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目的 :观察川芎嗪注射液 (TMRI)对脑缺血再灌注损伤 (CIRI)家兔血清白细胞介素 8(IL 8)的合成和释放的影响 ,并探讨其脑保护机制。方法 :制备家兔 CIRI模型 ,随机分为假手术对照组、缺血再灌注组和TMRI组 ,分别在缺血前、缺血 30分钟、再灌注 30、6 0、12 0分钟取静脉血 ,测定血清 IL 8浓度 ,实验结束取脑皮质 HE染色 ,光镜观察脑组织病理学改变。结果 :缺血再灌注组在脑缺血再灌注期间不同时间点血清 IL 8水平随脑缺血再灌注时间延长呈进行性升高 ,分别为缺血前的 1.38、1.6 2、1.93和 2 .2 9倍 ,明显高于假手术组 ,光镜下白细胞大量浸润、神经元明显损伤 :TMRI组不同时间点血清 IL 8浓度显著低于缺血再灌注组 ,光镜下白细胞浸润、神经元损伤程度较缺血再灌注组明显减轻 ,而与假手术组比较均无显著性差异。结论 :TMRI能有效抑制 IL 8的合成和释放 ,这可能是它减轻 CIRI的又一重要机制。
Objective: To observe the effect of Ligustrazine Injection (TMRI) on the synthesis and release of interleukin 8 (IL 8) in rabbits with cerebral ischemia-reperfusion injury (CIRI) and to explore its brain protection mechanism. METHODS: Rabbit CIRI models were prepared and randomly divided into sham operation control group, ischemia reperfusion group and TMRI group. Venous blood was taken before ischemia, 30 minutes of ischemia, 30, 60, and 120 minutes of reperfusion. The concentration of serum IL-8 was measured. The end of the experiment was taken for HE staining of the cerebral cortex, and light pathology was used to observe the pathological changes of the brain. RESULTS: In the ischemia-reperfusion group, serum IL-8 levels increased progressively with cerebral ischemia-reperfusion time at different time points during cerebral ischemia-reperfusion, and they were respectively 1.38, 1.62, 1.93, and 2. 9 times, significantly higher than that in the sham operation group. Leukocyte infiltration and neuronal damage were significantly observed under light microscope. Serum IL-8 levels in the TMRI group were significantly lower than those in the ischemia-reperfusion group at the different time points. Leukocyte infiltration and neuronal injury were observed under light microscope. Compared with the sham operation group, the degree of ischemia was significantly reduced, but there was no significant difference compared with the sham operation group. Conclusion: TMRI can effectively inhibit the synthesis and release of IL-8, which may be another important mechanism for reducing CIRI.