血清RAGE、HMGB1水平与重症肺炎急性呼吸窘迫综合征发病及IFN-γ/IL-4变化的关系

目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至2022年2月我院收治的100例SP患儿为研究对象,根据患儿是否发生继发性ARDS将患儿分为ARDS组(n=56)和对照组(n=44),收集患儿一般资料,采集外周血以酶联免疫吸附法进行RAGE、HMGB1、IFN-γ和IL-4表达水平检测,采用多因素logistic回归分析SP患儿继发ARDS的影响因素,采用Pearson相关性分析其与IFN-γ/IL-4的相关性,并采用受试者工作曲线(ROC)分析RAGE、HMGB1表达对SP患儿继发ARDS的预测价值。结果两组SP患儿性别、年龄、体温以及发病季节之间无显著差异,ARDS组致病菌种类多于对照组,PaO_(2)/FiO_(2)和APS评分、血清RAGE、HMGB1、IFN-γ和IL-4表达水平以及IFN-γ/IL-4比值均高于对照组(P<0.05)。经多因素logistic回归分析可知,致病菌种类、PaO_(2)/FiO_(2)、RAGE、HMGB1表达、IFN-γ、IL-4和IFN-γ/IL-4均为SP患儿继发ARDS的影响因素。经Pearson相关检验,SP患儿血清RAGE、HMGB1表达水平与IFN-γ、IL-4和IFN-γ/IL-4均呈正相关(P<0.05)。经ROC曲线分析可得,血清RAGE、HMGB1水平预测SP患儿发生ARDS的AUC分别为0.707和0.750,灵敏度分别为73.2%、64.3%,特异度分别为68.2%、77.3%,两者联合预测的AUC为0.848,灵敏度和特异度分别为80.4%和81.8%。结论SP继发ARDS患儿血清中RAGE、HMGB1表达水平较高,与IFN-γ/IL-4呈正相关,监测患儿血清RAGE、HMGB1表达对SP患儿继发ARDS的风险有一定的预测价值。

IFNα-2b治疗323例HBeAg阳性慢性乙型肝炎的效果

目的 探讨IFNα-2b抗病毒治疗乙型肝炎e抗原(HBeAg)阳性慢性乙型肝炎(CHB)患者的效果。方法回顾性分析2010年1月至2014年1月就诊于南昌大学第二附属医院并接受IFNα-2b治疗的323例HBeAg阳性CHB患者的临床资料,按丙氨酸氨基转移酶(ALT)水平将其分为3组:ALT<2×ULN(A1组,n=111)、2×ULN≤ALT≤5×ULN(A2组,n=111)以及ALT>5×ULN(A3组,n=101)。观察临床疗效及不良反应,并比较3组间的抗病毒效果。结果 在停药时及停药后第12、24、48、72、96、144、192、240周,323例患者的HBV-DNA阴转率分别为39.9%、40.2%、39.0%、36.2%、34.1%、33.4%、31.3%、30.7%、30.7%;HBsAg阴转率分别为6.2%、6.2%、6.2%、5.9%、5.9%、5.9%、5.6%、5.6%、5.6%;HBeAg血清学转换率分别为28.2%、31.0%、32.8%、34.4%、33.7%、33.1%、32.8%、32.5%、31.6%。在各随访时间点,3组患者的HBV-DNA阴转率和HBeAg血清学转换率比较,A3组显著高于A2组,A2组显著高于A1组(P<0.05);3组患者的HBsAg阴转率比较,差异无统计学意义(P>0.05)。323例患者均出现发热及类流感样症状,238例(73.7%)出现白细胞及中性粒细胞降低,35例(10.8%)甲状腺功能异常,5例(1.5%)斑秃,1例(0.3%)睡眠障碍,经过密切观察和对症处理后,患者均顺利完成疗程,各指标均基本正常。结论 IFNα-2b治疗HBeAg阳性CHB患者在停药时及停药后随访期间均表现出较好的效果,大多数患者可耐受IFNα-2b的不良反应。IFNα-2b的抗病毒效果可能与ALT水平有关。

