大鼠p-MCAO后延迟给予长时间亚低温对NFkB和中性粒细胞的抑制.pdfVIP

after Or observed24hoursisehemia positivenegative)are by withnuclear ThenumberofinfilWated andthecells neurophils in two issmallerthanthat证 stainanti-NFkB the by p65antibody hypothermicgroups the fortheNFkB cell control numbers,one group．As p65immunopositive way ofvarianceshowsnOdifferencethethree the analysis among groups，although numbercontroltendstobe inthe group higher． Conclusion：ThemaIe activationandnuclear infiltration,NFkB neurophil in 24 after translocationthe a嘲in modelshours ischemi p-MCAO pcri-infarct 2and6hoursinhibit infiltration hypothermiadelayedby Can neuuophil Prolonged andNFkBnuclearwanslocation．Theinhibitionof isconsideredthe NFkB,which central of thereductionofinflammation relatorinflammatoryresponse，and may bethe the mechanismsof and probablyoneof neuroprotective delayedprolonged mild hypothermia． Key 4 2中文摘要 大鼠p-MCAO后延迟给予长时间亚低温对NFkB和中性粒细胞的抑制 低温在动物实验中已被证明具有强大的缺血后神经保护作用。常用的大脑局 部缺血的动物模型有两种：一过性大脑中动脉阻塞(toMCAO)和持续性大脑中 时间窗只有1小时。这限制了低温治疗的临床可行性。有一项报道在大鼠全脑一 过性缺血模型中，缺血后6小时给予48小时的低温可以减少CA