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1.
目的探讨氧化修饰低密度脂蛋白(ox-LDL)是否能作为抗原被树突状细胞(DC)直接递呈给淋巴细胞。方法以贴壁法从人外周血分离单核细胞,加入500IU/ml的rhGM-CSF和500IU/ml的rhIL-4,培养6d后加入LPS(20ng/ml)、LDL(10μg/ml)、ox-LDL(10μg/ml),作用48h,以流式细胞仪检测DC表型(CD14、CD86和HLA-DR)的变化,与同种异体T淋巴细胞以1∶5和1∶10的比例行混合淋巴细胞增殖反应,培养4d,以MTT法检测增殖反应。结果ox-LDL10μg/ml可促进DCCD86和HLA-DR的表达,有效激发同种异体淋巴细胞反应。结论ox-LDL可在体外作为抗原被DC递呈,ox-LDL和DC均可能参与致动脉粥样硬化(AS)的特异性免疫反应。  相似文献   

2.
目的:探讨Toll样受体4/核因子-κB(TLR4/NF-κB)信号通路在氧化性低密度脂蛋白(ox-LDL)诱导的血管平滑肌细胞(VSMCs)分泌单核细胞趋化因子-1(MCP-1)中的作用。方法:取SD大鼠胸主动脉中膜培养血管平滑肌细胞,以2.5mg/L、5.0mg/L、10.0mg/L的TLR4中和抗体(TLR4阻断剂)、5μmol/L、10μmol/L、、20μmol/LPDTC(NF-κB特异性阻断剂)分别进行干预,并分别设置空白对照组和ox-LDL组,观察其对血管平滑肌细胞中ox-LDL诱导的MCP-1表达的影响。结果:与空白对照组比较,ox-LDL组VSMCs MCP-1mRNA及蛋白的表达明显升高(P<0.05);与ox-LDL组比较,用TLR4中和抗体预孵育后Anti-TLR4三组MCP-1mRNA[(1.23±0.21)比(0.81±0.02)、(0.75±0.01)、(0.49±0.01)]及其蛋白的表达[(0.64±0.05)ng/ml比(0.41±0.12)ng/ml、(0.32±0.07)ng/ml、(0.21±0.02)ng/ml]明显降低(P均<0.01),且呈浓度依赖性;用PDTC预孵育后PDTC三组MCP-1mRNA[(1.37±0.19)比(1.02±0.08)、(0.87±0.01)、(0.56±0.02)]及其蛋白的表达[(0.65±0.07)ng/ml比(0.51±0.07)ng/ml、(0.30±0.08)ng/ml、(0.19±0.02)ng/ml]亦明显降低(P均<0.01),且呈浓度依赖性。结论:氧化性低密度脂蛋白是TLR4的内源性配体;氧化性低密度脂蛋白通过或部分通过TLR4/NF-κB信号通路介导血管平滑肌细胞单核细胞趋化因子-1的表达。  相似文献   

3.
目的:探讨氧化型低密度脂蛋白(ox-LDL)刺激人单核/巨噬细胞对Notch1表达的影响.方法:将人单核细胞株(THP1)经氟波酯(PMA)刺激转化为巨噬细胞后给予不同浓度ox-LDL刺激,采用RT-PCR及Western blot法检测巨噬细胞中Notch1受体mRNA及蛋白水平的表达,采用RT-PCR及ELISA法测定血管细胞黏附分子1(VCAM-1)和单核细胞趋化因子1(MCP-1)的表达.结果:与对照组比较,ox-LDL能显著上调巨噬细胞中Notch1受体mRNA及蛋白水平的表达(P<0.05),增加促炎细胞因子VCAM-1和MCP-1的分泌,并在一定范围内与ox-LDL呈浓度相关性.结论:ox-LDL能够激活巨噬细胞Notch1信号,增加促炎细胞因子分泌,促进巨噬细胞活化.  相似文献   