PEG-IFNα-2b联合替诺福韦治疗慢性乙型肝炎的疗效及对HBeAg转阴率、免疫功能的影响

目的:分析聚乙二醇干扰素α-2b(PEG-IFNα-2b)联合替诺福韦治疗慢性乙型肝炎的效果及对HBeAg转阴率、免疫功能的影响。方法:选取某院2019年3月—2022年3月收治的慢性乙型肝炎患者88例作为研究对象,依据随机抽签法分成研究组与对照组,每组44例。对照组接受替诺福韦治疗,研究组接受PEG-IFNα-2b联合替诺福韦治疗,比较2组HBeAg转阴率、HBsAg转阴率、治疗前后肝功能指标[谷氨酰转肽酶(GGT)、天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)]、免疫功能指标(CD3^(+)、CD4^(+)/CD8^(+)、C3、C4)及血清炎性因子[视黄酸受体相关孤核受体(RORγt)、白细胞介素-17(IL-17)、IL-4]水平。结果:研究组HBeAg转阴率、HBsAg转阴率分别为45.45%、13.64%,高于对照组的11.36%、0,差异有统计学意义(P<0.05)。治疗后,研究组GGT、AST、ALT、IL-4、IL-17、RORγt分别为(30.42±5.39)U/L、(31.08±6.64)U/L、(29.37±4.68)U/L、(1.32±0.42)pg/mL、(0.64±0.19)pg/mL、(0.80±0.30),均低于对照组的(56.93±8.75)U/L、(38.72±5.83)U/L、(49.61±6.42)U/L、(3.91±1.14)pg/ml、(3.01±0.87)pg/ml、(1.61±0.36),差异有统计学意义(P<0.05)。研究组CD3^(+)、CD4^(+)/CD8^(+)、C3、C4分别为(66.81±8.55)%、(1.53±0.16)、(1.22±0.01)g/L、(0.42±0.07)g/L,均高于对照组的(61.03±8.49)%、(1.26±0.2)、(0.73±0.09)g/L、(0.22±0.06)g/L,差异有统计学意义(P<0.05)。结论:PEG-IFNα-2b联合替诺福韦治疗慢性乙型肝炎效果明显,可提高HBeAg、HBsAg转阴率,改善肝功能,增强免疫功能,抑制炎性反应。

急性冠状动脉综合征患者血浆sRAGE、IFN-γ浓度及其与冠状动脉病变严重程度的关系

目的 探讨不同类型急性冠状动脉综合征患者血浆中可溶性晚期糖基化终末产物受体(soluble receptor for advanced glycation end product,sRAGE)、γ-干扰素(interferon-γ,IFN-γ)浓度及其与冠状动脉病变严重程度的关系。方法 纳入2016年6月至2018年6月于首都医科大学附属北京天坛医院行冠状动脉造影的236例患者,分为急性心肌梗死组(n=42)、不稳定型心绞痛组(n=119)、非冠状动脉粥样硬化性心脏病(以下简称冠心病)组(n=75)。用酶联免疫法检测各组血浆中sRAGE和IFN-γ浓度并比较。分别分析急性心肌梗死患者、不稳定型心绞痛患者sRAGE、IFN-γ在不同Gensini评分分组中的差异及其与冠状动脉病变支数的相关性。分析急性心肌梗死患者sRAGE、IFN-γ与心肌梗死标志物心肌肌钙蛋白(cardiac troponin I,cTnI)、肌红蛋白(myoglobin,Myo)、肌酸激酶同工酶(creatine kinase isoenzyme,CK-MB)的相关性。结果 急性心肌梗死组患者sRAGE浓度最高,非冠心病组最低。急性心肌梗死组IFN-γ浓度高于不稳定型心绞痛组和非冠心病组,不稳定型心绞痛组和非冠心病组差异无统计学意义。多因素Logistics回归分析显示sRAGE浓度升高是急性心肌梗死和不稳定型心绞痛的独立危险因素,且与急性心肌梗死的关系更为密切。急性心肌梗死患者血浆中sRAGE与IFN-γ浓度呈正相关,两者均与心肌梗死标志物cTnI、Myo、CK-MB呈正相关,与Gensini评分、冠状动脉病变支数未见明显相关性。不稳定型心绞痛患者,高Gensini组sRAGE及IFN-γ浓度大于中Gensini组和低Gensini组,sRAGE浓度以三支病变组最高、单支病变组最低,IFN-γ浓度以双支病变组最高、单支病变组最低。结论 急性冠状动脉综合征患者血浆中sRAGE浓度明显升高,并且急性心肌梗死者高于不稳定型心绞痛患者。不稳定型心绞痛患者中sRAGE及IFN-γ浓度与冠状动脉病变严重程度呈正相关。

