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Salvianolic acid A alleviates renal injury in systemic lupus erythematosus induced by pristane in bALb/c mice

Acta Pharmaceutica Sinica b 2017年第2期7卷 159-166页

作者： Yihuang Lin Yu Yan Huifang Zhang Yucai Chen Yangyang He Shoubao Wang Lianhua Fang Yang Lv Guanhua Du State Key Laboratory of bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular Diseases beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

The purpose of this study was to investigate the effects of salvianolic acid A(SAA) in systemic lupus erythematosus(SLE) induced by pristane in bALb/c mice.Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Mice were then treated with daily oral doses of SAA for 5 months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E) and periodic acid-Schiff(PAS) staining.Western blot analysis of renal tissue was also employed.SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,Iκb and nfκb in renal tissues of lupus mice.In conclusion,the results suggest that SAA alleviates renal injury in pristane-induced SLE in bALb/c mice through inhibition of phosphorylation of IKK,Iκb and nfκb.

关键词： Salvianolic acid A SLE Renal injury Autoantibodies Pristane bALb/c mice nfκb

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Inflammatory response and insulin signaling alteration induced by PCb77

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Journal of Environmental Sciences 2010年第7期22卷 1086-1090页

作者： Jing Wang Xiaowen Lv Yuguo Du State Key Laboratory of Environmental Chemistry and Ecotoxicology Research Center for Eco-Environmental Sciences Chinese Academy of Sciences Beijing 100085 China Feed Safety Reference Laboratory of Ministry of Agriculture Feed Research Institute Chinese Academy of Agricultural Sciences Beijing 100081 China

A specific mechanism whereby inflammation may contribute to cardiovascular diseases （CVD）, insulin resistance （IR） and type Ⅱ diabetes is the induction of endothelial dysfunction placing the vascular endothelium in a key unifying position for the shared pathogenesis of these diseases. However, the mechanisms by which PCbs induce endothelial cell dysfunction are not clearly understood. In the present study, we used human umbilical vascular endothelial cells （HUVEC） as model, and inflammatory response and insulin signaling alteration induced by PCbs were examined. Results showed that PCb77 induced the expression of proinflammatory cytokines including IL-6 and Tnfα and induced U937 adhesion to HUVEC cells consistent with increased nfr, b transcription activity. On the other hand, PCb77 blocked insulin-activated Akt signaling pathway, which was restored by pretreatment with Tnfα neutralization antibody. In conclusion, PCb77 showed the potential to induce the expression of proinflammatory cytokines including IL-6, which has been shown to be powerful independent risk predictor of CVD. And PCb77 was observed to alter insulin-activated Akt signaling by Tnfa secretion for the first time.

关键词： PCb77 pro-inflammatory cytokines IL-6 Tnfα nfκb Akt

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Ubiquitin-mediated nfκb degradation pathway

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Cellular & Molecular Immunology 2015年第6期12卷 653-655页

作者： Huimin Xu Mengli You Haifeng Shi Yongzhong Hou Institute Of Life Sciences Jiangsu University Zhenjiang China

The nuclear factor κb （nfκb） transcription factor plays critical roles in inflammation and immunity. The dysregulation of nfKb is associated with inflammatory and autoimmune diseases and cancer. nfKb activation is negatively regulated by the ubiquitin-dependent proteasomal degradation pathway. In the present review, we discuss recent advances in our understanding of how ubiquitin ligases regulate the nfκb degradation pathway.

关键词： nfκb ubiquitination degradation pathway

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Potential Mechanisms Involved in Ceramide-induced Apoptosis in Human Colon Cancer HT29 Cells

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biomedical and Environmental Sciences 2009年第1期22卷 76-85页

作者： JING WANG XIAO-WEN LV AND Yu-Guo DU State Key Laboratory of Envtronmental Chemistry and Ecotoxicology Research Center for Eco-Environmental Sciences Chinese Academy of Sciences Beijing 100085 China Feed Research Institute Chinese Academy of Agricultural Sciences Beijing 100081 China

