CAJ | 학술논문

目的：观察吡格列酮对内脂素诱导人脐静脉内皮细胞（HUVECs）炎症损伤过程中的影响，探讨吡格列酮改善内皮功能的信号转导机制。方法将HUVECs随机分组，给予不同浓度的内脂素进行诱导，运用蛋白印迹法（Western blotting）检测各组细胞Toll样受体4（TLR4）、细胞间黏附分子-1（ICAM-1）、核因子-κB（NF-κB）和NK-κB抑制蛋白α（IκB-α）的表达；再给予过氧化物酶体增殖物激活受体γ（PPARγ）激动剂吡格列酮，观察各组指标表达变化。结果与正常对照组相比，内脂素呈浓度依赖性地增加ICAM-1含量，下调IκB-α蛋白的表达，同时上调TLR4的表达，差异具有统计学意义（P＜0.05），且当内脂素浓度为1×10-5mol/L时效果最显著。而吡格列酮呈浓度依赖性地抑制内脂素所诱导的上述效应，差异具有统计学意义（P＜0.05），当吡格列酮浓度为20μmol/L时效果最显著。结论吡格列酮对内脂素诱导的HUVECs炎症损伤有保护作用，其机制可能与抑制TLR4/NF-κB信号转导通路有关。
목적：관찰필격렬동대내지소유도인제정맥내피세포（HUVECs）염증손상과정중적영향，탐토필격렬동개선내피공능적신호전도궤제。방법장HUVECs수궤분조，급여불동농도적내지소진행유도，운용단백인적법（Western blotting）검측각조세포Toll양수체4（TLR4）、세포간점부분자-1（ICAM-1）、핵인자-κB（NF-κB）화NK-κB억제단백α（IκB-α）적표체；재급여과양화물매체증식물격활수체γ（PPARγ）격동제필격렬동，관찰각조지표표체변화。결과여정상대조조상비，내지소정농도의뢰성지증가ICAM-1함량，하조IκB-α단백적표체，동시상조TLR4적표체，차이구유통계학의의（P＜0.05），차당내지소농도위1×10-5mol/L시효과최현저。이필격렬동정농도의뢰성지억제내지소소유도적상술효응，차이구유통계학의의（P＜0.05），당필격렬동농도위20μmol/L시효과최현저。결론필격렬동대내지소유도적HUVECs염증손상유보호작용，기궤제가능여억제TLR4/NF-κB신호전도통로유관。
Objective To determine the effect of pioglitazone on visfantin-induced inflammatory injury in human vascular endothelial cells and investigate the underlying signal pathway of pioglitazone in improving endothelial functions. Methods Human umbilical vein endothelial cells (HUVECs) were treated by different concentrations of visfantin. Then Western blotting was used to detect the expression of Toll-like receptor4 (TLR4), intercellular cell adhesion molecule-1 (ICAM-1), nuclear factor-κB (NF-κB) and inhibitor of NK- κB-α (IκB-α). Their expression levels were measured again after the cells were respectively exposed to the agonist of peroxisome proliferator activated receptor gamma (PPARγ), pioglitazone. Results Compared with the control group, visfantin enhanced the expression of ICAM-1 in a dose-dependent manner, and also induced TLR4 up-regulation and IκB-α down-regulation (P<0.05), with visfantin at dose of 1×10-5mol/L showing the strongest effect. However, pioglitazone inhibited the above effects of visfatin in a dose-dependent manner, with dose of 20 μmol/L having the maximal effect. Conclusion Pioglitazone exerts protective effect on visfantin-induced inflammatory injury in human vascular endothelial cells, which may be due to its blocking TLR4/NF-κB signal pathway.