4.
目的 探讨类风湿关节炎(RA)患者外周血单核细胞高迁移率族蛋白-1(HMGBl)的释放和细胞内定位及沙立度胺对其的影响.方法 抽取19例RA患者和20例健康对照者外周静脉血5 ml,Ficoll密度梯度离心法分离外周血单核细胞,分别用100 ng/ml TNFα、100 ng/ml TNFα+40 μ/md沙立度胺处理细胞后,Western blot检测外周血单核细胞HMGB1的释放;细胞免疫荧光法观察外周血单核细胞中HMGB1的胞内定位.结果 (1)在无刺激因素作用下,RA患者外周血单核细胞培养液的上清中HMGBl蛋白水平较健康对照组显著增高(P<0.05).100 ng/ml TNα并不增加RA患者外周血单核细胞中HMGBl的释放,40μg/ml沙立度胺能明显降低RA患者外周血单核细胞HMGBl的释放(P<0.05).(2)RA患者外周血单核细胞中HMGB1主要分布于胞核.100 ng/m1TNFα刺激外周血单核细胞24 h后HMGB1向胞质移位,40 μg/m1沙立度胺能明显抑制TNFα所致的HMGBl胞质移位.结论 RA患者外周血单核细胞在TNFα刺激下HMGB1从核内移位至胞质,最后释放到细胞外,沙立度胺能抑制HMGB1的胞质移位和释放.  相似文献   

5.
慢性乙型肝炎患者外周血树突状细胞功能的研究   总被引:23,自引:2,他引:21  
目的研究慢性乙型肝炎患者外周血树突状细胞(DC)的免疫功能.方法从慢性乙型肝炎患者外周血中分离单个核细胞,用无血清培养法分离培养DC,用流式细胞仪检测DC表型,用液闪计数仪观察DC对T细胞的增殖作用,用ELISA法检测混合淋巴细胞反应(MLR)中细胞因子的分泌水平.结果患者组DC的CD86的表达率为(70.2±5.2)%,明显低于正常人组(95.3±3.8)%,P<0.01;其诱导T细胞增殖能力每分钟液闪计数cpm为10000±2000,明显低于正常人组(cpm为30000±3000),P<0.01患者MLR中IL-12为(120.0±19.7)pg/ml,γ-干扰素为(799.0±161.3)pg/m1,明显低于正常人组的(280.0±41.1)pg/ml和(3359.0±635.4)pg/ml,P<0.01.结论慢性乙型肝炎患者外周血DC免疫功能低下,并与DC表面CD86的表达率下降及DC分泌IL-12减少密切相关.  相似文献   

6.
目的 探讨前列腺素E1(PGE1)对人脐静脉内皮细胞单核细胞趋化蛋白-1(monocyte chemoattactant protein-1,MCP-1)表达的影响及可能机制.方法 用培养的人脐静脉内皮细胞观察氧化低密度脂蛋白(ox-LDL)对MCP-1、核因子(NF)-κB表达的影响及PGE1的干预作用.采用ELISA检测上清液MCP-1浓度,原位杂交检测MCP-1 mRNA的表达,免疫印迹检测NF-κB蛋白表达.结果 (1)PGE1(0.001、0.010、0.100 mol/L)组与ox-LDL(100 μg/ml)组比较,MCP-1蛋白表达为(0.327±0.051)、(0.214±0.213)、(0.247±0.228)pg/ml对(0.655±0.013)pg/ml,MCP-1mRNA表达为(0.061±0.008)、(0.033±0.006)、(0.026±0.004)吸光度(A)/μm2对(0.220±0.032)A/μm2,PGE1显著抑制了ox-LDL所诱导的MCP-1改变.(2)Western blot结果显示,PGE1呈浓度依赖性抑制ox-LDL所诱导的NF-κB P65蛋白表达.结论 PGE1可抑制ox-LDL诱导的内皮细胞MCP-1及NF-κB表达上调,这可能与PGE1介导的血管内皮保护作用有关.  相似文献   

