罗格列酮对人腹膜间皮细胞和脐静脉内皮细胞水孔蛋白-1的影响

目的探讨体外条件下核受体Peroxisome proliferator-activated receptor gamma（PPAR-gamma）激动剂罗格列酮（RosiglitazoneRGZ）对人腹膜间皮细胞（human peritoneal mesothelial cells HPMCs）、人脐静脉内皮细胞（Human Umbilical Vein Endothelial Cells HUVECs）水孔蛋白-1（aquaporin 1 AQP1）增殖以及基因水平的影响。方法以HPMCs和HUVECs为研究对象,将实验分成四组：对照组、RGZ组（10uMRGZ）、GW9662组（peroxisome proliferator-activated receptor gamma antagonist 20uMGW9662）以及GW9662＋R组（20uMGW9662提前作用1H后加入10uMRGZ）。应用比色法（CCK-8）观察RGZ等对HPMCs和HUVECs增殖的影响。应用Realtime-PCR方法检测罗格列酮等对水孔蛋白-1基因水平表达的影响。结果①GW9662＋R组与对照组相比,可以明显抑制HPMCs增殖（P〈0.01）,其他组对HPMCs增殖没有明显影响（P〉0.05）。而对HUVECs,RGZ组、GW9662组以及GW9662＋R组都可以促进其增殖（P〈0.01）;②罗格列酮上调这两种细胞AQP1基因水平的表达。结论在体外,罗格列酮可影响HPMCs和HUVECs水孔蛋白质1基因水平的表达。其作用机制可能是通过激活PPAR-gamma从而影响上述两种细胞的AQP1的表达。

Effect of rosiglitazone on aquaporin-1 expression in human peritoneal mesothelial cells and human umbilical vein endothelial cells

Objective To study the effect ofrosiglitazone （RGZ）, a ligand ofperoxisome proliferatoractivated receptor γ （PPAR-γ）, on the cell-proliferation and expression ofaquaporin- 1 mRNA in human peritoneal mesothelial cells （HPMCs） and human umbilical vein endothelial cells （HUVECs） in vitro. Methods Each kind of cells were divided into 4 groups： the control group, the RGZ group （10μM RGZ）, the GW9662 group （GW9662, a PPAR-γ antagonist, 20μM） and the GW9662＋RGZ group （cells were cultured for 1 h in the medium containing 20μM GW9662 and then in the medium containing 10μM RGZ）. Cell-proliferation affected by RGZ was assayed by using a CCK-8 cell-counting kit. Aquaporin-1 mRNA in HPMCs and HUVECs was measured by quantitative real-time PCR. Results Proliferation of HPMCs was inhibited in the GW9662＋RGZ group （P〈0.01） as com- pared with that of the control group, The inhibition was not found in the RGZ group and the GW9662 group （P〉 0.05）. However, proliferation of HUVECs presented in the 3 treated groups （P〈0.01）. RGZ up-regulated aquaporin- 1 mRNA in HPMCs and HUVECs. Conclusion RGZ can up-regulate the expression of aquaporin-1 at the mRNA level, probably through the activation of the PPARγ pathway in HPMCs and HUVECs.