白细胞介素-23及核因子-κB在大鼠脑梗死模型中的表达

Expression of IL-23 and NF-κB in rat models with cerebral infarction

目的探讨白细胞介素-23(IL-23)及核因子-κB(NF-κB)在脑梗死模型大鼠脑梗死区域炎性损伤组织中的表达情况。方法健康成年雄性SD大鼠50只,随机分为梗死组和假手术组,每组25只。梗死组用线栓法制作左侧大脑中动脉闭塞模型,2组均于手术后6 h、24 h、48 h、72 h、7 d随机取5只大鼠取材,采用免疫组化染色,观察脑梗死区域光镜下形态学变化及IL-23、NF-κB的表达。比较2组大鼠在同一时间点脑组织形态学变化及IL-23、NF-κB表达的异同。结果梗死组IL-23、NF-κB阳性细胞数各时间点均高于假手术组(P均<0.01)。梗死组IL-23在梗死后6 h表达增高,并且在梗死后48 h达到高峰,3d后阳性细胞数表达逐渐减少,各时间点比较具有显著性差异(P均<0.01)。梗死组NF-κB在梗死后48 h达到高峰,3 d后阳性细胞数表达逐渐减少,各时间点比较具有显著性差异(P均<0.01)。结论 IL-23和NF-κB在大鼠脑梗死区域表达增高,参与了梗死区域的炎性反应。

Objective It is to explore the expression of IL-23 and NF-κB in the inflammatory injury tissue in cerebral infarction area in rats with cerebral infarction.Methods 50 healthy aged male SD rats were randomly divided into infarction group and sham operation group,25 rats in each group.The models of left middle cerebral artery occlusion in infarction group were established by thread embolism method.The tissue of 5 rats were randomly collected in both groups in 6h,24h,48h,72h and 7d after operation to observe the changes of pathology in infarction area under light microscope and observe the expression of IL-23 and NF-κB after immunecytochemistry.The differences in the changes and expression at the same time in the rats between both groups were compared.Results The cells with positive IL-23 and NF-κB in infarction group at every time point were all more than that in sham group（P0.01）.The expression of IL-23 in infarction group began to increase in 6h after infarction,then reached its peak point after 48h,the expression gradually decreased after 3d.Compared with each other,the differences of every time point were significant（P0.01）.The expression of NF-κB reached its peak time in 48h after infarction in infarction group,then the expression gradually decreased after 3d.Compared with each other,the differences of every time point were significant（P0.01）.Conclusion The expression of IL-23 and NF-κB increased in the infarction area in the rats with cerebral infarction,which played a part in the inflammatory reaction in infarction area.