7.
目的观察药物普罗布考及血红素加氧酶1小干扰RNA(HO-1 siRNA)干扰后对氧化型低密度脂蛋白(ox-LDL)诱导的人单核细胞源性树突状细胞(DCs)免疫功能的影响,探讨普罗布考抗动脉粥样硬化的潜在机制。方法分离人外周血单核细胞,加入rhGM-CSF和IL-4促其分化为未成熟DC,随机分不同组别于予普罗布考(50 mg/L),低密度脂蛋白(LDL)或ox-LDL 50mg/L干预后,流式细胞术检测DC表型平均荧光强度(MFI)值,FITC-Dextran检测DCs吞噬功能,ELISA检测细胞培养上清液细胞因子(IL-4,TNF-α)浓度,Western blot分析STAT1、phosphoTyr 701 STAT1、HO-1的表达情况。结果 (1)ox-LDL干预组DCs的MFI值(CD1a、CD40、CD86、HLA-DR)显著升高,吞噬功能减弱,促炎因子TNF-α升高,抗炎因子IL-4降低;普罗布考干预组较未干预前MFI值均有降低,吞噬功能升高,TNF-α降低,IL-4升高,差值以ox-LDL干预组最显著(P均<0.05)。(2)HO-1 siRNA干扰后普罗布考组较单纯普罗布考干预组MFI值升高,...  相似文献   

8.
目的探讨白细胞介素(IL)37对动脉粥样硬化(AS)患者单核巨噬细胞脂蛋白相关磷脂酶A2(Lp-PLA2)的抑制作用。方法选取2018年12月~2019年5月滨海县人民医院就诊的AS患者96例为AS组和健康体检者40例为对照组,收集受试者一般临床资料,检测血清IL-37和Lp-PLA2水平。2组均随机选择7例,分离培养外周血单核细胞,将对照组来源细胞分为空白1组(A组)、氧化型LDL(ox-LDL)组(B组)及IL-37+ox-LDL组(C组),将AS组来源细胞分为空白2组(D组)、AS+ox-LDL组(E组)及AS+IL-37+ox-LDL组(F组),检测各组单核细胞凋亡率和单核细胞中Lp-PLA2 mRNA水平。结果对照组与AS组性别、年龄及HDL-C比较,无统计学差异(P0.05)。与对照组比较,AS组体质量指数、单核细胞、TC、TG、LDL-C及血清Lp-PLA2和Lp-PLA2 mRNA表达明显升高(P0.01),AS组血清IL-37和IL-37 mRNA表达水平明显降低,差异有统计学意义[(4.41±0.92)ng/L vs(5.04±1.03)ng/L,4.25±2.11 vs 5.28±1.88,P0.01]。IL-37+ox-LDL刺激培养外周血单核细胞48 h后,B组较A组,E组较D组单核细胞凋亡率及Lp-PLA2 mRNA表达明显升高(P0.05);C组较B组,F组较E组单核细胞凋亡率及Lp-PLA2 mRNA表达明显降低,差异有统计学意义(P0.05)。结论 IL-37对ox-LDL诱导的单核/巨噬细胞Lp-PLA2表达可能具有抑制作用。  相似文献   

9.
目的:通过观察非对称性二甲基精氨酸(ADMA)对树突状细胞(dendritic cells,DCs)成熟及免疫的影响来探讨AS形成的可能机制。方法:贴壁法分离人外周血单核细胞,在含重组人粒-巨噬细胞集落刺激因子(rhGM-CSF 20ng/ml)和重组人白细胞介素-4(rhIL-4,10ng/ml)的完全培养基中培养,五天后收集imDC,用1、8、16umol/L的ADMA干预未成熟DC 24h。用流式细胞术检测DC细胞表面分子的表达、吞噬能力及DC的凋亡,用混合淋巴细胞反应检测成熟DC刺激T淋巴细胞增殖的能力,用ELISA检测DC细胞因子的分泌。结果:生理浓度ADMA并不刺激DC成熟及分化;但病理浓度ADMA抑制DC成熟;抑制DC诱导的T淋巴细胞增殖;诱导DC凋亡:抑制DC分泌IL-12细胞因子、TNF-α及IL-10细胞因子。结论:生理浓度ADMA并不刺激DC成熟及分化;但病理浓度AD-MA抑制DC成熟和免疫。  相似文献   

