新疆医科大学学报
新疆醫科大學學報
신강의과대학학보
JOURNAL OF XINJIANG MEDICAL UNIVERSITY
2014年
9期
1149-1151
,共3页
陈龙%秦纹%连玉龙%刘继文
陳龍%秦紋%連玉龍%劉繼文
진룡%진문%련옥룡%류계문
慢性温和应激%大鼠%血管内皮
慢性溫和應激%大鼠%血管內皮
만성온화응격%대서%혈관내피
chronic mild stress%rat%vascular endothelial
目的:探讨慢性温和应激对大鼠血管内皮功能的影响及其作用机制。方法采用孤养与慢性轻度不可预见性应激模型相结合建立慢性温和应激动物模型,随机分为实验组和对照组,采用 ELISA法检测两组大鼠血清皮质醇、细胞间黏附因子1(ICAM-1)、白介素6(IL-6)、血浆内皮素1(ET-1)的含量,透射电镜观察大鼠血管内皮超微结构的改变。结果实验组大鼠第2周和第3周体质量显著低于对照组(P <0.05);血清皮质醇的含量显著增加(P <0.05);血清 ICAM-1、IL-6、血浆 ET-1均较对照组明显升高(P <0.05);血管内皮超微结构改变明显。结论慢性温和应激可导致大鼠血管内皮功能损伤。
目的:探討慢性溫和應激對大鼠血管內皮功能的影響及其作用機製。方法採用孤養與慢性輕度不可預見性應激模型相結閤建立慢性溫和應激動物模型,隨機分為實驗組和對照組,採用 ELISA法檢測兩組大鼠血清皮質醇、細胞間黏附因子1(ICAM-1)、白介素6(IL-6)、血漿內皮素1(ET-1)的含量,透射電鏡觀察大鼠血管內皮超微結構的改變。結果實驗組大鼠第2週和第3週體質量顯著低于對照組(P <0.05);血清皮質醇的含量顯著增加(P <0.05);血清 ICAM-1、IL-6、血漿 ET-1均較對照組明顯升高(P <0.05);血管內皮超微結構改變明顯。結論慢性溫和應激可導緻大鼠血管內皮功能損傷。
목적:탐토만성온화응격대대서혈관내피공능적영향급기작용궤제。방법채용고양여만성경도불가예견성응격모형상결합건립만성온화응격동물모형,수궤분위실험조화대조조,채용 ELISA법검측량조대서혈청피질순、세포간점부인자1(ICAM-1)、백개소6(IL-6)、혈장내피소1(ET-1)적함량,투사전경관찰대서혈관내피초미결구적개변。결과실험조대서제2주화제3주체질량현저저우대조조(P <0.05);혈청피질순적함량현저증가(P <0.05);혈청 ICAM-1、IL-6、혈장 ET-1균교대조조명현승고(P <0.05);혈관내피초미결구개변명현。결론만성온화응격가도치대서혈관내피공능손상。
Objective To study the endothelial function damage of rat under chronic stress.Methods En-zyme linked immunosorbent assay (ELISA)was applied to determining plasma levels of ET-1,serum lev-els of IL-6,ICAM-1,Cortisol.The Vascular endothelial morphological changes were identified via trans-mission electron microscope.Results From the second week,the body weight of rats in the experimental group were significantly lower than the control group (P <0.05).A significant increase in serum cortisol (P <0.05).The content of ICAM-1,IL-6,plasma ET-1 levels were higher in experimental group than in controlled group (P <0.05).Ultrastructural of Vascular endothelial were changed significantly.Conclu-sion Chronic mild stress can lead to vascular endothelial dysfunction in rats.