国际脑血管病杂志
國際腦血管病雜誌
국제뇌혈관병잡지
INTERNATIONAL JOURNAL OF CEREBROVASCULAR DISEASES
2012年
11期
843-848
,共6页
脑缺血%受体,肿瘤坏死因子,Ⅰ型%肿瘤坏死因子-α%新生血管化,生理性%神经发生%炎症%小鼠
腦缺血%受體,腫瘤壞死因子,Ⅰ型%腫瘤壞死因子-α%新生血管化,生理性%神經髮生%炎癥%小鼠
뇌결혈%수체,종류배사인자,Ⅰ형%종류배사인자-α%신생혈관화,생이성%신경발생%염증%소서
Brain Ischemia%Receptors,Tumor Necrosis Factor,Type Ⅰ%Tumor Necrosis Factor-α%Neurogenesis%Neovascularization,Physiologic%Inflammation%Mice
目的 探讨肿瘤坏死因子受体1(tumor necrosis factor receptor 1,TNFRI)在脑缺血小鼠血管发生和神经发生中的作用.方法 24只野生型和24只TNFR1基因敲除小鼠随机分为假手术组和局灶性脑缺血组(每组12只),在脑缺血和假手术后第3天腹腔注射5-溴脱氧尿苷(5-bromodeoxyuridine,BrdU).脑缺血后第7和第28天,应用葡萄糖载体-1(glucose transporter-I,Glut-1)/BrdU免疫荧光染色双标记评价梗死周围区新生血管,标记BrdU检测侧脑室下区神经干细胞增殖,分别采用双皮质素(doublecortin,DCX)/3rdU和神经元核抗原(neuronal nuclei antigen,NeuN)/BrdU双标记检测神经干细胞迁移和存活.结果 在正常情况下,野生型(418.000±28.404)和TNFR1基因敲除(528.000±60.597)小鼠血管发生和室管膜下区(subventricular zone,SVZ)的BrdU阳性细胞数无显著性差异(t=-1.644,P=0.131)；脑缺血后第7天,TNFR1基因敲除小鼠Glut-I/BrdU阳性细胞数量显著少于野生型小鼠(14.833±2.182对27.500±4.209；t=2.672,P=0.023),DCX/BrdU阳性细胞数也显著少于野生型小鼠(163.000±11.106对257.168±12.213；t=5.705,P=0.000)；脑缺血后第28天,TNFR1基因敲除小鼠NeuN/BrdU阳性细胞数显著少于野生型小鼠(6.000±0.577对11.000±1.571;t =2.988,P=0.014).结论 TNFR1可能在脑缺血后期的神经血管再生中起着促进作用.
目的 探討腫瘤壞死因子受體1(tumor necrosis factor receptor 1,TNFRI)在腦缺血小鼠血管髮生和神經髮生中的作用.方法 24隻野生型和24隻TNFR1基因敲除小鼠隨機分為假手術組和跼竈性腦缺血組(每組12隻),在腦缺血和假手術後第3天腹腔註射5-溴脫氧尿苷(5-bromodeoxyuridine,BrdU).腦缺血後第7和第28天,應用葡萄糖載體-1(glucose transporter-I,Glut-1)/BrdU免疫熒光染色雙標記評價梗死週圍區新生血管,標記BrdU檢測側腦室下區神經榦細胞增殖,分彆採用雙皮質素(doublecortin,DCX)/3rdU和神經元覈抗原(neuronal nuclei antigen,NeuN)/BrdU雙標記檢測神經榦細胞遷移和存活.結果 在正常情況下,野生型(418.000±28.404)和TNFR1基因敲除(528.000±60.597)小鼠血管髮生和室管膜下區(subventricular zone,SVZ)的BrdU暘性細胞數無顯著性差異(t=-1.644,P=0.131)；腦缺血後第7天,TNFR1基因敲除小鼠Glut-I/BrdU暘性細胞數量顯著少于野生型小鼠(14.833±2.182對27.500±4.209；t=2.672,P=0.023),DCX/BrdU暘性細胞數也顯著少于野生型小鼠(163.000±11.106對257.168±12.213；t=5.705,P=0.000)；腦缺血後第28天,TNFR1基因敲除小鼠NeuN/BrdU暘性細胞數顯著少于野生型小鼠(6.000±0.577對11.000±1.571;t =2.988,P=0.014).結論 TNFR1可能在腦缺血後期的神經血管再生中起著促進作用.