10.
目的 探讨氧化低密度脂蛋白(ox-LDL)对人单核细胞基质金属蛋白酶-9(MMP-9)、组织金属蛋白酶抑制物-1(TIMP-1)mRNA表达调控的机制,以及血凝素样氧化低密度脂蛋白受体-1(Lox-1)在其表达调控中的作用.方法 分离收集冠心病患者的外周血单核细胞,分为空白对照组(在不含血清的RPMI-1640中孵育24 h)、ox-LDL组(在不含血清的RPMI-1640中加ox-LDL 40 μg/ml孵育24 h)、多聚肌苷酸(PIA)组(在不含血清的RPMI-1640中先加PIA 250 μg/ml培育1 h,之后加入ox-LDL 40 μg/ml继续孵育24 h).收集单核细胞及细胞上清液,采用异硫氰酸胍-酚-氯仿抽提法提取总RNA,扩增目的 基因Lox-1、MMP-9、TIMP-1mRNA,并采用ELISA法测定上清液中sLox-1、MMP-9、TIMP-1浓度.结果 单核细胞经ox-LDL刺激后Lox-1、MMP-9 mRNA表达增加(0.813±0.131 vs 0.304±0.047,P<0.01;1.130±0.089 vs 0.595±0.091,P<0.01),细胞上清液中sLox-1、MMP9蛋白含量增加(16.517±2.064 vs 7.277±1.979,P<0.01;2.213±1.071 vs 0.967±0.500,P<0.01).与ox-LDL组相比,多聚肌苷酸预刺激后单核细胞Lox-1、MMP-9 mRNA表达减少(0.277±0.029 vs 0.813±0.131,P<0.01;0.715±0.286 vs 1.130±0.089,P<0.05),细胞上清液中sLox-1、MMP9蛋白含量显著减少(11.127±2.560 vs 16.517±2.064,P<0.05;1.040±0.312 vs 2.213±1.071,P<0.05),但与对照组比较无差异.TIMP-1 mRNA表达及细胞上清液中TIMP-1蛋白含量在各组间无显著差异.结论 ox-LDL可诱导人单核细胞Lox-1、MMP-9表达增加,并且Lox-1介导了ox-LDL对MMP-9表达的促进作用,但对TIMP-1表达无影响.  相似文献   

11.
目的探讨急性冠状动脉综合征(ACS)患者血管因子与冠状动脉斑块特征的相关性。方法选择56例ACS患者,年龄(60±11)岁,男37例,女19例,发病时取血,应用液相蛋白芯片结合流式细胞分析方法测定7种血管因子:可溶的P选择素(sPE)、组织血纤维蛋白溶酶原激活物(tPA)、单核细胞趋化蛋白1(MCP-1)、白细胞介素(IL)-8、IL-6、可溶的血管细胞间黏附分子1(sVCAM-1)和可溶的黏附分子40配体(sCD40L),以及相应的炎症因子;常规冠状动脉造影,并用血管内超声(IVUS)检测56个靶病变处动脉粥样斑块形态学及性质特征。分析急性心肌梗死(AMI)与不稳定性心绞痛(UA)患者、易损斑块与非易损斑块组发生斑块破裂时的血管因子改变以及斑块形态学指标与血管因子的相关性。结果存在密切相关的血管因子有sVCAM-1和sPE、sVCAM-1和sCIMOL、sCD40L和sPE、IL-6和IL-8、IL-8和MCP1、以及MCP1和sVCAM-1;易损斑块组的高敏C反应蛋白(hs-CRP)为(18.9±4.9)mg/L,IL-6为[19.5ng/L(9.2—44.6ng/L)],明显高于非易损斑块组[hs-CRP:(5.8±3.6)mg/L,IL-6:5.3ng/L(2.3—13.4ng/L),均P〈0.05];与非斑块破裂组比较,斑块破裂组的sCD40L[(474±126)ng/L比(238±35)ng/L],sPE[(107.2±39.9)ng/L比(49.1±5.6)μg/L]和MCP-1[(132±18)ng/L比(127±13)ng/L]明显升高(均P〈0.05);tPA与斑块形态之间存在一定的相关性(均P〈0.05)。sCIMOL、MCP—1,sPE和TC水平升高是发生斑块破裂的独立危险因素(均P〈0.05)。结论炎症反应作为中间过程,IL-6和CRP标志易损斑块的生物特点,对AMI可能有一定的诊断意义,而sCIMOL、MCP-1和sPE可能是另一个潜在的反映ACS严重发作的标志。  相似文献   

