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作 者:尉秀清[1] 文卓夫[1] 郑丰平[1] 姚集鲁[2]
机构地区:[1]中山大学附属第三医院消化内科,广州510630 [2]中山大学附属第三医院感染科,广州510630
出 处:《中华肝脏病杂志》2007年第8期585-588,共4页Chinese Journal of Hepatology
摘 要:目的了解CHB患者肝组织趋化因子RANTES水平与肝脏炎症程度和临床分度的相关性,探讨肝组织趋化因子RANTES表达变化的可能原因。方法研究对象包括64例CHB患者和10名正常人,CHB患者按临床严重程度分为轻度、中度、重度,按肝组织炎症程度分为G0~G4五级,用免疫组织化学染色定性及图像分析系统定量检测肝组织趋化因子RANTES表达情况。ELISA法和RT-PCR法检测HepG2和HepG2.2.15细胞的基础RANTES蛋白和mRNA表达情况以及10 ng/ml浓度的TNFα作用下HepG2细胞在不同时间点的RANTES蛋白和mRNA表达情况。结果CHB组的肝组织RANTES的表达量较正常人组增高,阳性单位值分别为25.9±11.9和3.7±1.5(P<0.01);随着CHB患者临床分度和肝脏组织炎症分级的增加,肝组织RANTES的表达强度逐渐升高,正常人和轻、中、重度CHB患者RANTES阳性单位值分别为3.7±1.5,15.6±6.9,24.0±4.0,37.9±11.1;G0~G4患者肝组织RANTES的阳性单位值分别为3.7±1.5,15.0±5.7,21.6±5.9,30.3±8.2和40.9±12.3。各级之间比较差异均有统计学意义(P<0.05)。HepG2.2.15细胞RANTES蛋白和mRNA表达均明显强于HepG2细胞;TNFα作用下HepG2细胞RANTES蛋白和mRNA表达均明显增加。结论趋化因子RANTES可能参与CHB的发病,而肝脏内趋化因子RANTES的增高可能与HBV和TNFα的作用有关。Objectives To study the relationship between intra-hepatic levels of regulated on activation, normal T-cell expressed and secreted (RANTES) and the disease severity and liver inflammatory degrees in patients with chronic hepatitis B and the possible mechanism of the changes of intra-hepatic levels of RANTES. Methods The expression of RANTES of the livers was studied using immunohistochemical stainings and morphometric quantitative measurements in liver specimens from 10 normal subjects and 64 patients with chronic hepatitis B with different degrees of liver inflammation and different clinical severity. The expressions of RANTES protein and mRNA in cell line HepG2, HepG2.2.15 and HepG2 treated with 10 ng/ml TNF α at different times were quantified by ELISA and one-step RT-PCR. Results The expression of RANTES of the livers in patients was significantly higher than that in the normal controls. Hepatic RANTES levels increased significantly and the increases were parallel to the increases of the severity of the hepatitis, from mild, moderate to severe hepatitis (the positive units were 3.7 ±1.5, 15.6±6.9, 24.0±4.0, 37.9 ± 11.1, respectively) and from GO degree to G4 degrees of liver inflammation (the positive units were 3.7 ±1.5, 15.0 ± 5.7, 21.6 ±5.9, 30.3 ± 8.2, 40.9± 12.3, respectively). The expressions of RANTES protein and mRNA of HepG2.2.15 were higher than that of HepG2. RANTES protein and mRNA were induced in HepG2 by TNF α. Conclusion RANTES may have an important role in the pathogenesis of chronic hepatiffs B. The elevation of hepatic RANTES may be caused by hepatitis B virus and TNF α.
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