罗格列酮对尿酸致腹膜间皮细胞损伤的干预作用

目的观察PPAR-γ激动剂罗格列酮对尿酸致腹膜间皮细胞（HPMC）增殖、损伤作用的影响。方法①细胞培养及分组：待生长状况良好的HPMC株60％-80％细胞贴壁后，无血清培养基同步24h，采用15μmol／L罗格列酮预处理细胞4h后，给予600μmol／L尿酸不同作用时间（24h、48h、72h）进行干预。②指标检测：采用细胞活性检测法检测HPMC增殖情况；采用乳酸脱氢酶测定试剂盒，检测培养液中乳酸脱氢酶（LDH）水平。结果①600μmol／L尿酸作用HPMC24h、48h、72h后，抑制HPMC增殖；与对照组比较，抑制增殖作用明显（P〈0．05），差异有统计学意义；罗格列酮干预后，各不同时间点，尿酸对HPMC抑制作用减弱。②600μmol／L尿酸作用HPMC24h、48h、72h后，HPMC培养液中LDH水平增高，与对照组比较，差异有统计学意义（P〈0．05）；罗格列酮干预后，各不同时间点，HPMC培养液中LDH水平降低（P〈0．05）。结论罗格列酮能够降低尿酸对HPMC增殖抑制、损伤作用。

Effects of Rosiglitazone on Proliferation and Injury in Human Peritoneal Mesothelial Cells Induced by Uric Acid

Objective To observe the role of rosiglitazone, a peroxisome proliferator-activated reeeptor-γ（PPAR-γ） agonists in vivo proliferation and cell injury in human peritoneal rnesothelial cells （HPMC） responding to uric acid. Methods （1）Cell culture. HPMC were grown in DMEM/F12 containing 10% fetal bovine serum. When 60% -80% cells were stick on the well, they were euhured for 24 h in free serum medium so as to maintain synchronization at the phase of G0/G1. （2）Index 15 μmol/L of rosiglitazone was pre-ineubated for 4 h and cells were stimulated with 600 μmol/L of uric acid for 24,48,72 h respectively, cell proliferation which was induced by uric acid by the CellTiter-Blue Cell Viability assay, meanwhile, the levels of LDH in cultivating medium was detected by LDH Kit. Results （1）Comparison with the control group, uric acid could inhibit the proliferation of HPMC remarkably in 600 μmol/L eoneentratian for different times（24,48,72 h） ,P 〈0.05. After pre-ineubated in rosiglitazone for 4 hours, rosiglitazone could prevent the inhibition effect of uric acid on cell proliferation of HPMC at different time points （P 〈 0.05 ）. （2）Ineubation with 600 μmol/L concentrations uric acid increased the levels of LDH for different times （24,48,72 h ） in HPMC. After pre-ineubated in rosiglitazone for 4 hours, rosiglitazone could decrease the raised levels of LDH induced by uric acid （ P 〈 0.05 ）. Conclusion The results indicated that rosiglitazone could prevent the inhibition of HPMC induced by uric acid and reduced uric acid-related HPMC damage in vitro.