12.
AIM: To investigate the in vitro effect of entecavir (ETV on the function of dendritic cells (DCs) derived from chronic hepatitis B (CHB) patients. METHODS: Mononuclear cells were isolated from peripheral blood of patients with CHB. DCs wer incubated with RPMI-1640 medium supplemented wit fetal bovine serum, IL-4, granulocyte-macrophag colony-stimulating factor (GM-CSF). DCs were treate with or without ETV on the fourth day. Cell surfac molecules, including CD1a, CD80, CD83 and HLA-DR were assessed by flow cytometry. Concentrations of IL- and IL-12 in the supernatant were assayed by enzyme linked immunosorbent assay (ELISA). The ability of th generated DCs to stimulate lymphocyte proliferation wa observed. RESULTS: Compared with CHB control group, th expression levels of CD1a (29.07 ± 3.20 vs 26.85 ± 2.80 CD83 (25.66 ± 3.19 vs 23.21 ± 3.10), CD80 (28.00 ± 2.7 vs 25.75 ± 2.51) and HLA-DR (41.96 ± 3.81 vs 32.20 ± 3.04) in ETV-treated group were higher (P 〈 0.05). ETV treated group secreted significantly more IL-12 (157.6 ± 26.85 pg/mL vs 132.60 ± 22.00 pg/mL (P 〈 0.05) an had a lower level of IL-6 in the culture supernatant (83.0 ± 13.88 pg/mL vs 93.60 ± 13.61 pg/mL, P 〈 0.05) tha CHB control group. The ability of DCs to stimulate th proliferation of allogeneic lymphocytes was increase in ETV-treated group compared with CHB control grou (1.53 ± 0.09 vs 1.42 ± 0.08, P 〈 0.05).CONCLUSION: Entecavir can enhance the biological activity of DCs derived from CHB patients.  相似文献   

13.
AIM: To investigate if the nucleoside analogue lamivudine (LAM), a potent inhibitor of HBV replication, could restore the function of dendritic cells derived from patients with chronic hepatitis B (CHB) in an Asian population. METHODS: Dendritic cells (DCs) derived from mononuclearcytes of patients with chronic HBV infection were cultured in the presence of IL-4, granulocyte-macrophage colony-stimulating factors (GM-CSF) and gradient concentrations of LAM (0-2 mmol/L). Cell morphology was observed under light microscopy. Cell surface molecules, including HLA-DR, CD80, CD83, and CD1α, were analyzed with flow cytometry. The concentrations of IL-6 and IL-12 in the supernatant were assayed by ELISA. T cell proliferation was assayed by methyl thiazolyl tetrazolium (MTT). RESULTS: The expression of CD1α on DC treated with 0.5 mmol/L LAM (LAM-DC 0.5 mmol/L) was significantly higher than that of DC untreated with LAM (54.1 ± 4.21 vs 33.57 ± 3.14, P < 0.05), and so was the expression of CD83 (20.24 ± 2.51 vs 12.83 ± 2.12, P < 0.05) as well as the expression of HLA-DR (74.5 ± 5.16 vs 52.8 ± 2.51, P < 0.05). Compared with control group, LAM-DC group (0.5 mmol/L) secreted significantly more IL-12 (910 ± 91.5 vs 268 ± 34.3 pg/mL, P < 0.05), had lower levels of IL-6 in the culture supernatant (28 ± 2.6 vs 55 ± 7.36 pg/mL, P < 0.05), markedly enhanced the stimulatory capacity in the allogeneic mixed leukocyte reaction (MLR) (1.87 ± 0.6 vs 1.24 ± 0.51, P < 0.05).CONCLUSION: The lower expression of phenotypic molecules and impaired allogeneic mixed lymphocyte reaction function of dendritic cells derived from patients with HBV infection could be restored in vitro by incubation with LAM.  相似文献   

