中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2012年
4期
234-237
,共4页
刘业成%何桂珍%齐志伟%徐军%朱华栋%王仲%于学忠%马遂
劉業成%何桂珍%齊誌偉%徐軍%硃華棟%王仲%于學忠%馬遂
류업성%하계진%제지위%서군%주화동%왕중%우학충%마수
缺血性脑卒中%肠黏膜屏障功能%凋亡%紧密连接%闭锁蛋白%闭锁小带蛋白1
缺血性腦卒中%腸黏膜屏障功能%凋亡%緊密連接%閉鎖蛋白%閉鎖小帶蛋白1
결혈성뇌졸중%장점막병장공능%조망%긴밀련접%폐쇄단백%폐쇄소대단백1
Ischemic stroke%Intestinal barrier function%Apoptosis%Tight junction%Occludin%Zonula occludens-1
目的 研究缺血性脑卒中对犬肠黏膜屏障功能的影响以及细胞凋亡和紧密连接蛋白在其中的可能机制.方法 杂犬20只,按随机数字表法分为梗死组和假手术组,每组10只.梗死组采用双硅柱置入法制作缺血性脑卒中模型,假手术组动物不置入栓子,其他同梗死组.光镜下观察肠黏膜形态;免疫组织化学法分析肠黏膜紧密连接蛋白闭锁蛋白和闭锁小带蛋白1的表达;采用TdT介导的dUTP缺口末端标记技术检测肠上皮细胞凋亡.结果 梗死组动物均形成脑梗死.和假手术组相比,梗死组紧密连接蛋白闭锁蛋白和闭锁小带蛋白1表达均明显降低(闭锁蛋白平均光密度值:0.20±0.01比0.22±0.01,P=0.007;闭锁小带蛋白1平均光密度值:0.20±0.01比0.22±0.02,P=0.008);梗死组凋亡指数明显增高(29.04 ±3.79比6.44±1.24,P=0.002);闭锁蛋白与闭锁小带蛋白1呈正相关(R=0.71,P=0.02);凋亡指数与闭锁蛋白和闭锁小带蛋白1均呈负相关(R=-0.91,P=0.00;R=-0.77,P=0.01).光镜下梗死组存在小肠病理损伤,假手术组小肠结构正常.结论 缺血性脑卒中时,肠道屏障功能发生损害.紧密连接蛋白闭锁蛋白和闭锁小带蛋白1表达降低,从而导致紧密连接破坏.肠黏膜细胞凋亡上调是肠屏障障碍的细胞学基础,凋亡是缺血性脑卒中时肠上皮细胞死亡的重要形式.
目的 研究缺血性腦卒中對犬腸黏膜屏障功能的影響以及細胞凋亡和緊密連接蛋白在其中的可能機製.方法 雜犬20隻,按隨機數字錶法分為梗死組和假手術組,每組10隻.梗死組採用雙硅柱置入法製作缺血性腦卒中模型,假手術組動物不置入栓子,其他同梗死組.光鏡下觀察腸黏膜形態;免疫組織化學法分析腸黏膜緊密連接蛋白閉鎖蛋白和閉鎖小帶蛋白1的錶達;採用TdT介導的dUTP缺口末耑標記技術檢測腸上皮細胞凋亡.結果 梗死組動物均形成腦梗死.和假手術組相比,梗死組緊密連接蛋白閉鎖蛋白和閉鎖小帶蛋白1錶達均明顯降低(閉鎖蛋白平均光密度值:0.20±0.01比0.22±0.01,P=0.007;閉鎖小帶蛋白1平均光密度值:0.20±0.01比0.22±0.02,P=0.008);梗死組凋亡指數明顯增高(29.04 ±3.79比6.44±1.24,P=0.002);閉鎖蛋白與閉鎖小帶蛋白1呈正相關(R=0.71,P=0.02);凋亡指數與閉鎖蛋白和閉鎖小帶蛋白1均呈負相關(R=-0.91,P=0.00;R=-0.77,P=0.01).光鏡下梗死組存在小腸病理損傷,假手術組小腸結構正常.結論 缺血性腦卒中時,腸道屏障功能髮生損害.緊密連接蛋白閉鎖蛋白和閉鎖小帶蛋白1錶達降低,從而導緻緊密連接破壞.腸黏膜細胞凋亡上調是腸屏障障礙的細胞學基礎,凋亡是缺血性腦卒中時腸上皮細胞死亡的重要形式.
목적 연구결혈성뇌졸중대견장점막병장공능적영향이급세포조망화긴밀련접단백재기중적가능궤제.방법 잡견20지,안수궤수자표법분위경사조화가수술조,매조10지.경사조채용쌍규주치입법제작결혈성뇌졸중모형,가수술조동물불치입전자,기타동경사조.광경하관찰장점막형태;면역조직화학법분석장점막긴밀련접단백폐쇄단백화폐쇄소대단백1적표체;채용TdT개도적dUTP결구말단표기기술검측장상피세포조망.결과 경사조동물균형성뇌경사.화가수술조상비,경사조긴밀련접단백폐쇄단백화폐쇄소대단백1표체균명현강저(폐쇄단백평균광밀도치:0.20±0.01비0.22±0.01,P=0.007;폐쇄소대단백1평균광밀도치:0.20±0.01비0.22±0.02,P=0.008);경사조조망지수명현증고(29.04 ±3.79비6.44±1.24,P=0.002);폐쇄단백여폐쇄소대단백1정정상관(R=0.71,P=0.02);조망지수여폐쇄단백화폐쇄소대단백1균정부상관(R=-0.91,P=0.00;R=-0.77,P=0.01).광경하경사조존재소장병리손상,가수술조소장결구정상.결론 결혈성뇌졸중시,장도병장공능발생손해.긴밀련접단백폐쇄단백화폐쇄소대단백1표체강저,종이도치긴밀련접파배.장점막세포조망상조시장병장장애적세포학기출,조망시결혈성뇌졸중시장상피세포사망적중요형식.
Objective To explore the impact of ischemic stroke on intestinal barrier changes in dogs.Methods Totally 20 mongrel dogs were divided into 2 groups by random number table with 10 in each.Double silicone cylinders measuring 1.1 mm in diameter and 8 mm in length were placed into their internal carotid arteries in all dogs of group A.Group B served as a control group and received sham operation.Light microscopy was performed for morphological measurement of intestinal epithelial cell.Immunohistochemistry was used to analysis the changes of protein zonula occludens-1(ZO-1)localizing at tight junction of intestinal epithelial cells.Results Ischemic stroke was confirmed by cranial CT scanning in all dogs of group A.Compared with the test results in group B,the occludin and Zo-1 protein levels in group A were significantly lower than those in group B(occludin:0.20 ±0.01 vs 0.22 ±0.01,P =0.007; ZO-1:0.20 ±0.01 vs 0.22 ±0.02,P =0.008).The apoptotic index in group A was significantly higher than in group B(29.04 ± 3.79 vs 6.44 ± 1.24,P =0.002).There was a positive correlation between occludin and ZO-1(R =0.71,P =0.02),and the apoptotic index was negatively correlated with levels of occludin,ZO-1(R =-0.91,P =0.00; R =-0.77,P =0.01).Light microscopy showed that the dogs in group A had intestinal mucousal injuries while no obvious change was detected in group B.Conclusions Dogs with ischemic stroke tend to develop intestinal barrier dysfunction,during which the destruction of tight junction plays a key role.The up-regulated apoptosis of intestinal epithelial cell constitutes one of the cellular bases of intestine injury.