论文部分内容阅读
目的；探索细胞因子介导的中性粒细胞化学吸附剂（CINC）在脑缺血损伤中的作用。方法：用线栓法制备大鼠局灶性脑缺血模型，观察不同脑缺血时程血浆（sera）和脑组织内CINC浓度与髓质过氧化物酶（MPO）活性。结果：缺血组，血浆中CINC浓度的高峰在缺血6小时，脑组织内CINC浓度和髓质过氧化物酶（MPO）活性均呈低水平，其中CINC浓度高峰在缺血12小时，与对照组比较，差异均有极显著性意义（P＜0．01）；血浆中MPO活性随着缺血时间延长而逐渐升高，缺血6小时以上各组与对照组比较差异均有极显著性意义（P＜0．01）；脑组织内各组MPO活性差异无显著性意义（P＜0．05）。结论：缺血时，脑组织内表达的CINC可能是启动缺血性脑损伤的因素之一
Objective To explore the role of cytokine-mediated neutrophil chemisorbent (CINC) in cerebral ischemic injury. Methods: The model of focal cerebral ischemia in rats was established by thread occlusion. The concentration of CINC and the activity of medulla peroxidase (MPO) in different sera and brain tissue were observed. Results: In the ischemic group, the peak of CINC concentration in plasma was 6 hours after ischemia, and the CINC concentration and MPO activity in brain tissue were all low. The peak of CINC concentration was at 12 hours of ischemia, (P <0.01). The activity of MPO in plasma increased gradually with the prolongation of ischemia, and there was a significant difference in the MPO activity between plasma and control group at 6 hours after ischemia (P <0.01). There was no significant difference in MPO activity between groups (P <0.05). Conclusions: CINC expressed in brain tissue may be one of the factors to start ischemic brain injury during ischemia