CAJ | 학술논문

目的：探讨罗格列酮对人腹膜微血管内皮细胞水孔蛋白1（ AQP1）、血管内皮生长因子A （ VEGF-A）及环氧合酶2（COX-2）蛋白的影响。方法：（1）体外培养人腹膜微血管内皮细胞并分为4组；用倒置显微镜观察细胞形态学变化；（2） Western blotting 检测细胞AQP1、VEGF-A和COX-2蛋白的表达；（3） real-time PCR检测细胞AQP1、VEGF-A及COX-2 mRNA的表达。结果：罗格列酮可促进人腹膜微血管内皮细胞增殖，上调AQP1蛋白及基因的表达（P＜0.05），下调VEGF-A和COX-2蛋白和mRNA的表达，过氧化物酶体增殖物激活受体γ（PPAR-γ）拮抗剂GW9662可部分抑制罗格列酮上调的AQP1表达（P＜0.05），但对VEGF-A及COX-2表达无明显影响（P＞0.05）。结论：罗格列酮能够上调腹膜微血管内皮细胞AQP1的表达，下调VEGF-A 及COX-2的表达，这可能与罗格列酮增加腹膜水转运、减轻腹膜纤维化有关。
목적：탐토라격렬동대인복막미혈관내피세포수공단백1（ AQP1）、혈관내피생장인자A （ VEGF-A）급배양합매2（COX-2）단백적영향。방법：（1）체외배양인복막미혈관내피세포병분위4조；용도치현미경관찰세포형태학변화；（2） Western blotting 검측세포AQP1、VEGF-A화COX-2단백적표체；（3） real-time PCR검측세포AQP1、VEGF-A급COX-2 mRNA적표체。결과：라격렬동가촉진인복막미혈관내피세포증식，상조AQP1단백급기인적표체（P＜0.05），하조VEGF-A화COX-2단백화mRNA적표체，과양화물매체증식물격활수체γ（PPAR-γ）길항제GW9662가부분억제라격렬동상조적AQP1표체（P＜0.05），단대VEGF-A급COX-2표체무명현영향（P＞0.05）。결론：라격렬동능구상조복막미혈관내피세포AQP1적표체，하조VEGF-A 급COX-2적표체，저가능여라격렬동증가복막수전운、감경복막섬유화유관。
AIM:To investigate the effect of rosiglitazone on the expression of aquaporin-1 (AQP1), vascular endothelial growth factor-A ( VEGF-A ) and cyclooxygenase-2 ( COX-2 ) in human peritoneal microvascular endothelial cells.METHODS: Cultured peritoneal microvascular endothelial cells were divided into 4 groups.The morphological changes of the cells were observed under inverted microscope .The protein expression of AQP1, VEGF-A and COX-2 in hu-man peritoneal microvascular endothelial cells was determined by Western blotting .The mRNA expression of AQP1, VEGF-A and COX-2 in the cells was measured by real-time PCR.RESULTS:Rosiglitazone stimulated the proliferation of the cells.Rosiglitazone up-regulated the expression of AQP1, and down-regulated the expression of VEGF-2 and COX-2 at mRNA and protein levels in the cells .The PPAR-γantagonist GW9662 partly inhibited the up-regulation of AQP1 expres-sion by rosiglitazone (P<0.05), but had no obvious effect on the expression of VEGF-A and COX-2 (P>0.05).CON-CLUSION:Rosiglitazone up-regulates the expression of AQP 1 and down-regulates the expression of VEGF-A and COX-2 in human peritoneal microvascular endothelial cells , thus promoting water transportation and attenuating peritoneal fibrosis during peritoneal dialysis .