急性重症肝炎小鼠肝脏趋化因子IP-10 mRNA的表达及意义

目的 探讨急性重症肝炎小鼠肝脏趋化因子IP-10 mRNA的表达及意义。方法 通过腹腔注射3型鼠肝炎病毒（MHV-3）建立急性重症肝炎小鼠模型,常规HE染色后进行肝组织HAI积分评估,常规生化检测感染后各时间点血清ALT的水平,实时定量PCR技术检测感染MHV-3 0、24、48、72 h后的Babl/cJ小鼠肝内趋化因子IP-10 mRNA的表达水平。结果 感染后的Balb/cJ小鼠血清ALT的水平以及肝脏HAI积分均显著升高,肝内IP-10 mRNA水平也显著上升,在48h和72h分别为感染前的 99倍和150倍。Persion相关分析证实感染后肝内趋化因子IP-10 mRNA的表达与血清ALT及肝组织HAI积分显著正相关(P<0.05)。结论 趋化因子IP-10在小鼠急性重症肝炎肝内淋巴细胞的募集及随后的坏死性炎症和急性肝衰竭中可能发挥着重要作用。     

胃癌组织中CXCR4蛋白表达及临床意义

目的:探讨趋化因子受体4(chemokine receptor 4,CXCR4)蛋白在胃癌中的表达及其临床意义。方法:免疫组织化学法检测60例胃癌和30例远癌胃组织中CXCR4蛋白的表达,分析其与临床病理特征的关系。结果:胃癌组织中CXCR4蛋白表达明显高于远癌胃组织(P<0.05)。CXCR4在胃癌原发灶中的表达与肿瘤分期、分化程度及淋巴结转移有相关性(P<0.05),与年龄、性别、肿瘤大小无相关性(P>0.05)。结论:CXCR4高表达与胃癌进展有关,CXCR4可作为判断胃癌进展的一个指标。     

miR-106调控CC趋化因子配体2对增生型糖尿病视网膜病变中人视网膜微血管内皮细胞增殖、血管生成和炎症反应的影响

目的 探讨miR-106调控CC趋化因子配体2(CCL2)对增生型糖尿病视网膜病变(PDR)中人视网膜微血管内皮细胞(HRMEC)增殖、血管生成、炎症反应的影响.方法 GEO数据库筛选PDR中差异表达的miRNAs.高糖(25.0 mmol·L-1葡萄糖,HG)诱导HRMEC建立PDR细胞模型,qRT-PCR检测miR...     

Tissue factor antisense deoxyoligonucleotide prevents monocrotaline/LPS hepatotoxicity in mice

Tissue factor (TF) is a membranous glycoprotein that functions as a receptor for coagulation factor VII/VIIa and activates the coagulation system when blood vessels or tissues are damaged. TF was upregulated in our monocrotaline (MCT)/lipopolysaccharide (LPS) hepatotoxicity model. We tested the hypothesis that TF‐dependent fibrin deposition and lipid peroxidation in the form of oxidized low‐density‐lipoprotein (ox‐LDL) accumulation contribute to liver inflammation induced by MCT/LPS in mice. In the present study, we blocked TF using antisense oligodeoxynucleotides against mouse TF (TF‐ASO). TF‐ASO (5.6 mg kg^?1) was given i.v. to ND4 male mice 30 min after administration of MCT (200 mg kg^?1) p.o. followed after 3.5 h by LPS i.p. (6 mg kg^?1). Blood alanine aminotransferase (ALT), TF, ox‐LDL, platelets, hematocrit and keratinocyte‐derived chemokine (KC) levels were evaluated in different treatment groups. Fibrin deposition and ox‐LDL accumulation were also analyzed in the liver sections using immunofluorescent staining. The results showed that TF‐ASO significantly restored blood ALT, hematocrit and KC levels, distorted after MCT/LPS co‐treatment, as well as preventing the accumulation of ox‐LDL and the deposition of fibrin in the liver tissues, and thereby inhibited liver injury caused by MCT/LPS. In a separate experiment, TF‐ASO administration significantly prolonged animal survival. The current study demonstrates that TF is associated with MCT/LPS‐induced liver injury. Administration of TF‐ASO successfully prevented this type of liver injury. Copyright © 2012 John Wiley & Sons, Ltd.     