Objective To investigate the potential mechanisms of cell death after the treatment with ceramide. Methods MTT assay, DNA ladder, reporter assay, FACS and Western blot assay were employed to investigate the potential mechanisms of cell death after the treatment with C2-ceramide. Results A short-time treatment with C2-ceramide induced cell death, which was associated with p38 MAP kinase activation, but had no links with typical caspase activation or PARP degradation. Rather than caspase inhibitor, Inhibitor of p38 MAP kinase blocked cell death induced by a short-time treatment with ceramide （〈12 h）. However, inhibition of p38 MAP kinase could not block cell death induced by a prolonged treatment with ceramide （〉12 h）. Moreover, incubation of cells with ceramide for a long time （〉12 h） increased subG1, but reduced S phase accompanied by caspase-dependent and caspase-independent changes including nfr, b activation. Conclusion Ceramide-induced cell apoptosis involves both caspase-dependent and -independent signaling pathway. Caspase-independent cell death occurring in a relatively early stage, which is mediated via p38 MAP kinase, can progress into a stage involving both caspase-dependent and -independent mechanisms accompanied by cell signaling of MAPKs and nfκb.

关键词： Ceramide HT29 cells Apoptosis Cell signaling p38 MAPK nfκb

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Development of an in vitro macrophage screening system on the immunomodulating effects of feed components

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Journal of Animal Science and biotechnology 2021年第2期12卷 639-648页

作者： S.E.Sivinski L.K.Mamedova R.A.Rusk C.C.Elrod T.H.Swartz J.M.McGill b.J.bradford Department of Animal Sciences and Industry Kansas State UniversityManhattan 66506USA Department of Diagnostic Medicine/Pathobiology Kansas State UniversityManhattan 66506USA Natural biologics NewfieldNY 14867USA 2265K Anthony Hall 474 S.Shaw LaneEast LansingMI 48824USA

background:While feed components capable of modulating the immune system are highly sought after and marketed,often little evidence is available to support functional immune response claims.Thus,a high-throughput in vitro cell screening system was developed to test these compounds for innate immune signaling effects,using Saccharomyces cerevisiae and its cell wall components in addition to lauric acid and its esters as models in two separate experiments.This screening system utilized RAW 264.7 murine macrophages to assess live S.cerevisiae cells and S.cerevisiae-derived cell wall componentsβ-glucan,mannan,and zymosan(a crude cell wall preparation containing bothβ-glucan and mannan).D-mannose was also evaluated as the monomer of mannan.We also examined the effect of a saturated fatty acid(C12:0,lauric acid)and its esters(methyl laurate and glycerol monolaurate)on innate immune cell activation and cellular metabolism.RAW cells were transfected with a vector that drives expression of alkaline phosphatase upon promoter activation of nuclear factorκ-light-chain-enhancer of activated b cells(nfκb),a major inflammatory/immune transcription factor.RAW cells were incubated with 0.01,0.1 or 1 mg/mL of yeast compounds alone or RAW cells were challenged with LPS and then incubated with yeast compounds.In a separate experiment,RAW cells were incubated with 0,0.5,2.5,12.5,62.5,and 312.5μmol/L of lauric acid,methyl laurate,or glycerol monolaurate alone,or RAW cells were challenged with LPS and then incubated with fatty acid treatments.Results:Treatment with zymosan orβ-glucan alone induced nfκb activation in a dose-dependent manner,whereas treatment with D-mannose,mannan,or live S.cerevisiae cells did not.Post-treatment with mannan after an LPS challenge decreased nfκb activation,suggesting that this treatment may ameliorate LPS-induced inflammation.Slight increases in nfκb activation were found when fatty acid treatments were applied in the absence of LPS,yet substantial reductions in nfκb activation were seen when treatments

关键词： Inflammation In vitro screening system nfκb

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The role of LRRK2 on PKA-nfκb pathway in microglia cells: implications for Parkinson’s disease

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Neural Regeneration Research 2019年第10期14卷 1713-1714页

作者： Isabella Russo biology and Genetic Unit Department of Molecular and Translational Medicine University of Brescia

Leucine-rich repeat kinase 2 (LRRK2), a gene linked to autosomal- dominantly inherited and sporadic Parkinson’s disease (PD) as a risk factor, encodes a large and complex protein with a dual enzymatic activity. LRRK2 contains several domains involved in protein-protein interactions, however, the presence of both a kinase and GTPase domain points to intracellular signaling functions (Marin, 2006). While LRRK2 has been linked to several molecular pathways important for neuronal activity (Martin et al., 2014), the observation that its expression is high in microglia has attracted the attention of different groups to understand whether LRRK2 dysfunctions in these cells may impact neuronal activity as secondary event.

