中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2010年
4期
681-685
,共5页
臧婵媛%康毅%温克%娄建石
臧嬋媛%康毅%溫剋%婁建石
장선원%강의%온극%루건석
微血管通透性%1-磷酸鞘氨醇%血小板活化因子%静水传导性%血管内皮钙粘蛋白
微血管通透性%1-燐痠鞘氨醇%血小闆活化因子%靜水傳導性%血管內皮鈣粘蛋白
미혈관통투성%1-린산초안순%혈소판활화인자%정수전도성%혈관내피개점단백
Microvessel permeability%Sphingosine 1-phosphate%Platelet activating factor%Hydraulic conductivity%Vascular endothelial-cadherin
目的:探讨1-磷酸鞘氨醇(S1P)对血小板活化因子(PAF)引起的大鼠肠系膜微血管通透性增高的影响.方法:本研究拟采用大鼠在体肠系膜微血管灌注的方法,通过测定微静脉的静水传导性(Lp),观察S1P对外源性PAF引起的微血管通透性增高的影响;并利用激光共聚焦显微镜技术,观察S1P对PAF引起的微血管荧光强度变化以及血管内皮细胞钙粘蛋白(VE-cadherin)变化的影响.结果:给予10 nmol/L PAF作用后,大鼠肠系膜微血管Lp值明显增高,而经1 μmol/L S1P预处理后,再给予PAF并未引起Lp的明显变化;PAF作用微血管后可见微血管内皮细胞间隙打开,微血管荧光强度明显增加,大量红色荧光微球(FMs)分布于内皮细胞间隙之中,S1P预处理后并未见内皮细胞间隙打开及FMs的明显积聚,微血管荧光强度与正常对照值比较无显著差异.结论:PAF可增加微血管的通透性,改变内皮细胞VE-cadherin正常结构,导致粘附连接断裂,细胞间隙形成,血管通透性增加可能与此结构变化有关.S1P能改善PAF引起的血管通透性增高,其作用与加强内皮细胞间粘附连接,抑制细胞间隙打开有关.
目的:探討1-燐痠鞘氨醇(S1P)對血小闆活化因子(PAF)引起的大鼠腸繫膜微血管通透性增高的影響.方法:本研究擬採用大鼠在體腸繫膜微血管灌註的方法,通過測定微靜脈的靜水傳導性(Lp),觀察S1P對外源性PAF引起的微血管通透性增高的影響;併利用激光共聚焦顯微鏡技術,觀察S1P對PAF引起的微血管熒光彊度變化以及血管內皮細胞鈣粘蛋白(VE-cadherin)變化的影響.結果:給予10 nmol/L PAF作用後,大鼠腸繫膜微血管Lp值明顯增高,而經1 μmol/L S1P預處理後,再給予PAF併未引起Lp的明顯變化;PAF作用微血管後可見微血管內皮細胞間隙打開,微血管熒光彊度明顯增加,大量紅色熒光微毬(FMs)分佈于內皮細胞間隙之中,S1P預處理後併未見內皮細胞間隙打開及FMs的明顯積聚,微血管熒光彊度與正常對照值比較無顯著差異.結論:PAF可增加微血管的通透性,改變內皮細胞VE-cadherin正常結構,導緻粘附連接斷裂,細胞間隙形成,血管通透性增加可能與此結構變化有關.S1P能改善PAF引起的血管通透性增高,其作用與加彊內皮細胞間粘附連接,抑製細胞間隙打開有關.
목적:탐토1-린산초안순(S1P)대혈소판활화인자(PAF)인기적대서장계막미혈관통투성증고적영향.방법:본연구의채용대서재체장계막미혈관관주적방법,통과측정미정맥적정수전도성(Lp),관찰S1P대외원성PAF인기적미혈관통투성증고적영향;병이용격광공취초현미경기술,관찰S1P대PAF인기적미혈관형광강도변화이급혈관내피세포개점단백(VE-cadherin)변화적영향.결과:급여10 nmol/L PAF작용후,대서장계막미혈관Lp치명현증고,이경1 μmol/L S1P예처리후,재급여PAF병미인기Lp적명현변화;PAF작용미혈관후가견미혈관내피세포간극타개,미혈관형광강도명현증가,대량홍색형광미구(FMs)분포우내피세포간극지중,S1P예처리후병미견내피세포간극타개급FMs적명현적취,미혈관형광강도여정상대조치비교무현저차이.결론:PAF가증가미혈관적통투성,개변내피세포VE-cadherin정상결구,도치점부련접단렬,세포간극형성,혈관통투성증가가능여차결구변화유관.S1P능개선PAF인기적혈관통투성증고,기작용여가강내피세포간점부련접,억제세포간극타개유관.
AIM: To study the effect of sphingosine 1-phosphate (S1P) on the increase in microvessel permeability induced by platelet activating factor (PAF). METHODS: The microvessel permeability was assessed by measuring hydraulic conductivity (Lp). To observe the effect of S1P and PAF on vascular endothelial-cadherin (VE-Cadherin), the microvessels were stained with immunofluorescence and examined by laser confocal microscopy. RESULTS: After giving PAF at concentration of 10 nmol/L, the Lp value of rat mesentery microvessel was significantly increased. However, after pretreatment with S1P, PAF did not give rise to a further significant change. The effect of PAF on microvascular endothelial cells could be seen: the formation of endothelial gap was induced, the microvascular fluorescence intensity significantly increased, a large number of fluorescent microspheres (FMs) distributed in the space among the endothelial cells. However, after pretreated with S1P, no obvious gap opening and the FMs accumulation were observed. Compared to normal control, no significant difference of the microvascular fluorescence intensity was found. CONCLUSION: PAF changes the structure of VE-Cadherin, leading to detachment of adherent junction, formation of intercellular gaps, which contributes to the increase in the permeability. S1P improves the increase in the microvessel permeability caused by PAF, which might be mediated by strengthening adherent junction and inhibiting the formation of endothelial gaps.