14.
Objective To investigate the relationships between vascular factors and plaque morphology in the patients with acute coronary syndrome(ACS). Methods Intravascular ultrasound(lVUS) was performed on 56 consecutively enrolled patients with ACS. Cytometric bead array for seven vascular factors(sPE,t-PA, MCP-1, IL-8,1L-6,sVCAM-1, and sCD40L) was measured by cytometry. The others biomarkers were tested by ELISA or biochemistry. Differences in bio-factors were compared between vulnerable plaque and non- vulnerable plaque groups, accte myocardial infarction (AMI) and ustable angina (UA) patients, and occurring plaque rupture. The relationship between the parameters of morphology and vascular factors was analyzed. Results There were positive correlations between sVCAM-lsPE, sVCAM-I-sCD40L, sCD40L-sPE, IL-6-ILS,ILS-MCP1, and MCPI-sVCAM-1; CRP (18.868±4.907mg/L vs 5.806±3.553 mg/L)and IL-6 (19.5 pg/ml [9.2 - 44.6 pg/ml]vs 5.3 pg/ml [2.3- 13.4 pg/ml])were elevated in the vulnerable plaque group(P 〈0.05). sCD40L(473.82± 126.11 vs 237.94± 34.78 pg/ml),sPE (107.21±39.90 vs 49.06 ±5.61ug/L) and MCP-1(132.42 ± 17.85 vs 127.17±13.27 pg/ml) were increased in the plaque rupture group(P 〈 0.05);There was correlation between tPA and plaque morphology(P 〈 0.05). Increases in sCD40L, MCP-1, sPE, and TC were independent factors for plaque rupture. Conclusions IL-6 and CRP may be biomarkers for vulnerable plaque and for diagnosis ofAMI, sCD40L, MCP-1 and sPE are potential markers when for plaque rupture patient present with severe ACS.  相似文献   

15.
AIMS: To determine the intra-vitreous levels of two pro-inflammatory cytokines [interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1)] and the anti-inflammatory cytokine interleukin-10 (IL-10) in patients with proliferative diabetic retinopathy (PDR). In addition, the relationship between the profile of cytokines and PDR activity has also been evaluated. PATIENTS AND METHODS: The study included 22 consecutive diabetic patients with PDR (4 Type 1 and 18 Type 2) on whom a vitrectomy was performed. Sixteen age-matched non-diabetic patients with other conditions requiring vitrectomy, but in which the retina was not directly affected by neovascularization served as a control group. IL-8, MCP-1 and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The vitreal levels of both IL-8 and MCP-1 were strikingly higher in diabetic patients with PDR in comparison with the control group [173.5 (64-1670) vs. 49 pg/ml (25-145), P < 0.001, and 2171 (388-6155) vs. 438 pg/ml (207-1344), P < 0.001, respectively]. In addition, the vitreous concentrations of IL-8 and MCP-1 were higher in patients with active PDR than in those patients with quiescent PDR [324.5 (80-1670) vs. 173.5 pg/ml (64-487), P = 0.06 and 3596 (1670-6155) vs. 1143 pg/ml (388-2500), P = 0.01, respectively]. However, vitreal levels of IL-10 in diabetic patients were similar to that obtained in the control group [2.89 (1.55-5.50) vs. 2.46 pg/ml (2.2-5.41), P = NS]. CONCLUSIONS: The pro-inflammatory cytokines IL-8 and MCP-1 are increased in the vitreous fluid of PDR patients without an increase in the anti-inflammatory cytokine IL-10. In addition, both IL-8 and MCP-1 intra-vitreous levels correlated with PDR activity, thus suggesting that these cytokines may be pathogenically important in PDR.  相似文献   