关键词： cells nfκb Parkinson protein GTPase impact gene has

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过表达TRIM27通过抑制nfκb/MAPK信号通路减轻小鼠重症急性胰腺炎

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中华急诊医学杂志 2022年第9期31卷 1186-1192页

作者：陈三洋宋耀东崔宗朝程波刘艳娜李孟可梅超鹏崔沪宁朱长举郑州大学第一附属医院急诊外科郑州450052 河南省急诊与创伤工程研究中心郑州450052

目的探讨过表达三基序蛋白27(tripartite motif-containing,TRIM27)对小鼠重症急性胰腺炎(severe acute pancreatitis,SAP)的保护作用及其可能机制。方法24只小鼠按随机数字表法分为假手术+对照病毒组(AAV-GFP组)、假手术+过表达TRIM27... 详细信息

目的探讨过表达三基序蛋白27(tripartite motif-containing,TRIM27)对小鼠重症急性胰腺炎(severe acute pancreatitis,SAP)的保护作用及其可能机制。方法24只小鼠按随机数字表法分为假手术+对照病毒组(AAV-GFP组)、假手术+过表达TRIM27组(AAV-TRIM27组)、SAP+对照病毒组(SAP+AAV-GFP组)、急性+过表达TRIM27组(SAP+AAV-TRIM27组),每组各6只。腹腔注射L-精氨酸(4mg/kg)制作小鼠SAP模型,假手术组注射等体积生理盐水,病毒组通过腹腔注射对照或者TRIM27过表达腺相关病毒(2×10^(11)μg/只)。各组小鼠建模后72h处死收集血清及胰腺组织标本,通过酶联免疫吸附试验检测小鼠血清淀粉酶、脂肪酶、肿瘤坏死因子-α(tumor necrosis factorα,Tnf-α)、白介素1b(interleukin-1b,IL-1b)、IL-6、人巨噬细胞趋化蛋白-1(macrophage chemoatractant protein-1,MCP-1)以及胰腺组织中丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽(glutathione,GSH)等表达,通过苏木精-伊红染色观察胰腺组织病理损伤,通过免疫组化观察小鼠胰腺组织中髓过氧化物酶(myeloperoxidase,MPO)、Ly6g阳性炎症细胞表达,通过蛋白免疫印迹试验测定胰腺组织中p-p65、p65、p-ASK1、ASK1、p-JNK、JNK、p-p38、p38等蛋白表达。结果小鼠SAP后胰腺组织中TRIM27表达显著下调(P0.05)。与SAP+AAV-GFP组相比,SAP+AAV-TRIM27组小鼠血清淀粉酶、脂肪酶以及Tnf-α、IL-1b、IL-6、MCP-1水平显著降低,胰腺组织中MDA降低、SOD和GSH升高,MPO、Ly6g等炎症细胞表达显著减少,同时p-p65、p-ASK1、p-JNK、p-p38等蛋白表达显著下调(Pnfκb/MAPK信号通路。

关键词：重症胰腺炎炎症氧化应激 TRIM27 nfκb

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Effect of Curcumin on Immune Function of Mice

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第2期25卷 137-140页

作者：李新建刘晓城 Department of Nephrology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Summary: To investigate the effect of curcumin on immune function of mice, the effect of curcumin was examined on the proliferation of spleen lymphocytes of mice and the function of phagocytosis of peritoneal macrophage by using MTT test and the expression of the nucleoprotein of nfκb p65 was determined in spleen lymphocytes by employing Western blot. Our results showed that curcumin could enhance the phagocytosis of peritoneal macrophages. Lowdose curcumin could upregulate the proliferation of spleen lymphocytes of mice, and highdose curcumin could suppress the proliferation of spleen lymphocytes. Curcumin could suppress the expression of nfκb p65. Our study suggested that curcumin can regulate immune function of mice in a dosedependent manner. The possible underlying mechanism might be its ability to suppress the activity of nfκb p65.