Nε-(carboxymethyl)lysine promotes lipid uptake of macrophage via cluster of differentiation 36 and receptor for advanced glycation end products

BACKGROUND Advanced glycation end products(AGEs)are diabetic metabolic toxic products that cannot be ignored.Nε-(carboxymethyl)lysine(CML),a component of AGEs,could increase macrophage lipid uptake,promote foam cell formation,and thereby accelerate atherosclerosis.The receptor for AGEs(RAGE)and cluster of differentiation 36(CD36)were the receptors of CML.However,it is still unknown whether RAGE and CD36 play key roles in CML-promoted lipid uptake.AIM Our study aimed to explore the role of RAGE and CD36 in CML-induced macrophage lipid uptake.METHODS In this study,we examined the effect of CML on lipid uptake by Raw264.7 macrophages.After adding 10 mmol/L CML,the lipid accumulation in macrophages was confirmed by oil red O staining.Expression changes of CD36 and RAGE were detected with immunoblotting and quantitative real-time polymerase chain reaction.The interaction between CML with CD36 and RAGE was verified by immunoprecipitation.We synthesized a novel N-succinimidyl-4-18Ffluorobenzoate-CML radioactive probe.Radioactive receptor-ligand binding assays were performed to test the binding affinity between CML with CD36 and RAGE.The effects of blocking CD36 or RAGE on CML-promoting lipid uptake were also detected.RESULTS The study revealed that CML significantly promoted lipid uptake by macrophages.Immunoprecipitation and radioactive receptor-ligand binding assays indicated that CML could specifically bind to both CD36 and RAGE.CML had a higher affinity for CD36 than RAGE.ARG82,ASN71,and THR70 were the potential interacting amino acids that CD36 binds to CML Anti-CD36 and anti-RAGE could block the uptake of CML by macrophages.The lipid uptake promotion effect of CML was significantly attenuated after blocking CD36 or RAGE.CONCLUSION Our results suggest that the binding of CML with CD36 and RAGE promotes macrophage lipid uptake.

MicroRNA-502-3p regulates GABAergic synapse function in hippocampal neurons

Gamma-aminobutyric acid(GABA)ergic neurons,the most abundant inhibitory neurons in the human brain,have been found to be reduced in many neurological disorders,including Alzheimer's disease and Alzheimer's disease-related dementia.Our previous study identified the upregulation of microRNA-502-3p(miR-502-3p)and downregulation of GABA type A receptor subunitα-1 in Alzheimer's disease synapses.This study investigated a new molecular relationship between miR-502-3p and GABAergic synapse function.In vitro studies were perfo rmed using the mouse hippocampal neuronal cell line HT22 and miR-502-3p agomiRs and antagomiRs.In silico analysis identified multiple binding sites of miR-502-3p at GABA type A receptor subunitα-1 mRNA.Luciferase assay confirmed that miR-502-3p targets the GABA type A receptor subunitα-1 gene and suppresses the luciferase activity.Furthermore,quantitative reve rse transcription-polymerase chain reaction,miRNA in situ hybridization,immunoblotting,and immunostaining analysis confirmed that overexpression of miR-502-3p reduced the GABA type A receptor subunitα-1 level,while suppression of miR-502-3p increased the level of GABA type A receptor subunitα-1 protein.Notably,as a result of the overexpression of miR-502-3p,cell viability was found to be reduced,and the population of necrotic cells was found to be increased.The whole cell patch-clamp analysis of human-GABA receptor A-α1/β3/γ2L human embryonic kidney(HEK)recombinant cell line also showed that overexpression of miR-502-3p reduced the GABA current and overall GABA function,suggesting a negative correlation between miR-502-3p levels and GABAergic synapse function.Additionally,the levels of proteins associated with Alzheimer s disease were high with miR-502-3p overexpression and reduced with miR-502-3p suppression.The present study provides insight into the molecular mechanism of regulation of GABAergic synapses by miR-502-3p.We propose that micro-RNA,in particular miR-502-3p,could be a potential therapeutic to rget to modulate GABAergic synapse function in neurological disorders,including Alzheimer's disease and Alzheimer's diseaserelated dementia.

