| 摘要: |
| 目的：探讨p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38MAPK)、核因子-κB (nuclear factor-κB，NF-κB ) 和环氧化酶-2 (cyclooxygenase-2,COX-2)之间的关系，从而研究p38MAPK和NF-κB、COX-2在糖尿病肾病中的作用机制。方法：分别以一定浓度的高葡萄糖(25 mmol/L)、高胰岛素(100 mmol/L)、过氧化氢(100 μmol/L)和糖基化终产物(100 mg/L)孵育大鼠肾小球系膜细胞系HBZY-1一定时间；先分别以一定浓度的p38MAPK特异抑制剂SB203580(10 μmol/L)预处理细胞系HBZY-1，再给予上述4种因素孵育细胞系HBZY-1，观察细胞系HBZY-1 p38MAPK、NF-κB和COX-2的表达。结果：高葡萄糖、高胰岛素、过氧化氢和糖基化终产物均可独立激活p38MAPK，使其磷酸化表达量增加，NF-κB、COX-2表达也明显增加，与对照组比较有显著性差异(P<0.01)；SB203580预处理后，NF-κB、COX-2表达显著降低，与相应刺激组比较差异有统计学意义(P<0.01)。结论：p38MAPK可通过激活NF-κB、COX-2而诱导DM时肾脏的损害， p38MAPK和NF-κB、COX-2在糖尿病肾病的发生发展过程中可能起重要作用。 |
| 关键词: p38丝裂原活化蛋白激酶类 NF-κB 环氧化酶2 糖尿病肾病 肾小球系膜细胞 |
| DOI：10.3724/SP.J.1008.2008.00241 |
| 投稿时间：2007-08-09修订日期：2008-01-09 |
| 基金项目:国家自然科学基金(30570744). |
|
| Role of p38MAPK in regulating expression of NF-κB and COX-2 in rat mesangial cell |
| WEI Qian-ping1,DENG Hua-cong1*,ZHAO Jie2 |
| (1.Department of Endocrinology, the First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China;2.Institute of Ultrasonic Engineering, the First Affiliated Hospital, Chongqing Medical University, Chongqing 400016) |
| Abstract: |
| Objective：To investigate the relationship between p38 mitogen-activated protein kinase (p38MAPK), nuclear factor-κB (NF-κB) and cyclooxygenase-2 (COX-2), so as to study the roles of p38MAPK, NF-κB and COX-2 in diabetic nephropathy. Methods: Rat mesangial cell line HBZY-1 was incubated with certain concentrations of glucose(25 mmol/L), insulin(100 mmol/L), H2O2(100 mmol/L) and glycation endproducts (AGEs)(100 mg/L) with or without pretreatment with SB203580, a specific inhibitor of p38MAPK, then the expression of p38MAPK, NF-κB and COX-2 in the HBZY-1 cells was examined. Results: High glucose, high insulin, H2O2 and AGEs independently activated p38MAPK, increased p38MAPK phosphorylation, and significantly up-regulated the expression of NF-κB and COX-2 compared with the control group (P<0.01). Pretreatment with SB203580 significantly decreased expression of NF-κB and COX-2 compared with the corresponding stimulating group (P<0.01). Conclusion: p38MAPK may induce renal damage during diabetic nephropathy by activating NF-κB and COX-2, indicating that p38MAPK, NF-κB and COX-2 may play important roles in the development of diabetic nephropathy. |
| Key words: p38 mitogen-activated protein kinases nuclear factor-kappa B cyclooxygenase-2 diabetic nephropathy mesangial cells |