关键词： curcumin lymphocytes macrophages nfκb

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阿司匹林抑制子宫创伤后胎盘植入发生的初步研究

阿司匹林抑制子宫创伤后胎盘植入发生的初步研究

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作者：杨思广州医科大学

学位级别：硕士

【背景】胎盘植入(placenta accreta spectrum,PAS)是胎盘绒毛外滋养细胞(extravillous trophoblasts,EVTs)异常侵袭子宫肌层的一类疾病,根据EVTs的侵入程度不同,可以分为胎盘粘连(placenta accreta,PA)、胎盘植入(placenta increta,PI)和穿透性胎盘植入(placenta percreta,PP)三种类型。PAS是目前造成孕产妇死亡的一大原因,主要的诊断方法是孕中、晚期超声或分娩后的病理检查,由于PAS具体病理机制仍不明确,早期筛查缺少有效的可行方案,为此需要我们进一步研究探索,以挖掘标志性预测分子。近年来,有研究发现PAS患者的胎盘中存在NK细胞和T细胞分布异常,提示母胎界面免疫环境紊乱可能是EVTs过度侵袭,引发PAS的原因。阿司匹林(aspirin,ASP)作为非甾体类抗炎药,早在多年前就用于治疗各种外伤引起的炎症,基于目前低剂量ASP在临床用于预防先兆子痫(preeclampsia,PE)的现状及其抗炎特性,我们推测ASP可能具有临床干预PAS的可行性。【研究目的】本研究的目的是通过模拟人剖宫产手术,建立PAS小鼠模型,探究妊娠周期中的PAS炎性病理机制以及ASP在此过程中的抗炎作用机理。【研究方法】1)通过模拟剖宫产手术,建立PAS小鼠模型,对术后妊娠E14.5胎盘进行病理检测,分析子宫创伤对胎盘组织形态、滋养巨细胞(trophoblast giant cells,TGCs)侵袭和血管生成的影响。2)建立PAS小鼠模型并给与不同浓度的ASP,分析ASP干预小鼠子宫创伤所致胎盘植入的有效性。3)检测子宫术后炎性调控因子的m RNA表达水平变化,探究子宫创伤对其免疫环境的影响。4)检测PAS小鼠用药后,妊娠早、中、晚期的子宫、蜕膜和胎盘组织中炎性调控因子的m RNA表达水平,分析PAS妊娠周期中母胎界面免疫调控的时空变化以及ASP对子宫创伤诱发的PAS的抑制机制。【结果】1)子宫创伤引起的内膜损伤可能导致小鼠子宫、蜕膜、胎盘内的炎性反应水平升高,促进NRF2相关通路分子的表达。2)ASP可以改善子宫创伤造成的小鼠妊娠胎盘中母体血管过度生成、血管周围炎性细胞浸润增加、滋养细胞过度侵袭和迷路层(labyrinth zone,LA)血窦过度生成的现象。3)ASP可以改善小鼠子宫创伤引起的子宫、蜕膜、胎盘组织中的免疫调控紊乱,从而抑制子宫创伤诱发的胎盘植入发生。【结论】ASP可以通过调控母胎界面的炎症因子表达水平,改善子宫创伤后母胎界面的免疫调控紊乱,从而抑制子宫创伤诱导的胎盘植入。

关键词：胎盘植入阿司匹林滋养细胞促炎因子抗炎因子 nfκb NRF2

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IL-37通过抑制中性粒细胞胞外诱捕网的形成缓解CVb3诱导的心肌损伤

IL-37通过抑制中性粒细胞胞外诱捕网的形成缓解CVB3诱导的心肌损伤

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作者：厉宝娜山东大学

学位级别：硕士

研究背景病毒性心肌炎(Viral myocarditis,VMC)是一种非缺血性炎症性心肌疾病,与多种病毒感染有关,其中,柯萨奇病毒b3(Coxsackievirus b3,CVb3)是最常见的病因。CVb3诱导的直接病毒损伤和其后继发的免疫反应决定了 VMC的严重程度。由于... 详细信息