16.
瑞舒伐他汀预处理对外周血树突状细胞的影响   总被引:1,自引:0,他引:1  
目的探讨瑞舒伐他汀对树突状细胞(dendritic cells,DCs)成熟程度及其功能的影响。方法体外分离培养外周血单核来源的DCs,第一部分给予不同剂量的瑞舒伐他汀预处理24 h,依次分为他汀1摩组、他汀5摩组、他汀10摩组和他汀15摩组;第二部分不同时间给予10 μmol/L瑞舒伐他汀预处理依次为他汀1 h组、他汀12 h组、他汀24 h组、他汀36 h组;第三部分选用10 μmol/L瑞舒伐他汀作用36 h为预处理组;各组均用TNF-α诱导DCs成熟的方式,三部分实验中,PBS预处理为空白组,仅加TNF-α处理为对照组,用流式细胞仪检测各组DCs表面分子CD86、CD83、CD40、HLA DR、CD80的表达,用ELISA法检测DCs分泌的趋化因子,~3H胸腺嘧啶核苷掺入法检测DCs诱导自体T淋巴细胞增殖反应。Western blot法检测DCs细胞质NF-κB抑制蛋白(IκBα)、NF-κB表达。结果与对照组比较,不同浓度和不同时间作用组CD86表达均有下降趋势;经终浓度10μmol/L瑞舒伐他汀处理36 h后DCs表面分子CD83、CD40、CD86、HLA-DR、CD80均有不同程度的下调,上清液中MCP-1浓度以及DCs促T淋巴细胞增殖的作用明显下降(P0.01)。Western blot检测表明,瑞舒伐他汀预处理后各组,IκBα表达均有不同程度增加,NF-κB含量则存在不同程度的减少,并表现一定的剂量和作用时间的依赖性,但当剂量达到10μmol/L,作用时间为24 h时,作用达到一个平台期。结论瑞舒伐他汀预处理可以抑制外周血单核来源的DCs成熟,并影响DCs的促T淋巴细胞增殖能力及迁移能力。  相似文献   

17.
AIMS: Inflammation plays an essential role in the atherosclerotic process, and chemokines such as monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) seem to play a pivotal role in the pathogenesis of atherosclerosis. A possible common inflammatory basis for the pathogenesis of type 2 diabetes, metabolic syndrome and atherosclerosis has been suggested. In this study we investigated the effect of physical exercise and the HMG-CoA reductase inhibitor pravastatin on peripheral markers of inflammation in subjects with the metabolic syndrome. METHODS: The study was an unmasked randomized 2x2 factorial trial of 12 weeks duration. RESULTS: In the combined exercise groups there was a significant reduction in MCP-1 and IL-8 of 48 pg/ml (P=0.04) and 1.0 pg/ml (P=0.007), respectively, as compared to the combined non-exercise groups. There was also a significant reduction vs baseline of 50 pg/ml (33%) (P=0.002) and 0.35 pg/ml (13%) (P=0.03) for MCP-1 and IL-8, respectively. Changes in MCP-1 were significantly correlated to changes in visceral fat (r=0.41, P=0.02). CONCLUSION: The protective effect of exercise might in part be due to suppression of the inflammatory process.  相似文献   

18.
目的 研究腺相关病毒(AAV)为载体的含有乙型肝炎病毒(HBV)C基因重组病毒(rAAV-HBV-C)感染树突状细胞(DC)的效率及对DC生长和成熟的影响。 方法 从正常人外周血中分离单个核细胞收取单核细胞进行体外培养,分别用rAAV-HBV-C和293细胞裂解物感染刺激单核细胞,感染后的单核细胞在粒细胞-巨噬细胞集落刺激因子(GM-CSF)、白细胞介素4(IL-4)和肿瘤坏死因子α(TNF α)存在的条件下继续培养获得成熟的DC。用逆转录聚合酶链反应及流式细胞仪细胞内染色检测目的基因(HBV-C)的转录及表达;通过观察不同时间DC的形态及检测收获DC时其表面分化抗原(CD)的表达来评价DC的生长和成熟状态。 结果 rAAV-HBV-c感染后的DC可转录HBV-C基因并表达HBV-C抗原,病毒感染组与对照组收获的DC在细胞形态与CD表达方面差异无统计学意义。 结论 rAAV-HBV-C可有效感染DC,感染的病毒对DC的生长及成熟没有显著影响。  相似文献   

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