목적 탐토종류배사인자수체1(tumor necrosis factor receptor 1,TNFRI)재뇌결혈소서혈관발생화신경발생중적작용.방법 24지야생형화24지TNFR1기인고제소서수궤분위가수술조화국조성뇌결혈조(매조12지),재뇌결혈화가수술후제3천복강주사5-추탈양뇨감(5-bromodeoxyuridine,BrdU).뇌결혈후제7화제28천,응용포도당재체-1(glucose transporter-I,Glut-1)/BrdU면역형광염색쌍표기평개경사주위구신생혈관,표기BrdU검측측뇌실하구신경간세포증식,분별채용쌍피질소(doublecortin,DCX)/3rdU화신경원핵항원(neuronal nuclei antigen,NeuN)/BrdU쌍표기검측신경간세포천이화존활.결과 재정상정황하,야생형(418.000±28.404)화TNFR1기인고제(528.000±60.597)소서혈관발생화실관막하구(subventricular zone,SVZ)적BrdU양성세포수무현저성차이(t=-1.644,P=0.131)；뇌결혈후제7천,TNFR1기인고제소서Glut-I/BrdU양성세포수량현저소우야생형소서(14.833±2.182대27.500±4.209；t=2.672,P=0.023),DCX/BrdU양성세포수야현저소우야생형소서(163.000±11.106대257.168±12.213；t=5.705,P=0.000)；뇌결혈후제28천,TNFR1기인고제소서NeuN/BrdU양성세포수현저소우야생형소서(6.000±0.577대11.000±1.571;t =2.988,P=0.014).결론 TNFR1가능재뇌결혈후기적신경혈관재생중기착촉진작용.
Objective To investigate the effect of tumor necrosis factor receptor 1 (TNFR1) in angiogenesis and neurogenesis during cerebral ischemia in mice.Methods Twenty-four wild-type and 24 TNFR1 knockout mice were randomly divided into either a sham operation group or a focal cerebral ischemia group (n =12 in each group).5-bromodeoxyuridine (BrdU) was injected intraperitoneally at day 3 after cerebral ischemia and sham operation.At day 7 and 28 after cerebral ischemia,the double-label immunofluorescence staining of glucose transporter-1(Glut-1)/BrdU was used to evaluate the angiogenesis surrounding the areas of infarction.A labeled BrdU was used to detect the neural stem cell proliferation in the subventricular zone.Double-labeled doublecortin (DCX)/BrdU and neuronal nuclei antigen (NeuN)/BrdU were used to detect the migration and survival of neural stem cells,respectively.Results Under the normal condition,there was no significant difference in angiogenesis and the number of BrdU-positive cells in the subependymal zone (SVZ) between the wild-type (418.000 ± 28.404) and TNFR1 knockout (528.000 ± 60.597) mice (t =-1.644,P =0.131).At day 7 after cerebral ischemia,the number of Glut-1/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wild-type mice (14.833 ± 2.182 vs.27.5 ± 4.209) (t =2.672,P =0.023),and the number of DCX/B3rdU-positive cells was also significantly less than that in the wild-type mice (163.000 ± 11.106 vs.257.168 ± 12.213) (t =5.705,P =0.000).At day 28 after cerebral ischemia,the number of NeuN/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wildtype mice (6.000 ± 0.577 vs.11.000± 1.571) (t=2.988,P=0.014).Conclusions TNFR1 may play a promoting role in the neurovascular reggeneration in late cerebral ischemia.