Interferon beta(IFN-β) treatment exerts potential neuroprotective effects through neurotrophic factors and novel neurotensin/neurotensin high affinity receptor 1 pathway

Multiple sclerosis（MS）is a chronic autoimmune disease of the central nervous system（CNS）characterized by coexisting processes of inflammation,demyelination,axonal neurodegeneration,and gliosis.It is the most common disabling neurological disease in young adulthood.

Effect of IFN-γ/IL-10 on IL-10 Receptor Expression of Human Decidual Stromal Cells in Early Pregnancy

Objective To study the role of IFN-γ/IL-10 cytokines protein expression of human decidual stromal cells（DSC） vitro. on IL-10 receptor gene and in human early pregnancy in vitro. Methods Human DSC was isolated and cultured in vitro, and the expression of IL-10R1 and IL-10R2 gene was analyzed after cells had been treated with TH2-type cytokines IL-10 and TH1-type cytokines IFN-γ within 60 rain with semiquantitative reverse transcriptase-PCR, then the influence of IL-10 and IFN-γ on expression of IL-10R protein was examined by first trimester DSC using flow cytometry. In addition, the vitality of DSC was detected by MTT. Results IL-10R1 mRNA levels of DSC treated with IL-10 （10 ng/ml） reached the peak level within 15 rain, and were significantly lower at 30 rain, then were not detected at 45 min. The expression of IL-10R1 were induced to moderate level by IFN-γ（10 ng/ml） within 30 rain, and reduced to undetected levels at 60 min. There was no significant difference of IL-10R2 expression （P〉0.05） between treated and not with the abovementioned cytokines. The IL-10R protein expression and vitality of DSC were significantly enhanced by IL-10 （10 ng/ml） and IFN-γ （10 ng/ml） which treated DSC 48 h （P〈0.05）. Coneclusion IL-10 and IFN-γ may play an important role of biologic function in early pregnancy by influencing IL-10R expression of DSC.

肿瘤坏死因子受体相关因子3调控STING/IFN-I信号通路改善狼疮肾炎足细胞损伤的机制研究

目的 探讨肿瘤坏死因子受体相关因子3(tumor necrosis factor receptor associated factor 3,TRAF3)对IgG诱导的人肾足细胞(human podocyte cell,HPC)凋亡和炎症的影响及机制。方法 体外培养HPC,用狼疮肾炎(lupus nephritis,LN)患者的纯化IgG诱导HPC细胞24 h营造炎症环境,将细胞分为对照组、IgG-LN组、IgG-LN联合siRNA组、IgG-LN联合si-TRAF3组、IgGLN联合STING抑制剂H-151(1μmol/L)组、 IgG-LN联合si-TRAF3和STING激活剂ADUS100(10μmol/L)组。CCK-8实验用于检测HPC细胞活力;流式细胞术检测HPC细胞凋亡;RTPCR用于检测各组HPC细胞中IFN-α mRNA水平;ELISA法检测各组HPC细胞中IFN-α、IL-6、IL-1β和TNF-α分泌水平;Western Blot法检测TRAF3和STING蛋白的表达;Co-IP实验验证TRAF3和STING的相互作用。结果 TRAF3沉默抑制IgG诱导的HPC细胞凋亡和炎症因子分泌(P<0.01)。TRAF3通过与STING结合抑制IgG诱导的HPC细胞中STING/IFN-I通路活化(P<0.01)。STING/IFN-I通路抑制改善IgG诱导的HPC细胞凋亡和炎症因子分泌(P<0.01)。STING/IFN-I通路活化可逆转TRAF3沉默对HPC细胞凋亡和炎症的缓解作用。结论 TRAF3沉默可抑制STING/IFN-I活化改善LN患者血清IgG诱导的HPC细胞凋亡和炎症反应。

