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机构地区:[1]贵阳医学院附属医院神经内科,贵州贵阳550004
出 处:《癫痫与神经电生理学杂志》2010年第2期74-76,共3页Journal of Epileptology and Electroneurophysiology(China)
摘 要:目的:通过观察糖尿病大鼠局灶性脑缺血再灌注后转录核因子NF-kBp65表达的动态变化,以探讨糖尿病在脑缺血再灌注损伤中的可能机制。方法:将SD大鼠随机分为正常对照组(A组)、假手术组(B组)、脑缺血再灌注组(C组)、糖尿病脑缺血再灌注组(D组),链脲佐菌素腹腔注射制作糖尿病模型,线栓法制作大鼠大脑中动脉缺血2h再灌注模型,免疫组织化学方法观察再灌注第3、第6、第24、第48小时脑组织中NFxBp65表达的动态变化。结果:脑缺血再灌注后,C组在第6小时、D组在第3小时即可见到NF-kBp65免疫阳性细胞,随着再灌注时间的延长,NF—KBp65免疫阳性细胞表达增加,第24小时达高峰,第48小时开始下降;NF_xBp65表达在各个缺血再灌注时间点上,D组较c组增加(P〈0.05)。结论:糖尿病可促进NF-kBp65活化加重脑缺血再灌注损伤。Objective:To study expression of NF -kBp65 after focal cerebral ischemic reperfusion in diabetic rats at different time points in order to investigate the mechanism of the cerebral ischemic reper- fusion injury aggravated by diabetes. Methods: Sprague-Dawley rats were randomly divided into the con- trol group (Group A), the sham operation group (Group B), the cerebral infarction group (Group C) and the diabetic cerebral infarction group (Group D). Diabetic model was made by injection of streptozotocin through abdomen. Transient focal ischemic reperfusion was produced by middle cerebral artery occlusion for 2 hours in Sprague Dawley rats. The expression of NF-k Bp65 was detected by immunohistochemistry in the 3th h,6th h, 24th h and 48th after reperfusion. Results: The immunohistochemistry results indica- ted that the expression of NF-k Bp65 in immuno positive cells increased at 6th h in Group C and increased at 3th h in Group D after ischemic reperfusion, peaked at 24t h, decreased gradually after 48th h. The ex- pression of NF--k Bp65 in Group D increased than that in Group C at different time points after reperfu- sion (P〈O. 05). Conclusion: In diabetic cerebral isc'hemic reperfusion rats the activation of NF-kBp65 may be a kind of effective mechanism of the cerebral ischemic reperfusion injury aggravated by diabetes.
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