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目的观察高压氧(HBO)对脑缺血再灌注大鼠核因子(NF-κB)及细胞间粘附分子-1(ICAM-1)表达的影响。方法采用改良栓线法阻断大脑中动脉建立大鼠局灶性脑缺血再灌注模型。将72只大鼠随机分为脑缺血再灌注组(CIR组)、脑缺血再灌注加高压氧治疗组(HBO组)和假手术对照组(SO组),分别观察各组大鼠脑梗死灶的大小,并用免疫组织化学染色检测再灌注24h、48h、72h、120h时相点大鼠脑组织NFκB和ICAM1表达的变化。结果HBO组大脑氯化三苯四氮唑(TTC)染色后梗死体积小于CIR组,差异有统计学意义(P<0.05)。再灌注各时相点CIR组和HBO组的NFκB及ICAM1表达均显著高于SO组(P<0.01);HBO组大鼠再灌注各时相点NF-κB及ICAM-1表达均显著低于CIR组(P<0.05)。结论脑缺血再灌注后NF-κB和ICAM-1明显上调,HBO治疗可以减轻大鼠脑缺血再灌注损伤的程度,其机制可能与抑制NF-κB活化,减少ICAM1的表达,进而降低缺血灶炎症反应的程度有关。
Objective To observe the effects of hyperbaric oxygen (HBO) on the expression of nuclear factor (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) after focal cerebral ischemia / reperfusion in rats. Methods The model of focal cerebral ischemia-reperfusion was established by blocking the middle cerebral artery with modified plug method. 72 rats were randomly divided into CIR group, cerebral ischemia-reperfusion plus hyperbaric oxygen therapy group (HBO group) and sham operation control group (SO group) The infarct size and the expression of NFκB and ICAM1 in brain tissue were detected by immunohistochemical staining at 24h, 48h, 72h and 120h after reperfusion. Results The volume of infarction in HBO group was less than that in CIR group after staining with triphenyltetrazolium chloride (TTC), the difference was statistically significant (P <0.05). The expression of NFκB and ICAM1 in CIR group and HBO group were significantly higher than those in SO group at each time point after reperfusion (P <0.01). The expressions of NF-κB and ICAM-1 in HBO group were significantly lower than those in reperfusion group CIR group (P <0.05). Conclusion The levels of NF-κB and ICAM-1 are significantly increased after cerebral ischemia-reperfusion in rats. HBO treatment can reduce the degree of cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the inhibition of NF-κB activation and the decrease of ICAM1 expression, Blood levels of inflammation related to the degree.