ANTIPROLIFERATIVE ACTIVITY OF HUMAN IFN-γ-EGF_3 FUSION PROTEIN ARE RELATED TO ITS EGF RECEPTOR COMPETITION

The relationship between antiproliferative effect of human IFN γ EGF 3 fusion protein and the influence of EGF receptor binding activity has been studied on A431 cell line. Antiproliferative activity of human IFN γ EGF 3 was higher than that of its parent IFN γ. In the 125 I EGF receptor competition experiment, the inhibition of EGF receptor binding capacity on the target cells was observed in the treatments of human IFN γ or IFN γ EGF 3, but the later was more significant. Our data suggests that the antiproliferative effects by IFN γ and its fusion protein are closely related to their EGF receptor competitions.

LncRNA AFAP1-AS1 exhibits oncogenic characteristics and promotes gemcitabine-resistance of cervical cancer cells through miR-7-5p/EGFR axis

Background:Drug resistance is the main factor contributing to cancer recurrence and poor prognosis.Exploration of drug resistance-related mechanisms and effective therapeutic targets are the aim of molecular targeted therapy.In our study,the role of long non-coding RNA(lncRNA)AFAP1-AS1 in gemcitabine resistance and related mechanisms were explored in cervical cancer cells.Methods:Gemcitabine-resistant cervical cancer cell lines HT-3-Gem and SW756-Gem were constructed using the gemcitabine concentration gradient method.The overall survival rates and recurrence-free survival rates were evaluated by Kaplan-Meier analysis.The interaction was verified through a Dual-luciferase reporter gene assay and a Biotinylated RNA pull-down assay.Cell proliferation ability was assessed through methyl-thiazolyl-tetrazolium(MTT),soft agar,and colony formation experiments.Cell cycle and apoptosis were detected byflow cytometry.Results:Up-regulation of AFAP1-AS1 in cervical cancer predicted a poor prognosis.Besides,patients in the gemcitabine-resistance group had higher levels of AFAP1-AS1 than the gemcitabine-sensitive group.AFAP1-AS1 promoted tumor growth and induced gemcitabine tolerance of cervical cancer cells.In addition,AFAP1-AS1 mediated epidermal growth factor receptor(EGFR)expression by serving as a molecular sponge for microRNA-7a-5p(miR-7-5p).This present study also proved that the knockdown of EGFR or overexpression of miR-7a-5p abolished the accelerative role of AFAP1-AS1 overexpression in cancer progression and gemcitabine tolerance.Conclusions:In general,the AFAP1-AS1/miR-7-5p/EGFR axis was tightly related to the progression and gemcitabine tolerance of cervical cancer,providing potential targets for the management of cervical cancer.

荨麻疹患者外周血单个核细胞产生IL-4、IL-10及IFNγ水平及意义

为研究荨麻疹患者外周血单个核细胞(PBMC)产生白细胞介素-4(IL-4),白细胞介素-10(IL-10)及γ干扰素(IFNγ)的水平,采用双抗体夹心ELISA方法,测定了23例荨麻疹患者PBMC产生IL-4、IL-10及IFNγ水平。结果表明荨麻疹患者PBMC产生IL-4水平明显高于正常人(P<0.01),而产生IL-10及IFNγ水平与正常人相差不显著(P>0.05)。IL-4在Ⅰ型变态反应荨麻疹发病中可能起一定作用。

