中文摘要：

目的观察肿瘤坏死因子a（TNF—a）对大鼠肺微血管内皮细胞表达白细胞介素17受体C（IL-17RC）的影响及甲泼尼龙的干预作用。方法体外培养肺微血管内皮细胞，根据TNF-a刺激浓度和时间的差异，将肺微血管内皮细胞分为TNF-a量效组和时效组：前者以0、0．1、1、10μg/LTNF—a与肺微血管内皮细胞孵育3h；后者以10μg／LTNF—a分别与肺微血管内皮细胞孵育0、1、3、6、12h。药物干预：分别以10μg／L的TNF．仅和200μg/L甲泼尼龙＋10μg／L的TNF-a与肺微血管内皮细胞孵育3h。用反转录-PCR，Western印迹及免疫细胞化学染色法检测IL-17RC表达。反转录-PCR检测TNF-a和甲泼尼龙对肺微血管内皮细胞表达IL-17RCmRNA的影响。结果反转录．PCR和Western印迹均证实肺微血管内皮细胞表达IL-17RC，免疫细胞化学染色发现IL-17RC主要分布在肺微血管内皮细胞胞膜和胞质。量效组IL-17RCmRNA相对表达量随TNF—a浓度（0、0．1、1、10μg／L）增加逐渐升高，分别为：0．241±0．010和0．372±0．017、0．452±0．017、0．643±0．042（F=46．460，P〈O．05）。时效组IL-17RCmRNA相对表达量于lh开始上升（0．417±0．038），3h达峰值（0．674±0．018），之后渐下降（6h：0．378±0．035，12h：0．318±0．032），但均高于孵育0h组（0．197±0．008），各时相组间比较差异均有统计学意义（F=37．903，P〈0．05）。甲泼尼龙显著下调TNF．仪诱导IL-17RCmRNA过度表达（0．333±0．031比0．660±0．026，F=89．637，P〈0．05）。结论IL-17RC主要分布在肺微血管内皮细胞胞膜和胞质；TNF-a刺激诱导肺微血管内皮细胞过度表达IL．17RC；甲泼尼龙抑制TNF—a对肺微血管内皮细胞表达IL-17RC的诱导效应，从而减轻肺微血管内皮细胞的炎症反应。

英文摘要：

Objective To explore the effects of tumor necrosis factor-alpha （TNF-a） or methylprednisolone on the expression of interleukin-17 receptor C （IL-17RC） in rat pulmonary microvascular endothelial ceils （RPMVEC）. Methods Culture RPMVEC were randomly divided into dose-dependent and time-dependent groups. In dose-dependent group, cells were cultured with TNF-a （0, 0. 1, 1, 10 μg/L TNF-a） for 3 h. In time-dependent group, cells were cultured with TNF-a （ 10 μg/L） for 0, 1, 3, 6, 12 h. In the drug intervention group, cells were cultured with TNF-a （ 10 μg/L） or methylprednisolone （200 μg/L） ＋TNF-z （10 μg/L） for 3 h respectively. The expression of IL-17RC in isolated and cultured RPMVEC was identified by reverse transcription-polymerase chain reaction （RT-FCR）, Western blot and immunocytochemistry. The changes of IL-17RC mRNA were detected by RT-PCR after the stimulation of RPMVEC by TNF-a or rnethylprednisolone. Results RT-PCR and Western blot revealed that IL-17RC mRNA and protein were present in RPMVEC. The product of IL-17RC immunocytochemical reaction was predominantly located in cytoplasm and cytomembrane. In RPMVEC TNF-a significantly up-regulated IL- 17RC mRNA in a dose-dependent manner （0 μg/L TNF-agroup： 0. 241±0. 010, 0. 1 μg/L TNF-a group：0. 372 s 0. 017, 1 μg/L TNF-a group. 0. 452 s 0. 017, 10 μg,/L TNF-a group ： 0. 643 s 0. 042, F = 33.774, P 〈 0. 05）. In time-dependent group, the expression of IL-17RC mRNA rose at 1 h （0. 417 ± 0. 038）, peaked at 3 h （0. 674 s0. 018）, then decreased gradually at 6 h （0. 378 s0. 035） , but stayed higher at 12 h （0. 318 s0. 032）. When compared with 0 h group （0. 197 ±0. 008）, there were significant differences （F = 37. 903, P 〈 0. 05 ）. Methylprednisolone caused a marked attenuation of TNF-a-induced IL-17RC expression （0. 333 s 0. 031 vs 0. 660 s 0. 026, F = 89. 637, P 〈 0. 05 ）. Conclusions IL-17RC is predominantly present in cytomembrane and cytoplasm of RPMVEC. TNF-a up-regulates