中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
10期
1579-1584
,共6页
戚金威%程景林%周姝%李景荣%李雪翔%杨琴%张浩%万俊%王育林%张立新%陈赟赟%习秀霞%叶丽%唐茜%徐凤%江洋%胡乐义%刘泽岩
慼金威%程景林%週姝%李景榮%李雪翔%楊琴%張浩%萬俊%王育林%張立新%陳赟赟%習秀霞%葉麗%唐茜%徐鳳%江洋%鬍樂義%劉澤巖
척금위%정경림%주주%리경영%리설상%양금%장호%만준%왕육림%장립신%진빈빈%습수하%협려%당천%서봉%강양%호악의%류택암
干细胞%骨髓干细胞%低氧诱导因子1α%骨髓间充质干细胞%血管内皮生长因子%心肌梗死%动员%寡核苷酸
榦細胞%骨髓榦細胞%低氧誘導因子1α%骨髓間充質榦細胞%血管內皮生長因子%心肌梗死%動員%寡覈苷痠
간세포%골수간세포%저양유도인자1α%골수간충질간세포%혈관내피생장인자%심기경사%동원%과핵감산
stem cells%mesenchymal stem cells%hypoxia-inducible factor 1,alpha subunit%myocardial infarction
背景：设想通过增加自体干细胞动员达到有效修复心脏缺血区的目的，因此找到可利用的特异而有效的干细胞动员剂成为关键所在。
<br> 目的：观察心肌梗死时低氧诱导因子1α表达对骨髓间充质干细胞动员的影响。
<br> 方法：将90只远交群SD大鼠结扎冠状动脉前降支建立急性心肌梗死模型，随机分为3组：低氧诱导因子1α反义寡核苷酸组给予低氧诱导因子1α反义寡核苷酸干预抑制大鼠梗死缺血组织的低氧诱导因子1α的表达，低氧诱导因子1α错义寡核苷酸组和对照组分别给予等量低氧诱导因子1α错义寡核苷酸和生理盐水。
<br> 结果与结论：造模后30 h、7 d，对照组外周血骨髓间充质干细胞计数及血浆血管内皮生长因子水平与低氧诱导因子1α错义寡核苷酸组相近，但明显高于低氧诱导因子1α反义寡核苷酸组。造模后7 d，对照组心肌缺血组织低氧诱导因子1α蛋白、血管内皮生长因子蛋白及mRNA表达与低氧诱导因子1α错义寡核苷酸组相近，但明显高于低氧诱导因子1α反义寡核苷酸组。造模后7，14，28 d，对照组心肌缺血组织切片毛细血管密度分析与低氧诱导因子1α错义寡核苷酸组相近，明显高于低氧诱导因子1α反义寡核苷酸组。说明大鼠急性心肌梗死后高表达的低氧诱导因子1α与骨髓间充质干细胞动员、启动一系列心肌组织自我修复过程有因果关系。
揹景：設想通過增加自體榦細胞動員達到有效脩複心髒缺血區的目的，因此找到可利用的特異而有效的榦細胞動員劑成為關鍵所在。
<br> 目的：觀察心肌梗死時低氧誘導因子1α錶達對骨髓間充質榦細胞動員的影響。
<br> 方法：將90隻遠交群SD大鼠結扎冠狀動脈前降支建立急性心肌梗死模型，隨機分為3組：低氧誘導因子1α反義寡覈苷痠組給予低氧誘導因子1α反義寡覈苷痠榦預抑製大鼠梗死缺血組織的低氧誘導因子1α的錶達，低氧誘導因子1α錯義寡覈苷痠組和對照組分彆給予等量低氧誘導因子1α錯義寡覈苷痠和生理鹽水。
<br> 結果與結論：造模後30 h、7 d，對照組外週血骨髓間充質榦細胞計數及血漿血管內皮生長因子水平與低氧誘導因子1α錯義寡覈苷痠組相近，但明顯高于低氧誘導因子1α反義寡覈苷痠組。造模後7 d，對照組心肌缺血組織低氧誘導因子1α蛋白、血管內皮生長因子蛋白及mRNA錶達與低氧誘導因子1α錯義寡覈苷痠組相近，但明顯高于低氧誘導因子1α反義寡覈苷痠組。造模後7，14，28 d，對照組心肌缺血組織切片毛細血管密度分析與低氧誘導因子1α錯義寡覈苷痠組相近，明顯高于低氧誘導因子1α反義寡覈苷痠組。說明大鼠急性心肌梗死後高錶達的低氧誘導因子1α與骨髓間充質榦細胞動員、啟動一繫列心肌組織自我脩複過程有因果關繫。
배경：설상통과증가자체간세포동원체도유효수복심장결혈구적목적，인차조도가이용적특이이유효적간세포동원제성위관건소재。
<br> 목적：관찰심기경사시저양유도인자1α표체대골수간충질간세포동원적영향。
<br> 방법：장90지원교군SD대서결찰관상동맥전강지건립급성심기경사모형，수궤분위3조：저양유도인자1α반의과핵감산조급여저양유도인자1α반의과핵감산간예억제대서경사결혈조직적저양유도인자1α적표체，저양유도인자1α착의과핵감산조화대조조분별급여등량저양유도인자1α착의과핵감산화생리염수。
