ( VEGF) was analyzed by real-time PCR.RESULTS: Apoptotic MSCs released a large quantity of microparticles which were phenotypically similar to the parent MSCs and 100~1 000 nm in diameter.The cardiac functions of myocardial infarction rat model were improved at 7 d and 28 d after intramyocardial injection of MSC-MPs compared with control group . The myocardial infarct size was reduced and angiogenesis was promoted significantly in the infarcted heart injected with MSC-MPs 28 d after treatment .MSC-MPs treatment also increased the expression level of VEGF within 7 d.CONCLU-SION:MSC-MPs protect cardiac tissue from ischemic injury and improve cardiac function by promoting angiogenesis after myocardial infarction .