中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2008年
47期
3374-3377
,共4页
尿毒症%血清%肺微血管内皮细胞%单层通透性%F-肌动蛋白
尿毒癥%血清%肺微血管內皮細胞%單層通透性%F-肌動蛋白
뇨독증%혈청%폐미혈관내피세포%단층통투성%F-기동단백
Uremia%Serum%Rat pulmonary microvascular endothelial cell%Monolayer permeability%F-actin
目的 观察尿毒症患者血清对培养大鼠肺微血管内皮细胞(RPMVEC)单层通透性、肌动蛋白骨架(F-肌动蛋白)的影响,探讨尿毒症患者血清对肺微血管内皮细胞损伤的机制.方法 体外培养大鼠RPMVEC并鉴定;用针头式滤器观察尿毒症患者血清对RPMVEC单层通透性的影响;F-actin用流式细胞仪测定.结果 健康对照组6、12 h单层通透性系数分别为(0.0382 4±0.0022)、(0.0393±0.0016)ml·min-1·cm-2·kPa-1;尿毒症患者血清6、12 h单层通透性系数分别为(0.0687±0.0014)、(0.0772±0.0031)ml·min-1·cm-2·kPa-1;流式细胞仪测定F-肌动蛋白的值分别为:阴性对照组10.60±3.3、正常健康对照组1233.34±13.92、尿毒症血清组(6 h)712±51、尿毒症血清组(12 h)613.31±42.81;实验发现尿毒症患者血清100μl作用于RPMVEC 6、12 h可使RPMVEC的单层通透性增高(P<0.01);F-肌动蛋白解聚(P<0.01),且二者呈负相关(r=-0.927,P<0.01).结论 尿毒症患者血清作用于RPMVEC一定时间,可引起RPMVEC单层通透性的增高与F-肌动蛋白解聚.尿毒症患者血清引起内皮单层通透性的增高的机制与F-肌动蛋白解聚密切相关.
目的 觀察尿毒癥患者血清對培養大鼠肺微血管內皮細胞(RPMVEC)單層通透性、肌動蛋白骨架(F-肌動蛋白)的影響,探討尿毒癥患者血清對肺微血管內皮細胞損傷的機製.方法 體外培養大鼠RPMVEC併鑒定;用針頭式濾器觀察尿毒癥患者血清對RPMVEC單層通透性的影響;F-actin用流式細胞儀測定.結果 健康對照組6、12 h單層通透性繫數分彆為(0.0382 4±0.0022)、(0.0393±0.0016)ml·min-1·cm-2·kPa-1;尿毒癥患者血清6、12 h單層通透性繫數分彆為(0.0687±0.0014)、(0.0772±0.0031)ml·min-1·cm-2·kPa-1;流式細胞儀測定F-肌動蛋白的值分彆為:陰性對照組10.60±3.3、正常健康對照組1233.34±13.92、尿毒癥血清組(6 h)712±51、尿毒癥血清組(12 h)613.31±42.81;實驗髮現尿毒癥患者血清100μl作用于RPMVEC 6、12 h可使RPMVEC的單層通透性增高(P<0.01);F-肌動蛋白解聚(P<0.01),且二者呈負相關(r=-0.927,P<0.01).結論 尿毒癥患者血清作用于RPMVEC一定時間,可引起RPMVEC單層通透性的增高與F-肌動蛋白解聚.尿毒癥患者血清引起內皮單層通透性的增高的機製與F-肌動蛋白解聚密切相關.
목적 관찰뇨독증환자혈청대배양대서폐미혈관내피세포(RPMVEC)단층통투성、기동단백골가(F-기동단백)적영향,탐토뇨독증환자혈청대폐미혈관내피세포손상적궤제.방법 체외배양대서RPMVEC병감정;용침두식려기관찰뇨독증환자혈청대RPMVEC단층통투성적영향;F-actin용류식세포의측정.결과 건강대조조6、12 h단층통투성계수분별위(0.0382 4±0.0022)、(0.0393±0.0016)ml·min-1·cm-2·kPa-1;뇨독증환자혈청6、12 h단층통투성계수분별위(0.0687±0.0014)、(0.0772±0.0031)ml·min-1·cm-2·kPa-1;류식세포의측정F-기동단백적치분별위:음성대조조10.60±3.3、정상건강대조조1233.34±13.92、뇨독증혈청조(6 h)712±51、뇨독증혈청조(12 h)613.31±42.81;실험발현뇨독증환자혈청100μl작용우RPMVEC 6、12 h가사RPMVEC적단층통투성증고(P<0.01);F-기동단백해취(P<0.01),차이자정부상관(r=-0.927,P<0.01).결론 뇨독증환자혈청작용우RPMVEC일정시간,가인기RPMVEC단층통투성적증고여F-기동단백해취.뇨독증환자혈청인기내피단층통투성적증고적궤제여F-기동단백해취밀절상관.
Objective To observe the effects of uremia serum on monolayer permeability and Factin in cultured rat pulmonary microvascular endothelial cell (RPMVEC) and to investigate the mechanism of injury of RPMVEC induced by uremia serum.Methods RPMVEC was isolated and cultured from Wistar rat in vitro.The effects of serum of uremia patients on monolayer permeability of RPMVEC were observed with microfiher, and F-actin expression was evaluated by flow eytometry.Results Serum of uremia patients induced the increased permeability of RPMVEC monolayer for 6 h and 12 h( P <0.01), depolymerization of F-actin for 6 h and 12 h(P <0.01),the increased permeability of RPMVEC monolayer induced by serum of uremia patients is significandy correlated with the depolymerization of F-actin(r = - 0.927, P <0.01 ).Conclusion Serum of uremia patients may induce the elevation of permeability monolayer and the depolymerization of F-actin in RPMVEC.The elevation of permeability monolayer induced by serum of uremia patients in RPMVEC is significantly correlated with the depolymerization of F-actin.
