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作 者:李宏博[1] 张景坤[2] 吴超[1] 王冀[3] 张玉军 高丽霞[5]
机构地区:[1]河北医科大学基础医学院病理学教研室,河北石家庄050017 [2]河北医科大学国际合作与交流处,河北石家庄050017 [3]河北医科大学教务处,河北石家庄050017 [4]石家庄人民医学高等专科学校病理教研室,河北石家庄050091 [5]河北医科大学第二医院免疫风湿科,河北石家庄050000
出 处:《临床荟萃》2014年第8期891-895,共5页Clinical Focus
基 金:河北省教育厅自然科学研究计划(Z2009151);河北省卫生厅医学重点资助项目(08055)
摘 要:目的探讨高迁移率族蛋白1(high mobility group protein,HMGB-1)、Toll样受体4(Toll-like receptor4,TLR4)和血管细胞黏附因子1(vascular cell adhesion molecule-1,VCAM-1)与狼疮性肾炎(LN)血脂异常和动脉粥样硬化(atheroscleros,AS)的关系。方法收集20例正常健康人、30例系统性红斑狼疮(SLE)无肾脏损害和35例LN患者外周静脉血,检测血脂水平、HMGB1mRNA、TLR-4mRNA、血清HMGB1蛋白水平、外周血单核细胞CD14+/VCAM-1表达。结果 LN组患者血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)明显高于SLE组和正常对照组(P<0.01);LN组患者血清中HMGB1表达量(9.86±1.54)g/L高于正常对照组(7.85±0.75)g/L和SLE组(7.46±1.53)g/L;HMGB1mRNA和TLR4mRNA表达亦升高(P<0.01),SLE组和正常对照组差异无统计学意义;与SLE组和正常对照组比较,LN组单核细胞中CD14+/VCAM-1表达明显增强;在LN组患者外周血中HMGB1表达与TLR4、血脂(TG、LDL-C)呈正相关(r=0.915、0.536、0.448,P<0.05或<0.01)。结论在LN发病过程中晚期炎症介质HMGB1可能通过与TLR4结合,促进单核细胞表面VCAM-1表达,从而引起血脂异常,参与AS的形成。Objective To investigate the relationship of high mobility group protein 1(HMGB1),Toll-like receptors 4(TLR-4),vascular endothelial cell adhesion molecule-1(VCAM-1)with atheroscleros(AS)and abnormality of blood lipids in lupus nephritis(LN)patients.Methods Serum samples from 65 patients including 30 patients with systemic lupus erythematosus(SLE),35 patients with LN,and 20 healthy volunteers as controls were measured in lipid profiles;HMGB1,TLR-4mRNA expression and CD14+/VCAM-1in peripheral blood monocytes were detected.Results Serum triglycerides(TG),total cholesterol(TC)and low-density lipoprotein cholesterol(LDL-C)were significantly higher than those in SLE and normal control group(P〈0.01).The HMGB1protein(9.86±1.54)g/L in blood serum of patients with LN was higher than that in SLE(7.46±1.53)g/L and control group(7.85±0.75)g/L.HMGB1 mRNA and TLR-4mRNA expression in LN group were higher than those in SLE group and the control group(P〈0.01),while there was no significant difference between SLE group and control group.The expression of VCAM-1in CD14+monocytes of patients with LN was higher than that of patients with SLE and normal control group.In LN peripheral blood,the HMGB1 expression showed positive correlation with TLR4 and lipids(TG,LDL-C)(r=0.915,0.536,0.448,P〈0.05or〈0.01).Conclusion In LN pathogenesis,HMGB1,the later inflammatory mediators,may promote the expression of monocyte cell surface VCAM-1by binding to TLR4,causing dyslipidemia,and involved in the formation of AS.
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