GCs对慢性低灌注大鼠海马脑组织IL-2及KRT6A蛋白表达影响的实验研究

目的采用免疫组化及蛋白质组学技术观察慢性脑缺血大鼠海马脑组织IL-2及蛋白表达产物变化。方法 BCAO建立慢性脑缺血大鼠模型,随机分为假手术组、模型组,GCs低中高剂量组及阳性药物(奥拉西坦)对照组。免疫组化ABC法检测海马脑组织IL-2表达改变;蛋白质组学技术分析鉴定慢性脑缺血大鼠模型及GCs干预后差异蛋白表达改变。结果 (1)模型组大鼠海马脑区IL-2表达量显著上升(2.15±0.45),与假手术组相比差异显著,差异有统计学意义(P0.05),GCs低中高剂量干预后IL-2表达水平出现显著上升,分别是(2.01±0.54、1.76±0.61、1.56±0.31)(P0.01,P0.05);(2)研究发现,慢性脑缺血大鼠海马脑组织Ⅱ型细胞骨架蛋白(typeⅡcytoskeletal 6A,KRT 6A)表达发生显著下降。结论慢性脑缺血病理过程中存在炎性相关蛋白的活化,推测其病理生理机制与炎症反应及细胞活化密切相关。

Experimental research between IL-2 and KRT6A protein expression in rats after chronic cerebral hypoperfusion

Objective To observe the IL-2 and the protein expression of the hippocampal tissue in chronic cerebral ischemia rats by immunohistochemical and proteomics techniques .Methods Establishing the model of chronic cerebral is-chemia rats by BCAO,and were randomly divided into control group ,model group,GCs low、middle、high dosage group.IL-2 expression was detected using immunohistochemical method .Proteomics technology identified the difference expression pro-tein of chronic cerebral ischemia rats and the intervention rats by GCs .Results (1) The expression of IL-2 in hippocampal brain of model rats markedly increased (2.15 ±0.45);however,IL-2 expression level significantly rise after intervention by GCs,respectively (2.01 ±0.54、1.76 ±0.61、1.56 ±0.31)(P<0.01,P<0.05).(2)The typeⅡ cytoskeleton protein ( typeⅡcytoskeletal 6A) was founded significantly decreased after intervention by GCs .Conclusion Immuno-inflammato-ry may be exist in chronic ischemic .Speculated that the pathophysiological mechanism is closely related to inflammatory re -action and cell activation .