研究背景病毒性心肌炎(Viral myocarditis,VMC)是一种非缺血性炎症性心肌疾病,与多种病毒感染有关,其中,柯萨奇病毒b3(Coxsackievirus b3,CVb3)是最常见的病因。CVb3诱导的直接病毒损伤和其后继发的免疫反应决定了 VMC的严重程度。由于其发病机制尚未明确,临床上VMC患者多采用对症支持治疗,主要目的是抑制心律失常和心力衰竭。因此探索出一种新的有效的心肌炎治疗措施,对缓解心肌炎病人的症状,改善心肌炎病人的预后十分重要。中性粒细胞是人类体内含量最高的白细胞,在先天免疫与急性炎症中都发挥着至关重要的作用。在受到无菌性炎症和有菌性炎症的刺激后,中性粒细胞通过释放中性粒细胞胞外诱捕网(Neutrophil extracellular traps,NETs),捕获病原体,限制炎症的扩散。最近的研究表明,在心肌炎患者和VMC小鼠模型的心肌组织中检测到大量NETs的形成。因此,NETs的生成在心肌炎的疾病进展中可能具有重要的作用,而阻断这一过程很有希望成为治疗VMC的新靶点。白细胞介素-37(Interleukin-37,IL-37)是一种固有免疫和适应性免疫的天然保护剂,在多种炎症、癌症、自身免疫性疾病和老化中发挥了保护作用。多项研究表明,IL-37可以通过抑制核因子κb(nuclear factor kappa-b,nfκb)信号通路减轻炎症细胞的浸润,抑制细胞的凋亡及免疫反应。nfκb在多种疾病中发挥着促炎作用,触发炎症反应并刺激促炎细胞因子(如IL-1β、IL-6、Tnf-α等)的分泌,从而加速疾病的进展。因此,我们提出假设:在VMC中,IL-37可以通过调节nfκb信号通路抑制NETs的形成,减轻CVb3诱导的心肌损伤并改善其心功能。实验目的1.通过尾静脉注射IL-37腺相关病毒9(Adeno-associated virus-9,AAV9),使IL-37在小鼠体内稳定表达。2.通过腹腔注射CVb3构建VMC小鼠模型,AAV9-IL-37或DNASE1干预VMC小鼠,观察CVb3、IL-37以及DNASE1对小鼠体重、生存状态、死亡率的影响。3.通过检测各组小鼠血清中炎症因子的表达,心肌组织病理学的改变以及通过心脏超声评估心功能,探究IL-37、DNASE1对VMC小鼠心肌炎症和心功能的调节作用。4.通过检测各组小鼠血清及心肌组织中NETs的表达量,探究IL-37对NETs形成的作用。5.收集健康人外周血,分离外周血中性粒细胞,使用佛波酯(Phorbol 12-myristate 13-acetate,PMA)诱导NETs的表达,在IL-37干预中性粒细胞后,探究IL-37在体外对NETs形成的作用。6.探究nfκb信号通路在急性VMC及NETs形成中的作用,阐明IL-37在VMC小鼠炎症损伤及NETs形成中的机制。实验方法选取4-6周龄,bALb/c雄性小鼠,48只,随机分为4组:提前7天,向VMC+AAV9-NC组和VMC+AAV9-IL-37组小鼠尾静脉注射相应AAV9;第0天,向 VMC+AAV9-NC 组、VMC+AAV9-IL-37 组与 VMC+DNASE1组小鼠腹腔注射 CVb3(103TCID50)诱导小鼠急性 VMC;第 0至 7天,给予VMC+DNASE1组小鼠腹腔注射DNASE1(50μg/只,1天2次),对照组给予上述各组同体积的媒介物溶剂。每日监测小鼠体重及一般状况,并记录其生存率。第7天行心脏超声评估各组小鼠心功能,随后处死小鼠,通过ELISA法检测小鼠外周血血清中炎症因子(IL-1β、IL-6、Tnf-α)的表达,通过H&E染色评估其心肌炎症改变,通过picogreen试剂测定血清中dsDNA含量,通过免疫荧光染色检测心肌组织中MPO-DNA复合物的形成,通过western blot检测各组相关信号通路蛋白量(Iκbα、p-IKbα、nfκb、p-nfκb)的表达。在体外实验中,留取健康人外周血,分离获得中性粒细胞,通过佛波酯(Phorbol 12-myristate 13-acetate,PMA 100nM)刺激使其释放大量 NETs,IL-37(0.1ng/ml)或 bAY11-7082(2.5μM)进行干预。经过 4h 刺激后,通过 picogreen试剂测定细胞上清中dsDNA含量以及免疫荧光标记MPO-DNA复合物评估NETs的释放,另外,通过western blot检测其相关机制蛋白(Iκbα、p-Iκbα、nfκb、p-nfκb)的表达。实验结果1.IL-37改善CVb3诱导的急性VMC小鼠早期的一般状况及生存率。2.IL-37改善CVb3诱导的急性VMC小鼠的早期心功能。3.IL-37减轻CVb3诱导的急性VMC小鼠早期的心肌炎症反应。4.IL-37抑制CVb3诱导的急性VMC小鼠早期NETs的形成。5.IL-37和nfκb抑制剂(bAY1

关键词：白介素-37 病毒性心肌炎柯萨奇病毒b3 中性粒细胞胞外诱捕网 nfκb

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