中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2010年
1期
11-14,19
,共5页
孟辉%刘国龙%唐荣锐%宫国旗%冯华
孟輝%劉國龍%唐榮銳%宮國旂%馮華
맹휘%류국룡%당영예%궁국기%풍화
脑出血%脑积水%脑脊液%水通道蛋白1
腦齣血%腦積水%腦脊液%水通道蛋白1
뇌출혈%뇌적수%뇌척액%수통도단백1
Cerebral hemorrhage%Hgdrocephalus%Cerebrospinal fluid%Aquaporin 1
目的 观察大鼠脑室出血后水通道蛋白1(AQP1)在大鼠脑内的表达变化,探讨其与脑出血后慢性脑积水之间的关系. 方法 将45只Wister大鼠按照随机数字表法分为3组:正常对照组(5只,不作任何处理)、假手术对照组(20只,侧脑室内注入0.1 mL生理盐水)、实验组(20只,侧脑室内注入0.1 mL枸橼酸化的自体静脉血),后2组再分别分为术后3 d、7 d、14 d、30 d4个时相点,每时相点5只.分别采用免疫组化、原位杂交方法观察大鼠脑室出血后不同时间AOP1蛋白及AQP1 mRNA在大鼠脑内的表达变化. 结果 实验组30 d时相点4只大鼠出现脑积水(4/5)、其余组别未出现慢性脑积水.正常对照组大鼠AQP1蛋白在脉络丛上皮细胞顶质膜强烈表达,室管膜、纵裂池、软脑膜、蛛网膜、硬脑膜也有较强烈表达;实验组大鼠脑室出血后3 dAQP1蛋白表达减少,7 d表达继续减少,14 d表达最弱,与正常对照组、假手术对照组比较,差异均有统计学意义(P<0.05),30d表达仍较弱.大鼠AQP1 mRNA在脑内的表达强度较AQP1蛋白弱,表达部位及变化与AQP1蛋白基本一致. 结论 AQP1作为水通道蛋白不仅参与脑脊液的分泌,可能也参与脑脊液的循环吸收过程;大鼠实验性脑室出血后AQP1表达下调导致脑脊液吸收减少可能也参与脑出血后慢性脑积水的形成.
目的 觀察大鼠腦室齣血後水通道蛋白1(AQP1)在大鼠腦內的錶達變化,探討其與腦齣血後慢性腦積水之間的關繫. 方法 將45隻Wister大鼠按照隨機數字錶法分為3組:正常對照組(5隻,不作任何處理)、假手術對照組(20隻,側腦室內註入0.1 mL生理鹽水)、實驗組(20隻,側腦室內註入0.1 mL枸櫞痠化的自體靜脈血),後2組再分彆分為術後3 d、7 d、14 d、30 d4箇時相點,每時相點5隻.分彆採用免疫組化、原位雜交方法觀察大鼠腦室齣血後不同時間AOP1蛋白及AQP1 mRNA在大鼠腦內的錶達變化. 結果 實驗組30 d時相點4隻大鼠齣現腦積水(4/5)、其餘組彆未齣現慢性腦積水.正常對照組大鼠AQP1蛋白在脈絡叢上皮細胞頂質膜彊烈錶達,室管膜、縱裂池、軟腦膜、蛛網膜、硬腦膜也有較彊烈錶達;實驗組大鼠腦室齣血後3 dAQP1蛋白錶達減少,7 d錶達繼續減少,14 d錶達最弱,與正常對照組、假手術對照組比較,差異均有統計學意義(P<0.05),30d錶達仍較弱.大鼠AQP1 mRNA在腦內的錶達彊度較AQP1蛋白弱,錶達部位及變化與AQP1蛋白基本一緻. 結論 AQP1作為水通道蛋白不僅參與腦脊液的分泌,可能也參與腦脊液的循環吸收過程;大鼠實驗性腦室齣血後AQP1錶達下調導緻腦脊液吸收減少可能也參與腦齣血後慢性腦積水的形成.
목적 관찰대서뇌실출혈후수통도단백1(AQP1)재대서뇌내적표체변화,탐토기여뇌출혈후만성뇌적수지간적관계. 방법 장45지Wister대서안조수궤수자표법분위3조:정상대조조(5지,불작임하처리)、가수술대조조(20지,측뇌실내주입0.1 mL생리염수)、실험조(20지,측뇌실내주입0.1 mL구연산화적자체정맥혈),후2조재분별분위술후3 d、7 d、14 d、30 d4개시상점,매시상점5지.분별채용면역조화、원위잡교방법관찰대서뇌실출혈후불동시간AOP1단백급AQP1 mRNA재대서뇌내적표체변화. 결과 실험조30 d시상점4지대서출현뇌적수(4/5)、기여조별미출현만성뇌적수.정상대조조대서AQP1단백재맥락총상피세포정질막강렬표체,실관막、종렬지、연뇌막、주망막、경뇌막야유교강렬표체;실험조대서뇌실출혈후3 dAQP1단백표체감소,7 d표체계속감소,14 d표체최약,여정상대조조、가수술대조조비교,차이균유통계학의의(P<0.05),30d표체잉교약.대서AQP1 mRNA재뇌내적표체강도교AQP1단백약,표체부위급변화여AQP1단백기본일치. 결론 AQP1작위수통도단백불부삼여뇌척액적분비,가능야삼여뇌척액적순배흡수과정;대서실험성뇌실출혈후AQP1표체하조도치뇌척액흡수감소가능야삼여뇌출혈후만성뇌적수적형성.
Objective To explore the possible pathogenesis of chronic posthemorrhagic hydrocephalus by observing the expression of AQP1 on rats after experimental intraventricular hemorrhage. Methods Fourty-five rats were randomly divided into normal control(n=5),sham-operated(n=20)and experimental(n=20)groups.The 0.1mL saline and 0.1mL citrated autologous blood were injected into the lateral ventricle of the rats in the sham-operated and the experimental groups,respectively.The later two groups were divided into four subgroups according to different time points at 3,7,14 and 30 d(n=5).The change of protein expression of AQP1 at different time points of bleeding were detected by immunohistochemical techniques and that of mRNA expression of AQP1 was obsevred by in situ hybridization,respectively.and then,the possible pathogenesis of chronic posthemorrhagic hydrocephalus was discussed. Results At the time point of 30 d after intraventricular hemordmge,chronic hydrocephalus appeared in 4 rats(80%)in the experimental group.High protein expression of AQP1 was found in the apical of cuboidal epithelium of choroids plexus,the ependyma, the pia mater, the arachnoid and the dura in the normal control group;the protein expression of AQP1 gradually weakened in the experimental group 3 d aftea intraventricular hemorrhage and dropped to the bottom on the 14th d,which was significantly different from the normal control and sham-operative groups(P<0.05).The mRNA expression of AQP1 was weaker than the protein expression of AQP1,and the expression locations of them were basically in concordance. Conclusion AQP1 is involved not only in the secretion of cerebrospinal fluid,but also in the process of the CSF absorption.The decrease of CSF absorption induced by the decreased expression of AQP1 after intraventrieular hemorrhage in rats may also relate to the development of chronic posthemorrhagic hydrocephalus.
