卒中与神经疾病
卒中與神經疾病
졸중여신경질병
Stroke and Nervous Diseases
2015年
5期
273-276
,共4页
脑缺血%缺血后处理%缺血再灌注损伤%Toll 样受体 2
腦缺血%缺血後處理%缺血再灌註損傷%Toll 樣受體 2
뇌결혈%결혈후처리%결혈재관주손상%Toll 양수체 2
Brain ischemia%Ischemic postconditioning%Ischemic/reperfusion%TLR2
目的：探讨缺血后处理对大鼠局灶性脑缺血再灌注时 Toll 样受体2(TLR2)表达的影响。方法成年雄性 SD 大鼠90只，分为假手术组、缺血再灌注组、缺血后处理组各30只；用线栓法建立局灶性大脑中动脉闭塞模型(MCAO)，随机分为假手术组(sham)、缺血再灌注组(I/R)、缺血后处理组(IPC)，分别于再灌注24、48、72 h后留取大脑皮质组织；采用 Longa 的等级评分法进行神经行为学评分，免疫组化和蛋白质印记(Western blot)法检测 TLR2蛋白的表达水平，逆转录-聚合酶链反应(RT-PCR)检测 TLR2 mRNA 表达水平。结果(1)缺血后处理组大鼠神经行为学评分明显改善；(2)缺血再灌注组 TLR2蛋白在再灌注24、48、72 h表达水平明显升高(P <0.05)；缺血后处理组 TLR2蛋白表达在各时间点均减少(P <0.05)；TLR2 mRNA 的表达趋势与蛋白表达基本一致。结论缺血后处理可以降低 TLR2表达水平，这可能是其脑保护作用的部分机制之一。
目的：探討缺血後處理對大鼠跼竈性腦缺血再灌註時 Toll 樣受體2(TLR2)錶達的影響。方法成年雄性 SD 大鼠90隻，分為假手術組、缺血再灌註組、缺血後處理組各30隻；用線栓法建立跼竈性大腦中動脈閉塞模型(MCAO)，隨機分為假手術組(sham)、缺血再灌註組(I/R)、缺血後處理組(IPC)，分彆于再灌註24、48、72 h後留取大腦皮質組織；採用 Longa 的等級評分法進行神經行為學評分，免疫組化和蛋白質印記(Western blot)法檢測 TLR2蛋白的錶達水平，逆轉錄-聚閤酶鏈反應(RT-PCR)檢測 TLR2 mRNA 錶達水平。結果(1)缺血後處理組大鼠神經行為學評分明顯改善；(2)缺血再灌註組 TLR2蛋白在再灌註24、48、72 h錶達水平明顯升高(P <0.05)；缺血後處理組 TLR2蛋白錶達在各時間點均減少(P <0.05)；TLR2 mRNA 的錶達趨勢與蛋白錶達基本一緻。結論缺血後處理可以降低 TLR2錶達水平，這可能是其腦保護作用的部分機製之一。
목적：탐토결혈후처리대대서국조성뇌결혈재관주시 Toll 양수체2(TLR2)표체적영향。방법성년웅성 SD 대서90지，분위가수술조、결혈재관주조、결혈후처리조각30지；용선전법건립국조성대뇌중동맥폐새모형(MCAO)，수궤분위가수술조(sham)、결혈재관주조(I/R)、결혈후처리조(IPC)，분별우재관주24、48、72 h후류취대뇌피질조직；채용 Longa 적등급평분법진행신경행위학평분，면역조화화단백질인기(Western blot)법검측 TLR2단백적표체수평，역전록-취합매련반응(RT-PCR)검측 TLR2 mRNA 표체수평。결과(1)결혈후처리조대서신경행위학평분명현개선；(2)결혈재관주조 TLR2단백재재관주24、48、72 h표체수평명현승고(P <0.05)；결혈후처리조 TLR2단백표체재각시간점균감소(P <0.05)；TLR2 mRNA 적표체추세여단백표체기본일치。결론결혈후처리가이강저 TLR2표체수평，저가능시기뇌보호작용적부분궤제지일。
Objective To investigate the protective effect of ischemic postconditioning by examining the express of toll-like receptor 2 (TLR2)in cerebral ischemic reperfusion injury(I/R).Methods SD rats model of focal ischemic reperfusion was induced by intraluminal middle cerebral artery occlusion(MCAO)with a nylon monofilament suture.Ischemic animals were randomly assigned to 3 groups:sham group(n=30),I/R group (n=30)and IPC group (n=30).Each group was divided into 3 subgroups by the different times after reperfu-sion (t=24 h,t=48 h,t=72 h).In IPC group,animals were further subjected to postconditioning (3 cycles of 30s ischemia and 30s reperfusion)after MCAO.Neurologic scores and infarct volumes were assessed at 24, 48 and 72 hours.TLR2 was examined by immunohistochemistry,Western blot and RT-PCR.Results IPC treatment improved neurologic scores and reduced infarct volumes compared with the I/R group.Compared with the sham group,the expression of TLR2 increased in the rats undergoing I/R procedure.The level of TLR2 significantly reduced in ischemic postconditioning group.Conclusions Ischemic postconditioning can re-duce the expression of TLR2 which may be related to neuroprotective effects.