<br> 결과여결론：조모후30 h、7 d，대조조외주혈골수간충질간세포계수급혈장혈관내피생장인자수평여저양유도인자1α착의과핵감산조상근，단명현고우저양유도인자1α반의과핵감산조。조모후7 d，대조조심기결혈조직저양유도인자1α단백、혈관내피생장인자단백급mRNA표체여저양유도인자1α착의과핵감산조상근，단명현고우저양유도인자1α반의과핵감산조。조모후7，14，28 d，대조조심기결혈조직절편모세혈관밀도분석여저양유도인자1α착의과핵감산조상근，명현고우저양유도인자1α반의과핵감산조。설명대서급성심기경사후고표체적저양유도인자1α여골수간충질간세포동원、계동일계렬심기조직자아수복과정유인과관계。
BACKGROUND:Increasing autologous stem cellmobilization is conceived to achieve effectively repair of cardiac ischemic injury. Therefore, it is important to seek a specific and effective mobilization agent. OBJECTIVE:To observe the effects of hypoxia-inducible factor-1α(HIF-1α) on bone marrow mesenchymal stem cellmobilization in myocardial infarction. METHODS:Left anterior descending artery was ligated to establish a rat model of acute myocardial infarction in 90 outbreeding Sprague-Dawley rats, and then the models were randomly divided into three groups. In HIF-1α-antisense oligonucleotide (ASODN) group, HIF-1α-ASODN was infused into the tail vein to restrain the expression of HIF-1αin infarcted ischemic tissue. In HIF-1α-missense oligonucleotide (MSODN) group or control group, an equal volume of HIF-1α-MSODN or saline was injected. RESULTS AND CONCLUSION:After 30 hours and 7 days of modeling, the number of bone marrow mesenchymal stem cells and expression of vascular endothelial growth factor in the peripheral blood of the control group were similar to the HIF-1α-MSODN group, but significantly higher than the HIF-1α-ASODN group. After 7 days of modeling, the expressions of HIF-1αprotein, vascular endothelial growth factor protein and mRNA in the ischemic myocardial tissues of the control group were similar to the HIF-1α-MSODN group, but significantly higher than the HIF-1α-ASODN group. After 7, 14 and 28 days of modeling, the capil ary density in the ischemic myocardial tissues of the control group was similar to the HIF-1α-MSODN group, but significantly higher than the HIF-1α-ASODN group. These findings indicate that after acute myocardial infarction, high expression of HIF-1αexhibits a causal relationship with mobilization of bone marrow mesenchymal stem cells, initiating a series of self-healing process of myocardial tissues.
