CAJ | 학술논문

目的：观察高血压大鼠大脑皮质局灶梗死后病灶周围皮质及其同侧丘脑抑制性蛋白-硫酸软骨素蛋白多糖(chondroitin sulfate proteoglycans, CSPGs)的表达并探讨其对神经可塑性的可能作用。方法建立高血压大鼠的右侧大脑中动脉闭塞(middle cerebral artery occlusion, MCAO)模型，假手术(Sham)组仅暴露而不凝闭MCA，每组24只。MCAO或Sham后第7天和第14天，各组各时间点取12只大鼠按改良神经功能缺损评分(mod-ified neurological severity scores, mNSS)进行神经功能评分后，处死取脑，免疫荧光及western bolt检测梗死灶周围皮质及其同侧丘脑CSPGs及其组分NG2、Neurocan的表达。结果 MCAO后大鼠出现不同程度的神经功能缺损；MCAO术后第7天梗死灶周围皮质及其同侧丘脑CSPGs、NG2及全长Neurocan与Sham组相比表达均增加，并持续至第14天(P<0.05)，但第7天与第14天的表达相比无统计学差异(P>0.05)；术后第7天和第14天C端片段的Neurocan在上述部位的表达无统计学差异(P>0.05)。结论 CSPGs可能通过提供抑制性环境参与脑梗死后病灶局部及远隔丘脑的神经可塑性。
목적：관찰고혈압대서대뇌피질국조경사후병조주위피질급기동측구뇌억제성단백-류산연골소단백다당(chondroitin sulfate proteoglycans, CSPGs)적표체병탐토기대신경가소성적가능작용。방법건립고혈압대서적우측대뇌중동맥폐새(middle cerebral artery occlusion, MCAO)모형，가수술(Sham)조부폭로이불응폐MCA，매조24지。MCAO혹Sham후제7천화제14천，각조각시간점취12지대서안개량신경공능결손평분(mod-ified neurological severity scores, mNSS)진행신경공능평분후，처사취뇌，면역형광급western bolt검측경사조주위피질급기동측구뇌CSPGs급기조분NG2、Neurocan적표체。결과 MCAO후대서출현불동정도적신경공능결손；MCAO술후제7천경사조주위피질급기동측구뇌CSPGs、NG2급전장Neurocan여Sham조상비표체균증가，병지속지제14천(P<0.05)，단제7천여제14천적표체상비무통계학차이(P>0.05)；술후제7천화제14천C단편단적Neurocan재상술부위적표체무통계학차이(P>0.05)。결론 CSPGs가능통과제공억제성배경삼여뇌경사후병조국부급원격구뇌적신경가소성。
Objective To examine the expression of inhibitory chondroitin sulfate proteoglycans (CSPGs) and in-vestigate their potential effects on neural plasticity in the peri-infarct cortex and ipsilateral thalamus after focal cerebral infarction in hypertensive rats. Methods Twenty-four adult renovascular hypertensive Sprague-Dawley rats per group were subjected to permanent right middle cerebral artery occlusion(MCAO) or sham operation. Twelve rats which were se-lected randomly from per group at each time point were decapitated and their brains were removed and cut into coronal sections at 7 and 14 days post MCAO. The expression of CSPGs, NG2 and Neurocan was examined using immunostaining and western blot. Results All rats displayed neurological deficits to varying degrees and the expression of CSPGs, NG2 and full length Neurocan was increased in the peri-infarct cortex and ipsilateral thalamus at 7 and 14 days (P<0.05). However, there were no significant difference in either expression of CSPGs, NG2 and full-length Neurocan between 7 and 14 days or the expression of C-terminal fragment Neurocan at 7 and 14 days (all P>0.05). Conclusions CSPGs may play a negative role in neural plasticity through induction of inhibitory environment in the peri-infarct cortex and ipsilat-eral thalamus following focal cerebral infarction in hypertensive rats.