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作 者:李辉[1]
机构地区:[1]广州市花都区人民医院内科,广东广州510800
出 处:《中西医结合肝病杂志》2016年第4期210-212,216,共4页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
摘 要:目的:研究Toll样受体(TLRs)信号转导通路负性调控因子在慢性丙型肝炎患者免疫发病机制中的作用。方法:选择2015年1月-10月我院收治的慢性丙型肝炎患者19例为研究组,正常对照组为17例本院健康志愿者,使用荧光定量PCR检测研究组与对照组外周血单个核细胞TLRs信号通路负性调节因子A20、IRAK-M、MyD88s与TLR2基因的表达;采用ELISA法检测血浆TNF-α水平。结果:研究组TLR2表达水平(17.38±3.45),高于对照组(4.24±1.37)(P<0.05);研究组负性调节因子A20相对表达量(10.53±1.16),高于对照组(1.36±0.21)(P<0.05);研究组IRAK-M相对表达量(26.22±2.62),高于对照组(9.52±1.34)(P<0.05);研究组MyD88s相对表达量(4.51±1.57),高于对照组(P<0.05)。研究组血浆TNF-α水平为(58.45±4.36)Pg/ml,明显高于对照组(20.12±2.24)Pg/ml,两组比较差异有统计学意义(P<0.05)。研究组TLR2 mRNA和血清总胆红素(TBil)呈正相关(r=0.647,P<0.05);研究组TLR2 mRNA和凝血酶原活动度(PTA)呈负相关(r=-0.663,P<0.05);研究组TLR2基因表达和同组TNF-α水平呈正相关(r=0.892,P<0.01)。结论:TLRs信号通路负性调节因子参与慢性丙型肝炎的发生,A20、IRAK-M、MyD88s等负性调节因子参与了慢性丙型肝炎发病过程中的免疫损伤。Objective:To explore the role of negative regulators of toll-like receptor(TLRs) signal pathways in immunological pathogenesis of severe hepatitis C infection.Methods:mRNA expressions of MyD88 s,IRAK-M,SIGIRR,A20 and TLR2 in peripheral blood mononuclear cells(PBMCs) in 19 cases of chronic hepatitis C,and 17 healthy controls were detected by real time fluorescence quantitative PCR.Serum levels of tumor necrosis factor-α(TNF-a) was detected by ELISA assay.Results:Compared with control group,mRNA expressions of TLR2 were higher in research group(P〈0.05),mRNA expression levels of MyD88 s,IRAK-M and A-20 as well as serum levels of TNF-a were unregulated with the progression of diseases in research group(P〈0.05).TLR2 mRNA and serum total bilirubin(TBIL) were positively correlated(r =0.647,P〈0.05) in research group,TLR2 mRNA and prothrombin activity(PTA) showed a negative correlation(r=-0.663,P〈0.05) in research group,TLR2 gene expression and the same group of TNF alpha levels were positively correlated(r = 0.892,P〈0.01) in research group.Conclusion:Negative regulators of TLRs signaling pathway participate in the pathogenesis of chronic hepatitis C,negative regulators A20^IRAK-M、MyD88s may lead to immunosuppressive in patients with chronic hepatitis C.
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