儿童支原体肺炎IFN-γ、IL-4水平中西医研究现状

肺炎支原体肺炎是常见的社区获得性肺炎,其发病机制的研究结果各不相同。越来越多的实验结果表明肺炎支原体肺炎的发病与免疫学说密切相关。由Th1和Th2细胞分别释放的IFN-γ和IL-4可间接反映Th亚群的变化,在细胞的固有免疫和适应性免疫方面起到调节作用。细胞因子水平的研究有助于辅助诊断本病、判断预后及免疫治疗,使病程缩短、症状缓解。现就近几年肺炎支原体肺炎患儿血清、诱导痰及肺泡灌洗液中细胞因子IFN-γ、IL-4水平的研究进展及中药制剂对其水平的影响作一综述。

鼻腔结构异常与老年慢性鼻-鼻窦炎患者鼻腔分泌物IFN-γ、IL-5、IL-17的表达及相关性

目的探讨鼻腔结构异常与老年慢性鼻-鼻窦炎患者鼻腔分泌物干扰素(IFN)-γ、白细胞介素(IL)-5、IL-17的表达情况及相关性。方法取2014年12月至2016年12月医院收治鼻腔结构异常及老年慢性鼻-鼻窦炎患者100例为观察组。其中,鼻腔结构异常50例为结构异常组;慢性鼻-鼻窦炎患者50例为鼻窦炎组;取同期入院健康体检者50人为对照组。取3组鼻腔分泌物,采用酶联免疫吸附试验测定IFN-γ、IL-5、IL-17水平并分析其相关性。结果观察组IFN-γ、IL-5、IL-17水平显著高于对照组(P<0.05);结构异常组与鼻窦炎组显著高于对照组(P<0.05);鼻窦炎组显著高于结构异常组(P<0.05);鼻窦炎组病情比结构异常组重,鼻窦炎组鼻塞、喷嚏、鼻涕及鼻痒症状评分显著高于结构异常组(P<0.05);相关性研究显示,鼻腔结构异常、慢性鼻-鼻窦炎发病与IFN-γ、IL-5、IL-17水平呈正相关性(P<0.05)。结论鼻腔结构异常与老年慢性鼻-鼻窦炎患者均伴有IFN-γ、IL-5、IL-17水平高表达,并且患者病情越严重表达水平越高。

TLR4mAb对急性期溃疡性结肠炎小鼠结肠黏膜中促炎因子TNF-α、IFN-γ、IL-1β的影响

目的探讨TLR4单克隆抗体(toll like receptor4monoclonal antibodies,TLR4mAb)对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导的急性期溃疡性结肠炎(ulcerative colitis,UC)小鼠肠黏膜的促炎因子TNF-α、IFN-γ、IL-1β的影响。方法30只BALB/c小鼠分为A-E组,分别为对照组、模型组以及低、中、高剂量干预组。A组小鼠饮用蒸馏水7d;B-E组小鼠仅饮用5%DSS水溶液7d以产生急性期溃疡性结肠炎模型。造模开始的同时,3组干预组小鼠分别给予低、中、高剂量TLR4mAb腹腔内注射,对照组及模型组给予腹腔内注射生理盐水,以观察TLR4mAb的干预作用。观察指标包括疾病活动指数(disease activity index,DAI)、结肠组织病理学评分(histopathological score,HPS)。造模及干预7d后处死小鼠,RT-PCR法检测各组肠黏膜TNF-α、IFN-γ、IL-1β的mRNA表达。结果(1)与对照组相比,模型组小鼠结肠黏膜DAI及HPS明显增高(P<0.01)。与模型组相比,在使用TLR4mAb干预后低、中、高剂量组DAI和HPS均有不同程度的缓解,但无明显剂量依赖关系。(2)与模型组相比,在使用TLR4mAb后炎症因子TNF-α、IFN-γ、IL-1β在小鼠结肠黏膜中的表达均有不同程度的降低,并呈剂量依赖关系。结论TLR4mAb可能通过下调小鼠结肠黏膜促炎因子TNF-α、IFN-γ、IL-1β的mRNA表达而发挥其干预作用。

