山东大学学报(医学版)
山東大學學報(醫學版)
산동대학학보(의학판)
JOURNAL OF SHANDONG UNIVERSITY(HEALTH SCIENCES)
2015年
4期
31-36
,共6页
陈海丽%顾娇阳%张文静%袁琳冉%郑娟%袁中瑞
陳海麗%顧嬌暘%張文靜%袁琳冉%鄭娟%袁中瑞
진해려%고교양%장문정%원림염%정연%원중서
缺血性脑卒中%经典 Wnt 信号通路%β-catenin%血管新生%大鼠
缺血性腦卒中%經典 Wnt 信號通路%β-catenin%血管新生%大鼠
결혈성뇌졸중%경전 Wnt 신호통로%β-catenin%혈관신생%대서
Ischemic stroke%Canonical Wnt pathway%β-catenin%Angiogenesis%Rats
目的:研究缺血性脑卒中大鼠缺血周边脑组织的经典 Wnt 信号通路活性及干预该通路活性对缺血周边血管新生的影响。方法随机将50只雄性 Wistar 大鼠分为4组:假手术组(Sham 组,n =10),脑缺血对照组(MCAO 组,n =20),氯化锂干预组(LiCl 组,n =10),DKK1干预组(DKK1组,n =10)。免疫印迹法检测经典Wnt 信号通路成分,FITC-dextran 检测血管密度,多普勒血流仪检测血流量。结果脑缺血1 d 后,与 Sham 组相比,MCAO 组缺血周边脑组织细胞核蛋白及细胞浆蛋白中β-catenin 表达水平显著下降(P <0.05),7 d 时明显恢复,14 d 时接近正常水平。与 MCAO 组相比,LiCl 组β-catenin 表达水平及 p-GSK-3β/GSK-3β比值提高(P <0.05),并且缺血周边血管密度及血流量增加(P <0.05);DKK1组变化相反,β-catenin 表达水平及 p-GSK-3β/GSK-3β比值降低(P <0.05),血管密度及血流量下降(P <0.05)。结论经典 Wnt 信号通路参与调节缺血性脑卒中后缺血周边的血管新生。
目的:研究缺血性腦卒中大鼠缺血週邊腦組織的經典 Wnt 信號通路活性及榦預該通路活性對缺血週邊血管新生的影響。方法隨機將50隻雄性 Wistar 大鼠分為4組:假手術組(Sham 組,n =10),腦缺血對照組(MCAO 組,n =20),氯化鋰榦預組(LiCl 組,n =10),DKK1榦預組(DKK1組,n =10)。免疫印跡法檢測經典Wnt 信號通路成分,FITC-dextran 檢測血管密度,多普勒血流儀檢測血流量。結果腦缺血1 d 後,與 Sham 組相比,MCAO 組缺血週邊腦組織細胞覈蛋白及細胞漿蛋白中β-catenin 錶達水平顯著下降(P <0.05),7 d 時明顯恢複,14 d 時接近正常水平。與 MCAO 組相比,LiCl 組β-catenin 錶達水平及 p-GSK-3β/GSK-3β比值提高(P <0.05),併且缺血週邊血管密度及血流量增加(P <0.05);DKK1組變化相反,β-catenin 錶達水平及 p-GSK-3β/GSK-3β比值降低(P <0.05),血管密度及血流量下降(P <0.05)。結論經典 Wnt 信號通路參與調節缺血性腦卒中後缺血週邊的血管新生。
목적:연구결혈성뇌졸중대서결혈주변뇌조직적경전 Wnt 신호통로활성급간예해통로활성대결혈주변혈관신생적영향。방법수궤장50지웅성 Wistar 대서분위4조:가수술조(Sham 조,n =10),뇌결혈대조조(MCAO 조,n =20),록화리간예조(LiCl 조,n =10),DKK1간예조(DKK1조,n =10)。면역인적법검측경전Wnt 신호통로성분,FITC-dextran 검측혈관밀도,다보륵혈류의검측혈류량。결과뇌결혈1 d 후,여 Sham 조상비,MCAO 조결혈주변뇌조직세포핵단백급세포장단백중β-catenin 표체수평현저하강(P <0.05),7 d 시명현회복,14 d 시접근정상수평。여 MCAO 조상비,LiCl 조β-catenin 표체수평급 p-GSK-3β/GSK-3β비치제고(P <0.05),병차결혈주변혈관밀도급혈류량증가(P <0.05);DKK1조변화상반,β-catenin 표체수평급 p-GSK-3β/GSK-3β비치강저(P <0.05),혈관밀도급혈류량하강(P <0.05)。결론경전 Wnt 신호통로삼여조절결혈성뇌졸중후결혈주변적혈관신생。
Objective To investigate the involvement of canonical Wnt pathway in postischemic angiogenesis by using a rat model of ischemic stroke.Methods A total of 50 normal male Wistar rats were randomly divided into 4 groups:Sham group (n =10),cerebral ischemia group (MCAO group,n =20),LiCl treated group (LiCl group,n =10)and DKK1 treated group (DKK1 group,n =10).Western blotting was used to detect the expression of the elements of canonical Wnt pathway.FITC-dextran was used to detect the vessel volume,and Laser Doppler was used to measure the local cerebral blood flow in ischemic penumbral.Results The expressions of β-catenin in both the nuclear fraction and the cytoplasmic fraction in MCAO group decreased at 1 day post-cerebral ischemia,compared with Sham group (P <0.05).Nevertheless,the expressions of β-catenin in both the nuclear fraction and the cytoplasmic fraction at 7 day post-cerebral ischemia significantly increased (P <0.05),and reached normal level at 14 day post-cerebral ische-mia.Compared with MCAO group,the expressions of β-catenin in both the nuclear fraction and the cytoplasmic frac-tion LiCl group in were upregulated,accompanied with the elevated ratio of p-GSK-3β/GSK-3β,enhanced vessel vol-ume and local cerebral blood flow in ischemic penumbral(P <0.05).Compared with MCAO group,the expressions ofβ-catenin in DKK1 group in both the nuclear fraction and the cytoplasmic fraction were downregulated,accompanied with the decreased ratio of p-GSK-3β/GSK-3β,weakened vessel volume and local cerebral blood flow in ischemic penumbral(P <0.05).Conclusion The canonical Wnt pathway might be involved in postischemic angiogenesis.