上海交通大学学报(医学版)
上海交通大學學報(醫學版)
상해교통대학학보(의학판)
JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY(MEDICAL SCIENCE)
2009年
6期
633-636
,共4页
储光%严轶文%张治%王治%戴秋艳
儲光%嚴軼文%張治%王治%戴鞦豔
저광%엄질문%장치%왕치%대추염
ICAM-1%干细胞%冠心病%心肌梗死
ICAM-1%榦細胞%冠心病%心肌梗死
ICAM-1%간세포%관심병%심기경사
intercellular adhesion molecule-1%stem cells%coronary artery disease%myocardial infarction
目的 观察细胞间黏附分子-1(ICAM-1)在大鼠急性心肌梗死后外周血成体干细胞上调过程中的作用.方法 16只SD大鼠开胸结扎左前降支(LAD)近端,制作急性心肌梗死模型,分为对照组(n=8)和实验组(n=8).另取2只大鼠的心脏做正常心肌组织切片对照.实验组从尾静脉注入大鼠ICAM-1单克隆抗体,对照组未注射任何试剂.两组大鼠分别在术后1、3、7和14 d抽取尾静脉血.采用ELISA法检测血清中ICAM-1浓度变化,流式细胞仪检测外周血中CD34细胞阳性率,比较两组各时间点ICAM-1浓度和CD34细胞阳性率的变化.结果 实验组外周血中ICAM-1浓度较对照组明显下降,第7天达到最低值(59.01±2.22)pg/mL;其中第7、14天时与对照组比较差异有统计学意义(P<0.01).实验组外周血中CD34细胞阳性率较对照组明显上升,第7天时达到最高值(12±2.11)%;其中第3、7、14天时与对照组比较差异均有统计学意义(P<0.05或P<0.01).结论 初步显示ICAM-1在大鼠急性心肌梗死后抑制了外周血成体干细胞的上调.
目的 觀察細胞間黏附分子-1(ICAM-1)在大鼠急性心肌梗死後外週血成體榦細胞上調過程中的作用.方法 16隻SD大鼠開胸結扎左前降支(LAD)近耑,製作急性心肌梗死模型,分為對照組(n=8)和實驗組(n=8).另取2隻大鼠的心髒做正常心肌組織切片對照.實驗組從尾靜脈註入大鼠ICAM-1單剋隆抗體,對照組未註射任何試劑.兩組大鼠分彆在術後1、3、7和14 d抽取尾靜脈血.採用ELISA法檢測血清中ICAM-1濃度變化,流式細胞儀檢測外週血中CD34細胞暘性率,比較兩組各時間點ICAM-1濃度和CD34細胞暘性率的變化.結果 實驗組外週血中ICAM-1濃度較對照組明顯下降,第7天達到最低值(59.01±2.22)pg/mL;其中第7、14天時與對照組比較差異有統計學意義(P<0.01).實驗組外週血中CD34細胞暘性率較對照組明顯上升,第7天時達到最高值(12±2.11)%;其中第3、7、14天時與對照組比較差異均有統計學意義(P<0.05或P<0.01).結論 初步顯示ICAM-1在大鼠急性心肌梗死後抑製瞭外週血成體榦細胞的上調.
목적 관찰세포간점부분자-1(ICAM-1)재대서급성심기경사후외주혈성체간세포상조과정중적작용.방법 16지SD대서개흉결찰좌전강지(LAD)근단,제작급성심기경사모형,분위대조조(n=8)화실험조(n=8).령취2지대서적심장주정상심기조직절편대조.실험조종미정맥주입대서ICAM-1단극륭항체,대조조미주사임하시제.량조대서분별재술후1、3、7화14 d추취미정맥혈.채용ELISA법검측혈청중ICAM-1농도변화,류식세포의검측외주혈중CD34세포양성솔,비교량조각시간점ICAM-1농도화CD34세포양성솔적변화.결과 실험조외주혈중ICAM-1농도교대조조명현하강,제7천체도최저치(59.01±2.22)pg/mL;기중제7、14천시여대조조비교차이유통계학의의(P<0.01).실험조외주혈중CD34세포양성솔교대조조명현상승,제7천시체도최고치(12±2.11)%;기중제3、7、14천시여대조조비교차이균유통계학의의(P<0.05혹P<0.01).결론 초보현시ICAM-1재대서급성심기경사후억제료외주혈성체간세포적상조.
Objective To investigate the role of intercellular adhesion molecule-1 (ICAM-1) in the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats. Methods The models of acute myocardial infarction were established in 16 rata by ligation of left anterior descending branch of left coronary artery through chest incision, and the animal were divided into control group(n=8) and experiment group (n=8). The hearts of another 2 rats were obtained for normal myocardial tissue sections as controls. Monoclonal antibody of ICAM-1 was infused from the caudal vein in experimental group, and no invervention was conducted for control group. Blood samples were obtained from caudal vein on the first, third, seventh and fourteenth day after operation in these two groups. Serum concentration of ICAM-1 was measured by ELISA, positive rate of CD34 cells in peripheral blood was detected by flow cytometry, and the parameters of concentration of ICAM-1 and positive rate of CD34 cells at each time point were compared between groups. Results The concentration of ICAM-1 in peripheral blood of experiment group reached the lowest of (59.01±2.22) pg/mL on the seventh day. The concentrations of ICAM-1 in peripheral blood of experiment group were lower than those in control group, and there were significant differences between these two groups on the seventh and fourteenth day(P < 0.01). The positive rate of CD34 cells in peripheral blood of experiment group reached the highest of (12±2.11)% on the seventh day. The positive rates of CD34 cells in peripheral blood of experiment group were higher than those in control group, and there were significant differences between these two groups on the third, seventh and fourteenth day(P<0.05 or P<0.01). Conclusion ICAM-1 can inhibit the up-regulation of peripheral blood somatic stem cells after acute myocardial infarction in rats.