趋化因子受体CXCR5在肺癌中的表达及其意义

目的：探讨肺癌原发灶中趋化因子受体CXCR5的表达特点及与其临床病理的关系。方法：对79例肺癌手术切除标本组织采用免疫组化法检测CXCR5表达。结果：CXCR5在肺腺癌组织100％（46／46）中呈阳性表达,33例肺鳞癌中仅1例表达（3．0％）。CXCR5的表达与肺癌患者的性别、年龄、肿瘤大小无关（P〉0．05）,而与肺癌患者的组织学类型密切相关（P〈0．01）。结论：CXCR5表达与组织学类型密切相关。CX-CR5在肺腺癌选择性的表达值得进一步进行相关研究。     

Circulating CCL20: A potential biomarker for active vitiligo together with the number of Th1/17 cells

Background

Vitiligo is an autoimmune disease with varying pathological features. Activation of the CCL20-CCR6 axis plays an important role in chronic inflammatory diseases. However, whether CCL20-CCR6 and Th1/17 cells are indicative of active vitiligo is unclear.

CCR7信号通路与视网膜新生血管

视网膜新生血管性疾病是致盲的主要原因。趋化因子受体7(C-C chemokine receptor type 7, CCR7)可通过细胞外信号调节激酶(extracellular signal regulate kinase,ERK)通路促进血管内皮生长因子(vascular endothelial growth factor, VEGF)的表达,导致血管渗漏、血管内皮细胞增生以及新生血管形成等改变。趋化因子受体7的检测可指导视网膜新生血管性疾病的诊治。     

不同正畸力值对哺乳期大鼠正畸牙周组织中HO-1 CC类趋化因子受体1及其配体的影响

目的 探讨不同正畸力值对哺乳期大鼠正畸牙周组织中血红素氧合酶(HO-1)、CC类趋化因子受体1及其配体的影响。方法 选择3月龄Wistar大鼠126只制备哺乳期大鼠模型,成功制备72只,按随机数字表法分为0N组、0.29N组、0.49N组及0.98N组,每组18只。每组依次给予0N、0.29N、0.49N及0.98N的正畸力,比较干预前1天及干预第1、3、7 天后4组大鼠的CC趋化因子受体1(CCR1)及其配体(CCL3、CCL5)mRNA相对表达量、HO-1表达及抗酒石酸酸性磷酸酶(TRAP)破骨细胞染色阳性面积。结果 干预第1、3天,0.29 N组、0.49 N组及0.98 N组CCR1、CCR3和CCL5 mRNA表达水平及破骨细胞染色阳性面积较0N组均明显增加(P<0.05),0.49N组及0.98N组上述指标水平较0.29N组均明显增加(P<0.05),而0.49N组与0.98N组这些指标比较,差异均无统计学意义(P>0.05)。结论 正畸干预可通过促进哺乳期大鼠牙周组织中HO-1、CCR1及其配体的表达发挥作用。     

SDF‐1/CXCR4/CXCR7 is pivotal for vascular smooth muscle cell proliferation and chronic allograft vasculopathy

Chronic rejection remains a major obstacle in transplant medicine. Recent studies suggest a crucial role of the chemokine SDF‐1 on neointima formation after injury. Here, we investigate the potential therapeutic effect of inhibiting the SDF‐1/CXCR4/CXCR7 axis with an anti‐SDF‐1 Spiegelmer (NOX‐A12) on the development of chronic allograft vasculopathy. Heterotopic heart transplants from H‐2bm12 to B6 mice and aortic transplants from Balb/c to B6 were performed. Mice were treated with NOX‐A12. Control animals received a nonfunctional Spiegelmer (revNOX‐A12). Samples were retrieved at different time points and analysed by histology, RT‐PCR and proliferation assay. Blockade of SDF‐1 caused a significant decrease in neointima formation as measured by intima/media ratio (1.0 ± 0.1 vs. 1.8 ± 0.1, P < 0.001 AoTx; 0.35 ± 0.05 vs. 1.13 ± 0.27, P < 0.05 HTx). In vitro treatment of primary vascular smooth muscle cells with NOX‐A12 showed a significant reduction in proliferation (0.42 ± 0.04 vs. 0.24 ± 0.03, P < 0.05). TGF‐β, TNF‐α and IL‐6 levels were significantly reduced under SDF‐1 inhibition (3.42 ± 0.37 vs. 1.67 ± 0.33, P < 0.05; 2.18 ± 0.37 vs. 1.0 ± 0.39, P < 0.05; 2.18 ± 0.26 vs. 1.6 ± 0.1, P < 0.05). SDF‐1/CXCR4/CXCR7 plays a critical role in the development of chronic allograft vasculopathy (CAV). Therefore, pharmacological inhibition of SDF‐1 with NOX‐A12 may represent a therapeutic option to ameliorate chronic rejection changes.