中文摘要：

目的观察大鼠肾小管上皮细胞（NRK-52E细胞）缺氧复氧损伤时内质网应激蛋白和炎症细胞因子表达的改变及其意义,以探讨缺氧复氧诱导大鼠肾小管上皮细胞内质网应激与炎症反应的关系。方法 NRK-52E细胞用含5%胎牛血清的DMEM液培养于37℃、5%CO2恒温培养箱。将细胞分为正常对照组和缺氧/复氧损伤（hypoxia reoxygenation,H/R）组。采用全自动生化分析仪检测细胞培养液上清LDH活性,Western blot方法检测GRP78、CHOP蛋白表达,ELISA法检测细胞上清IL-β水平。结果①与对照组细胞培养液上清LDH（22.07±1.23）U/L比较,H/R损伤组（45.93±6.42）U/L显著增加（P〈0.05）。②与对照组肾小管上皮细胞GRP78表达（0.80±0.04）比较,H/R损伤组（1.24±0.04）明显增加（P〈0.05）。③与对照组肾小管上皮细胞CHOP表达（0.81±0.05）比较,H/R损伤组（1.19±0.05）明显增加（P〈0.05）。④与对照组IL-1β水平（6.55±2.03）pg/ml比较,H/R损伤组（14.93±2.26）pg/ml显著增加（P〈0.01）。结论缺氧复氧可以诱导大鼠肾小管上皮细胞内质网应激与炎症反应。内质网应激上调CHOP表达可能在肾小管上皮细胞缺氧复氧损伤炎症反应中具有重要作用。

英文摘要：

Objective To study the expression change of endoplasmic reticulum stress proteins and inflammatory cytokines during hypoxia/reoxygenation in rat renal tubular epithelial cell line NRK-52E,and to discuss the relationship between endoplasmic reticulum stress and hypoxia/reoxygenation-induced inflammation in NRK-52E cells.Methods NRK-52E cells were cultured in DMEM containing 5% fetal bovine serum in a thermostatic incubator（37 C,5% CO2）.The cells were divided into a normal control group and a hypoxia/reoxygenation（H/R） group.LDH activity in the supernatant of cell culture media was tested with an automatic biochemical analyzer.The expression of glucose-regulated protein 78（GRP78） and of CCAAT/enhancer-binding protein homologous protein（CHOP） was detected with Western blot analysis.The IL-β level in the supernatant of cell culture media was measured with ELISA.Results LDH activity in the supernatant of cell culture medium of the H/R group（45.93±6.42 U/L） increased significantly,as compared with that of the control group（22.07±1.23 U/L）（P 0.05）.GRP78 expression level（GRP78/β-actin） and CHOP expression level（CHOP/β-actin） in the cells of the H/R group was 1.24±0.04 and 1.19±0.05,respectively,significantly higher than those of the control group 0.80±0.04（P0.05） and 0.81±0.05（P0.05）,respectively.The IL-β level in the H/R group（14.93±2.26 pg/ml） had a remarkable difference from that in the control group（6.55±2.03 pg/ml）（P 0.01）.Conclusion Hypoxia/reoxygenation can induce endoplasmic reticulum stress and inflammation in rat renal tubular epithelial cells.CHOP expression up-regulated by endoplasmic reticulum stress is probably important in the hypoxia/reoxygenation-induced inflammation in renal tubular epithelial cells.