人IFN-β基因脂质体转染胶质瘤细胞及对其增殖的抑制作用

目的 观察β 干扰素 (IFN β)基因脂质体pSV2IFN β转染人胶质瘤细胞系SHG4 4及其对SHG4 4细胞增殖的影响。方法 应用流式细胞仪、酶联免疫吸附试验 (ELASA)及细胞免疫组织化学染色法检测脂质体 pSV2IFN β转染后 ,SHG4 4细胞IFN β的表达情况 ;应用四唑盐比色试验 (MTT)检测脂质体 pSV2IFN β转染后转染组与对照组SHG4 4细胞增殖的差异。 结果 IFN β基因脂质体pSV2IFN β转染SHG4 4胶质瘤细胞系后 4d和 6d ,对肿瘤细胞具有明显的增殖抑制作用 ,抑制率分别为 16 .7%和 32 .7%。ELASA及流式细胞仪蛋白检测均表明转染后胶质瘤细胞具有显著的IFN β表达 (P <0 .0 1) ,其中在转染后 72h和 96h ,IFN β表达量分别为 (35 .4± 2 .7)U/ml和 (4 0 .3± 3.2 )U/ml。免疫组织细胞化学实验也表明转染后的细胞有明显的IFN β的表达。 结论 IFN β基因脂质体 pSV2IFN β可转染SHG4 4胶质瘤细胞系 。

TLR2 mAb和TLR4 mAb对急性期溃疡性结肠炎小鼠结肠黏膜炎症因子IFN-γ、IL-4及IL-17表达的影响

目的探讨TLR2单克隆抗体(toll-like receptor 2 monoclonal antibodies,TLR2 mAb)和TLR4单克隆抗体(toll-like receptor 4 monoclonal antibodies,TLR4 mAb)对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导的急性期溃疡性结肠炎(ulcerative colitis,UC)小鼠结肠黏膜的炎症因子IFN-γ、IL-4及IL-17表达的影响。方法50只雄性BALB/c小鼠分为5组(每组10只):对照组(A)、模型组(B)及TLR2 mAb干预组(C)、TLR4mAb干预组(D)、TLR2 mAb和TLR4 mAb联合干预组(E)。A组小鼠饮用蒸馏水7 d;B-E组小鼠仅饮用5%DSS水溶液7 d以产生急性期溃疡性结肠炎模型。造模开始的同时,每隔48 h分别给予C、D、E干预组小鼠以TLR2 mAb(10μg)、TLR4 mAb(10μg)、TLR2 mAb(10μg)+TLR4 mAb(10μg)腹腔内注射,A、B组给予腹腔内注射生理盐水,以观察TLR2 mAb和TLR4 mAb的干预作用。观察指标包括疾病活动指数(disease activityindex,DAI)、结肠组织病理学评分(histopathological score,HS)。造模及干预7 d后处死小鼠,Real-ti me PCR法检测各组结肠黏膜TLR2、TLR4、IFN-γ、IL-4及IL-17的mRNA表达。结果(1)与A组相比,B组小鼠肠道DAI及HS明显增高(P<0.01)。与B组相比,E组小鼠肠道DAI(P<0.05)和HS(P<0.01)均明显降低。与D组相比,E组小鼠肠道HS明显降低(P<0.05)。(2)与A组相比,B组小鼠结肠黏膜TLR2、TLR4表达明显增高(P<0.01,P<0.05)。与B组相比,C、D、E组小鼠结肠黏膜TLR2、TLR4表达均有不同程度的降低。(3)与A组相比,B组小鼠结肠黏膜IFN-γ、IL-4及IL-17的mRNA表达明显增高(P<0.01,P<0.05,P<0.01)。与B组相比,C、D、E组小鼠结肠黏膜IFN-γ、IL-4及IL-17的mRNA表达均有不同程度的降低。结论TLR2 mAb和TLR4 mAb可能通过下调小鼠结肠黏膜的炎症因子IFN-γ、IL-4、IL-17的mRNA表达而发挥其干预作用。

