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江德富,童夏生,罗冬娇,亢晓冬,叶 辉,范广民,陈 琪.哮喘大鼠TLR1、 FasL和TRAF2表达及甲基强的松龙干预作用[J].浙江中西医结合杂志,2012,22(6):424-427
哮喘大鼠TLR1、 FasL和TRAF2表达及甲基强的松龙干预作用
Regulation with Methylprednisolone on the Expression of Toll like receptor 1, FasL, and Tumor NecrosisFactor Receptor Associated Factor 2 in Asthmatic Rats
投稿时间:2012-01-13  
DOI:
中文关键词:  大鼠 哮喘 TLR1 FasL TRAF2 肿瘤坏死因子受体相关因子 糖皮质激素
英文关键词:rats asthma Toll like receptor FasL tumor necrosis factor receptor associated factor glucocorti? coids
基金项目:浙江省医药卫生科技计划项目 (No.2007-B238), 浙江省温岭市科技局基金资助项目 (No.2009-2-55)
作者单位
江德富 浙江省温岭市第二人民医院 台州 317500 
童夏生 浙江省台州市中西医结合医院 
罗冬娇 杭州师范大学钱江学院 
亢晓冬 杭州师范大学钱江学院 
叶 辉 浙江省台州市第一人民医院 
范广民 浙江省台州市中心医院 
陈 琪 浙江省台州市中心医院 
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中文摘要:
      目的: 探讨TLR1、 FasL 和TRAF2在大鼠哮喘炎症机制中的作用, 观察甲基强的松龙对其 表达的影响。方法: 27只SD大鼠, 随机分成哮喘模型组、 正常对照组和甲基强的松龙组, 每组9只, 采用流式细胞术检测血淋巴细胞TLR1和FasL表达, 免疫组织化学法检测肺组织TRAF2表达。结 果: 哮喘组血淋巴细胞TLR1表达水平显著低于甲基强的松龙组 (P<0.05), 正常对照组血淋巴细胞 TLR1表达水平分别与哮喘组及甲基强的松龙组比较, 差异无统计学意义 (P均>0.05)。哮喘组和 甲基强的松龙组血淋巴细胞FasL表达水平均显著高于正常对照组 (P均<0.05), 而哮喘组血淋巴细 胞FasL表达水平与甲基强的松龙组比较差异无统计学意义 (P>0.05)。哮喘组TRAF2光密度值显 著高于正常对照组和甲基强的松龙组 (P均<0.01), 甲基强的松龙组TRAF2光密度值与正常对照组 比较, 差异无统计学意义 (P>0.05)。结论: 哮喘模型大鼠FasL和TRAF2表达增加, 而TLR1无变化; 甲基强的松龙能下调TRAF2和提升TLR1水平, 从而起到抗炎作用。
英文摘要:
      Objective: To investigate the potential effects of methylprednisolone on the expression of Toll like re? ceptor 1(TLR1), FasL, and tumor necrosis factor receptor associated factor 2(TRAF2) in asthmatic rats. Methods: Twenty-seven SD rats were randomly divided into 3 groups, including asthma group, control group, and methyl? prednisolone-treated group. The levels of TLR1 and FasL in blood lymphocyte were detected by flow cytometry. The expression of TRAF2 protein was detected by immunohistochemical methods. Results: The level of TLR1 in the asthma group(47.58 ± 1.46 )MFI was significantly lower than that in the methylprednisolone-treated group (52.89±3.92 ) MFI (P<0.05); The level of TLR1 in the control group did not differ to that in the asthma group or the methylprednisolone-treated group(all P>0.05) . The level of FasL in the asthma group(15.52±0.53 MFI) and the methylprednisolone-treated group (14.46±2.19 MFI)were both significantly higher than that in the con? trol group (11.73±1.39 MFI) (all P<0.05), but no significant difference was noted between the asthma group and the methylprednisolone-treated group(P>0.05). The expression of TRAF2 protein in the asthma group (0.317 ± 0.041 optical density) was dramatically higher than that in the control group (0.220±0.057 optical density) and the methylprednisolone treated group(0.235 ± 0.028 optical density) (all P<0.01) , but no significant difference was seen between the methylprednisolone-treated group and the control group(P>0.05) . Conclusion: The levels of FasL and TRAF2 were elevated and TLR1 had no change in asthmatic rats. The anti-inflammation role of meth? ylprednisolone may be partly through down-regulating TRAF2 and up-regulating TLR1, but had no effect on FasL.
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