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观察锌离子螯合剂N-二硫氨基甲酸(DEDTC)对大鼠缺血性脑损伤的炎症反应的影响并对其作用机制进行研究。随机将200只雄性SD大鼠分为假手术组、局灶性脑缺血再灌注(I/R)组及DEDTC治疗组。采用线栓法建立大鼠大脑中动脉闭塞(MCAO)模型。分别于再灌注6、12和24 h时处死大鼠并取材。借助2,3,5-氯化三苯基四氮唑(TTC)法检测大鼠脑梗死体积;采用Newport Green(NG)染色法观察缺血半暗带区域锌离子的变化情况;以酶标记免疫吸附法(ELISA)测定脑组织中TNF-α和IL-6的浓度;最后通过Western blot的方法对PI3K/Akt/NF-κB信号通路的表达变化进行检测。结果显示,DEDTC显著减小大鼠的脑梗死体积,改善大鼠的神经功能,降低缺血再灌注损伤后脑组织中炎性因子的释放,抑制PI3K/Akt/NF-κB信号通路的激活。以上结果表明,DEDTC对大鼠局灶性脑缺血损伤具有一定的保护作用,其作用机制可能与抑制PI3K/Akt/NF-κB信号通路,降低炎性因子释放有关。
To observe the effect of zinc ion chelator N-dithiocarbamic acid (DEDTC) on the inflammatory reaction of ischemic brain injury in rats and its mechanism of action. 200 male SD rats were randomly divided into sham operation group, focal cerebral ischemia reperfusion (I / R) group and DEDTC treatment group. The rat model of middle cerebral artery occlusion (MCAO) was established by thread occlusion. Rats were killed and harvested at 6, 12 and 24 h after reperfusion. The cerebral infarction volume was measured by 2,3,5-triphenyltetrazolium chloride (TTC) method. The changes of zinc ion in the ischemic penumbra were observed by Newport Green (NG) staining. The concentrations of TNF-α and IL-6 in brain tissue were determined by ELISA. Finally, the changes of PI3K / Akt / NF-κB signaling pathway were detected by Western blot. The results showed that DEDTC significantly reduced the volume of cerebral infarction, improved the neurological function, reduced the release of inflammatory cytokines and inhibited the activation of PI3K / Akt / NF-κB signaling pathway in ischemic postconditioning rats. The above results show that DEDTC has a protective effect on focal cerebral ischemic injury in rats, and its mechanism may be related to the inhibition of PI3K / Akt / NF-κB signaling pathway and the decrease of inflammatory factor release.