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目的探讨大鼠局灶性脑缺血再灌注时核因子κB(NFκB)、白细胞介素1(IL1)、肿瘤坏死因子α(TNFα)、细胞间黏附分子1(ICAM1)在异丙酚脑保护机制中的作用。方法对90只雄性Wistar大鼠,采用大脑中动脉线栓法建立局灶性脑缺血再灌注模型,并随机将大鼠分为假手术组、缺血再灌注组和异丙酚组,每组30只。在大鼠脑缺血2h后进行再灌注。在再灌注2、6、12、24h,应用免疫组织化学染色分析核因子κB的移位,蛋白质印迹检测大鼠脑组织中核核因子κB的表达量。在再灌注3、6、24、72h,采用免疫组织化学染色检测脑组织IL1、TNFα、ICAM1的表达。结果局灶性脑缺血再灌注后,核因子κB在再灌注2～24h明显从细胞浆移位于细胞核内,与假手术组比较,核因子κB的表达量显著增加,灰度值分别为86±10、89±9、87±10、94±8(均P<001),IL1、TNFα、ICAM1表达的峰值明显升高,灰度值分别为170±5、174±5、171±4(均P<001),但在时间上明显滞后于核核因子κB。应用异丙酚,脑缺血再灌注后核因子κB从细胞浆向细胞核的移位被明显抑制,与缺血再灌注组比较,核因子κB的表达量显著减少,灰度值分别为61±6、62±5、66±6、63±7(均P<005),IL1、TNFα、ICAM1表达的峰值明显降低,分别为150±4、152±5、152±4(均P<005)。结论异丙酚能抑制大鼠局?
Objective To investigate the protective effect of propofol on cerebral ischemia-reperfusion injury in rats with cerebral ischemic reperfusion (NF-κB), interleukin 1 (IL1), tumor necrosis factor α (TNFα) and intercellular adhesion molecule 1 Mechanism of the role. Methods Focal cerebral ischemia-reperfusion model was established in 90 male Wistar rats with middle cerebral artery occlusion. Rats were randomly divided into sham operation group, ischemia-reperfusion group and propofol group. Group of 30. Reperfusion was performed 2h after cerebral ischemia in rats. At 2, 6, 12 and 24 hours after reperfusion, nuclear translocation of NF-κB was analyzed by immunohistochemical staining. The expression of NF-κB in rat brain was detected by Western blotting. At 3, 6, 24 and 72h after reperfusion, the expression of IL1, TNFα and ICAM1 in brain tissue were detected by immunohistochemical staining. Results After focal cerebral ischemia / reperfusion, nuclear factor κB was significantly translocated from the cytoplasm to the nucleus within 2 to 24 hours after reperfusion. Compared with the sham operation group, the expression of NF-κB was significantly increased 86 ± 10,89 ± 9,87 ± 10,94 ± 8 (all P <001). The peak values of IL1, TNFα and ICAM1 expression were significantly increased with the gray values of 170 ± 5,174 ± 5,171 ± 4 (All P <001), but significantly lagged in nuclear factor kappa B in time. Application of propofol, nuclear factor κB translocation from the cytoplasm to the nucleus was significantly inhibited after cerebral ischemia-reperfusion, compared with the ischemia-reperfusion group, the expression of nuclear factor κB decreased significantly, the gray values were 61 ± 6,62 ± 5,66 ± 6,63 ± 7 (all P <005). The peak of expression of IL1, TNFα and ICAM1 were significantly decreased (150 ± 4,152 ± 5,152 ± 4, P < . Conclusion Propofol can inhibit the rat?