中文摘要：

目的观察小白菊内酯（PTL）对硝基酪氨酸（NT）诱导的大鼠肾小球系膜细胞核转录因子-κB（NF—κB）及单核细胞趋化蛋白-1（MCP-1）表达的影响。方法通过体外培养的系膜细胞进行研究。设立低糖对照组（糖浓度为5．6mmol／L）、NT试验组（100μmol／L）及吡咯二流氨基甲酸酯（PDTC）干预组（100μmol／L）和含PTL（1，5，10μmol／L）的干预组。以实时荧光定量PCR检测MCP-1mRNA的表达；用酶联免疫（ELISA）法检测培养细胞上清中MCP-1；WesternBlot方法检测系膜细胞核内NF—κBp65蛋白的表达。结果NT诱导系膜细胞24h后，MCP-1分泌明显增强（P〈0．01），小白菊内酯（1，5，10μmol／L）对NT诱导的系膜细胞分泌的MCP-1的抑制作用随浓度增大而逐渐增强。系膜细胞在低浓度葡萄糖作用下可低水平表达MCP-1mRNA，NT作用24h后MCP-1mRNA表达明显增强（P〈0．01），PTL可明显下调NT诱导的MCP-1mRNA表达（P〈0．01）。在NT作用1h后，系膜细胞核内的NF—κBp65蛋白核内表达增强（P〈0．05），PTL能部分抑制NT诱导的系膜细胞NF—κBp65进入细胞核内（P〈0．05）。结论在体外含NT培养条件下，小白菊内酯可部分逆转NT诱导的系膜细胞NF—κBp65进入细胞核内，进-步抑制MCP-1mRNA及蛋白在系膜细胞的表达，提示小白菊内酯对MCP-1的影响可能与NF—κB的抑制有关。

英文摘要：

Objective To observe the effect of parthenolide（PTL） on nitrotyrosine（NT） induced nuclear factor-κB（NF-κB） activation and monocyte chemoattractant protein- 1 （MCP- 1 ） expression in rat mesangial cells（MCs）. Methods MC cells were cultured in vitro. The low glucose control group （low glucose concentration of 5.6 mmol/L）, the NT test group（100 μmol/L）, the pyrrolidine dithiocar- bamate （PDTC） intervention group （100 μmol/L） and the PTL intervention groups （containing PTL 1, 5, 10 μmol/L respectively） were set up. The enzyme- linked immunoabsorbent assay （ELISA） method was adopted to detect MCP- 1 protein in the supernatant and the expression of NF- κB p65 protein in cell nucleus was detected by Western Blot. Results The MCP- 1 protein secretion was enhanced obviously after NT inducing MCs for 24 h（P 〈0.01）, the inhibiting effect of PTL（1, 5, 10 μmol/L） on MCP-1 se- creted by NT induced MCs was gradually enhanced with the concentration increase. MCs could express MCP- 1 mRNA in the low level under the low glucose action. MCP- 1 mRNA expression was enhanced obviously after NT action for 24 h （P 〈 O. 01）. PTL could obviously down-regulate NT induced MCP-1 mRNA expression（P〈 0.01）. The expression of NF-κB p65 protein in the eel1 nucleus was enhanced after NT action for l h （P 〈 0. 05）. PTL can partially restrain NT- induced NF- κB p65 to enter into cell nucleus（ P 〈 0. 05）. Conclusion PTL can partially reverse NT- induced NF- κB p65 to enter into cell nucleus, further inhibit the expression of MCP- 1 mRNA and protein in MCs, which indicating that the influence of PTL on MCP- 1 may be related with the inhibition of NF- κB.