肺癌早期患者术后心理应激现状及应激相关因子HSP70、IFN-γ关联性

目的探讨肺癌早期患者术后心理应激现状及应激相关因子热应激蛋白(HSP)70和干扰素(IFN)-γ表达情况。方法选取肺癌早期患者为研究对象,采用横断面调查研究方法,对研究对象进行问卷调查;调查问卷包括一般资料调查问卷和健康症状自评量表(SCL-90),用以评价肺癌早期患者术后心理应激程度;采用酶联免疫吸附试验检测血清HSP70、IFN-γ表达水平。结果共调查158例肺癌早期患者,其中男111例(70.2%)、女47例(29.8%)。患者SCL-90各项因子均高于常模,以焦虑、恐怖、躯体化、抑郁、人际关系敏感因子得分平均分较高(P<0.05)。血清HSP70表达水平在中度不适的肺癌早期患者表达水平最高(P<0.05),血清IFN-γ表达水平随着应激程度加重而降低(P<0.05);HSP70与躯体化因子呈正相关,与恐惧因子呈负相关,IFN-γ与恐惧因子呈负相关。结论肺癌早期患者术后广泛存在不同程度的心理问题,术后及时进行心理干预意义重大;HSP70、IFN-γ水平作为反映心理应激的监测指标存在一定的临床价值。

金欣口服液对呼吸道合胞病毒感染的BALB/c小鼠IFN-β表达的调控作用

目的通过研究金欣口服液对呼吸道合胞病毒(RSV)感染的BALB/c小鼠IFN-β表达的干预作用,探讨其抗病毒机制。方法 RSV感染BALB/c小鼠,不同剂量金欣口服液灌胃给药干预,并于首次滴鼻后24h、72h、144h取各组小鼠肺组织和肺泡灌洗液,检测IFN-β表达情况。结果 RSV感染BALB/c小鼠24h后,金欣不同剂量组均能下调RSV诱导的IFN-β的高表达(P<0.01),但金欣等效剂量组作用尤显著。RSV感染BALB/c小鼠72h后IFN-β仍呈高表达(P>0.05),但较24h模型组明显降低;金欣不同剂量组对RSV诱导的IFN-β含量显著上调(P<0.01),其中金欣等效剂量组尤显著。RSV感染BALB/c小鼠144h后IFN-β表达均明显下降(P<0.01),金欣不同剂量组均对RSV诱导的IFN-βmRNA低表达具有上调作用(P<0.01),且金欣等效剂量组尤显著。结论 RSV感染的BALB/c小鼠IFN-β表达呈现先增高后降低的趋势,金欣口服液能够影响该趋势,使小鼠体内IFN-β浓度维持在一个相对较高的水平,起到抗病毒效应,金欣口服液等效剂量组的影响尤为明显。

TNF-α和IFN-γ刺激的人脐静脉内皮细胞上IgG受体的表达

目的:检测IgG受体(FcγR)在炎症细胞因子刺激的人脐静脉内皮细胞(HUVEC)上的表达。方法:采用ELISA、免疫组化染色法、免疫荧光法和RT-PCR等方法,检测FcγRII及其表达。结果:未经细胞因子刺激的正常HU-VEC可表达低水平的FcγRIIa;经2×105U/L TNF-α和1×105U/L IFN-γ联合刺激3d后,FcγRIIa的表达提高16倍(P<0.01)。免疫荧光法检测显示,TNF-α和IFN-γ诱导的FcγRIIa表达于HUVEC表面。RT-PCR结果显示,FcγRIIamRNA表达量在TNF-α和IFN-γ刺激24h后有明显提高。结论:TNF-α和IFN-γ可通过调节FcγRIIa的转录和翻译,增强其在HUVEC上的表达。FcγRIIa的表达可能与血管炎条件下,免疫复合物在血管上的特异性定位有关。