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哮喘大鼠TLR1、 FasL和TRAF2表达及甲基强的松龙干预作用
引用本文: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.
作者姓名:江德富  童夏生  罗冬娇  亢晓冬  叶 辉  范广民  陈 琪
作者单位:1. 浙江省温岭市第二人民医院,台州,317500
2. 浙江省台州市中西医结合医院
3. 杭州师范大学钱江学院
4. 浙江省台州市第一人民医院
5. 浙江省台州市中心医院
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)
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。

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
收稿时间:2012/1/13 0:00:00

Regulation with Methylprednisolone on the Expression of Toll like receptor 1, FasL, and Tumor Necrosis Factor Receptor Associated Factor 2 in Asthmatic Rats
jiang de-fu,tong xia-sheng,luo dong-jiao,kang xiao-dong,ye hui,fan guang-min and chen qi.Regulation with Methylprednisolone on the Expression of Toll like receptor 1, FasL, and Tumor Necrosis Factor Receptor Associated Factor 2 in Asthmatic Rats[J].Zhejiang Journal of Integrated Traditional Chinese and Western Medicine,2012,22(6):424-427.
Authors:jiang de-fu  tong xia-sheng  luo dong-jiao  kang xiao-dong  ye hui  fan guang-min and chen qi
Institution:JIANG Defu, TONG Xiasheng, LUO Dongjiao, et al. The Second People’s Hospital of Wenling, Taizhou(317500), China
Abstract: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.
Keywords:rats asthma Toll like receptor FasL tumor necrosis factor receptor associated factor glucocorti coids
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