CAJ | 학술논문

目的：探讨过氧化物酶体增殖物受体γ（ PPARγ）对高糖介导的血管内皮细胞活性氧（ ROS）生成的影响及机制。方法：人脐静脉内皮细胞（ HUVECs ）以高糖（33 mmol／L D-葡萄糖）培养基培养，并以低糖培养基（5.5 mmol／L D-葡萄糖）作为对照。分别利用超氧阴离子和一氧化氮（ NO）的荧光探针观察PPARγ激动剂比格列酮对高糖环境下内皮细胞超氧阴离子和NO水平的影响，以Western blotting 法观察解偶联蛋白2（ UCP2）的表达。结果：PPARγ激动剂比格列酮可显著抑制高糖介导的ROS生成，并可防止高糖介导的内皮细胞NO水平的下降，而上述作用可被PPARγ的阻断剂GW9662所阻断。 PPARγ激动剂可上调内皮细胞UCP2的表达，而通过genipin抑制UCP2可显著减弱PPARγ激动剂的作用。结论：激活PPARγ可显著抑制高糖介导的ROS的生成，而该作用可能与其上调UCP2的表达有关。
목적：탐토과양화물매체증식물수체γ（ PPARγ）대고당개도적혈관내피세포활성양（ ROS）생성적영향급궤제。방법：인제정맥내피세포（ HUVECs ）이고당（33 mmol／L D-포도당）배양기배양，병이저당배양기（5.5 mmol／L D-포도당）작위대조。분별이용초양음리자화일양화담（ NO）적형광탐침관찰PPARγ격동제비격렬동대고당배경하내피세포초양음리자화NO수평적영향，이Western blotting 법관찰해우련단백2（ UCP2）적표체。결과：PPARγ격동제비격렬동가현저억제고당개도적ROS생성，병가방지고당개도적내피세포NO수평적하강，이상술작용가피PPARγ적조단제GW9662소조단。 PPARγ격동제가상조내피세포UCP2적표체，이통과genipin억제UCP2가현저감약PPARγ격동제적작용。결론：격활PPARγ가현저억제고당개도적ROS적생성，이해작용가능여기상조UCP2적표체유관。
AIM:To explore the effects of PPARγon the elevated level of reactive oxygen species ( ROS) in-duced by high glucose and its mechanism .METHODS:Human umbilical vein endothelial cells ( HUVECs) were cultured with DMEM containing high glucose (33 mmol/L D-glucose), and DMEM containing lower glucose (5.5 mmol/L D-glu-cose) was used as control .Superoxide anion and nitric oxide fluorescence probes were used to observe the effects of PPAR γagonist on ROS and NO productions in the HUVECs .The uncoupling protein 2 (UCP2) protein level in the HUVECs was detected by Western blotting .RESULTS:PPARγagonist pioglitazone inhibited the ROS generation and prevented the de-crease in NO level under high glucose condition , and these effects were reversed by pretreatment with PPARγantagonist GW9662.The results of Western blotting indicated that PPARγagonist pioglitazone up-regulated the UCP2 expression un-der high glucose condition , and this effect was also blocked by GW 9662.Inhibition of UCP2 by genipin attenuated the effect of pioglotazone on the ROS production .CONCLUSION: Activation of PPARγinhibits ROS generation under high glucose condition , and this effect may mediate by up-regulation of UCP2.