CAJ | 학술논문

目的探讨大鼠蛛网膜下腔出血(SAH)后G蛋白信号调节因子5(RGS5)表达变化与迟发缺血性神经功能障碍(DIND)之间的关系.方法 Sprague-Dawley (SD)大鼠90只,随机分为SAH组(A组,42只)、生理盐水组(B组,42只)和健康对照组(C组,6).A组采用枕大池二次注血法建立SAH模型,B组同法注射等量生理盐水.A、B组分别在二次注血(或生理盐水)后1、3、5、7、9、11、13 d取大脑,每组每时相取6个大脑,行脑组织HE染色观察脑组织病理形态,免疫组化检测RGS5蛋白,原位杂交法检测RGS5 mRNA.C组用以上同样方法观察检测.结果 A组二次注血后3～11d脑组织出现局部缺血梗死的病理形态,组织结构紊乱,间质水肿,神经元变性坏死.与B、C组相比,A组3～11 d RGS5蛋白及RGS5mRNA表达均增多(P＜0.05),第5天增多最明显(P＜0.05).结论 SAH后RGS5高表达与DIND的发生密切相关.
목적 탐토대서주망막하강출혈(SAH)후G단백신호조절인자5(RGS5)표체변화여지발결혈성신경공능장애(DIND)지간적관계.방법 Sprague-Dawley (SD)대서90지,수궤분위SAH조(A조,42지)、생리염수조(B조,42지)화건강대조조(C조,6).A조채용침대지이차주혈법건립SAH모형,B조동법주사등량생리염수.A、B조분별재이차주혈(혹생리염수)후1、3、5、7、9、11、13 d취대뇌,매조매시상취6개대뇌,행뇌조직HE염색관찰뇌조직병리형태,면역조화검측RGS5단백,원위잡교법검측RGS5 mRNA.C조용이상동양방법관찰검측.결과 A조이차주혈후3～11d뇌조직출현국부결혈경사적병리형태,조직결구문란,간질수종,신경원변성배사.여B、C조상비,A조3～11 d RGS5단백급RGS5mRNA표체균증다(P＜0.05),제5천증다최명현(P＜0.05).결론 SAH후RGS5고표체여DIND적발생밀절상관.
Objective To explore relationship between expression of regulators of G protein signaling 5 (RGS5) and delayed ischemic neurological deficit (DIND) after experimental subarachnoid hemorrhage(SAH) in rats.Methods 90 Sprague-Dawley rats were randomly divided into SAH group (n =42),saline-control group (n =42) and normal control group (n =6).SAH was developed with twice injections of 0.3 ml arterial blood into cisterna magna,and 0.3 ml saline injected for saline-control group.For SAH group and saline-control group,brains were harvested on 1 d,3 d,5 d,7 d,9 d,11 d and 13 d after second injection of blood.6 brains were harvested at each time for each group.Hematoxylin-eosin staining was used to observe pathomorphological changes of brain tissue.Proteins of RGS5 in brain tissue were evaluated by immunohistochemically staining.Expression changes of RGS5 mRNA were identified by insitu hybridization.Same methods were used for normal control group.Results For SAH group,ischemic pathomorphological changes including disordered tissue construction,edema of interstitial substance,degeneration and necrosis of neurons in brain tissue were identified from 3 d to 11 d.For salinecontrol and normal control group,there were no ischemic pathomorphological changes in brains at different time points.Compared with saline-control group and normal,the expression of RGS5 protein and mRNA increased at different time poiuts of SAH group group (P ＜ 0.05),and significantly increased on 5 d than other times (P ＜ 0.05).Conclusions The high expression of RGS5 in the rat brain may be associated with the delayed ischemic neurological deficit after subarachnoid hemorrhage.