简介：目的：观察表皮生长因子（EGF）对大鼠肠缺血-再灌注（I/R）后磷酸化丝裂原活化蛋白激酶（phospho-MAPK）表达的影响。方法：夹闭大鼠肠系膜上动脉根部45min之后放松血管夹形成再灌注，同时经颈静脉分别注入EGF100μg/Kg或生理盐水，分别于伤后2、6、12和24h检测血浆D-乳酸浓度，取水肠组织进行形态学观察，用免疫组织化学方法研究磷酸化p44/42MAPK、SAPK和p38的表达，设置对照组和单纯缺血组。结果：EGF显著降低D-乳酸水平升高的幅度(P<0.05），明显改善I/R引起的病理损害，使p44/42MAPK和p38的表达增强和提前，前减弱SAPK的表达。结论：肠道I/R激活磷酸化MAPK系统，EGF通过调节MAPK的表达参与细胞的应激反应和增殖与分化。

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简介：昆虫长是最丰富的草食动物，并且植物发展了复杂机制对他们的攻击保卫。特别地，植物能察觉与昆虫herbivory联系的织物损坏的特定的模式。某植物种类能在昆虫察觉某些elicitors在喂期间进入创伤，并且很快激活一系列缠绕的发信号的小径安排各种各样的防御代谢物的生合成的口头的分泌物(OS)。激活Mitogen的蛋白质kinases(MAPK)，对所有优核质普通，涉及许多细胞的进程的组织，包括开发和压力回答。在植物，至少二MAPK，水杨酸导致酸的蛋白质kinase(SIPK)和导致创伤的蛋白质kinase(WIPK)，被伤害或昆虫OS很快激活；重要地，用在MAPK发信号损害的转基因或变异的植物的基因研究显示MAPK在调整植物激素的导致herbivory的动力学起关键作用，例如jasmonic酸，乙烯和水杨酸酸，和MAPK也为草食动物的transcriptional激活被要求防御代谢物的防卫相关的基因和累积。在这评论，我们在在植物抵抗理解MAPK的功能到昆虫草食动物总结最近的开发。

简介：一、破骨细胞破骨细胞(osteoclast,OC)是由单核/巨噬形成的一种多核细胞,细胞家族中的单核细胞祖细胞融合后形成的一种多核细胞,巨噬细胞变成具有骨吸收能力的OC必须要有骨髓基质细胞/成骨细胞(osteoblast,OB)的存在[1].骨髓基质细胞/OB表达两个促进OC生成所必须的分子:一个是巨噬细胞集落刺激因子(macrophagecolony-stlimulatingfactor,MCSF),另一个是激活核因子NF-κB受体的配体(receptoractivatorofnuclearkappaBligand,RANKL)[2].在骨髓基质细胞和OB的存在下,M-CSF和RANKL分别与OC前体细胞上各自的受体结合并诱导其分化为成熟的OC.

简介：摘要丝裂原活化蛋白激酶(mitogen-activated protein kinase，MAPK)信号转导通路是调节细胞生长和存活的关键途径，异常的MAPK信号能促进癌症的发生发展，也决定了癌症的治疗反应。胃癌是中国常见消化道恶性肿瘤之一；近年来研究发现，在胃癌中存在诸多细胞信号传导通路的调控异常。细胞外信号调节激酶(extracellular signal-regulated kinase，ERK)信号通路是MAPK家族中的一条重要信号通路，该信号通路通过整合传递细胞外信号至细胞及其核内控制细胞的生长、凋亡和分化等。MAPK/ERK信号通路的异常激活可导致细胞丧失凋亡和分化能力，引发细胞异常增殖和恶性转化，促进胃癌的恶性表型；相反，阻断MAPK/ERK信号通路的相关组分则可逆转这一过程。本文结合国内外最新研究报道，对近年来在胃癌研究中发现MAPK/ERK信号通路的激活或失活在促进或抑制胃癌细胞恶性表型的重要作用及其相关的分子机制加以综述。

简介：丝裂原活化蛋白激酶（MAPK）超家族是介导细胞反应的重要信号系统,主要由MAPK、MAPK激酶（MAPKK）、MAPKK激酶（MAPKKK）等3类保守的蛋白激酶组成,通过级联反应不断磷酸化下游靶蛋白而参与细胞的增殖、分化、衰老、凋亡。辐射损伤使细胞膜受体和其他感应分子激活细胞内的MAPK信号通路,产生一系列应答反应。简要介绍MAPK家族中各条通路在辐射应答中的作用。

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简介：白念珠菌是人类最常见的条件致病菌。促分裂素原活化蛋白激酶（MAPK链）是真核生物信号传递网络中的重要途径之一，在基因表达调控和细胞质功能活动中发挥关键作用。在白念珠菌中主要有4条MAPK途径：Mkcl途径、Cekl途径、Cek2途径和HOG途径。其中HOG途径在白念珠菌MAPK信号通路起着重要的作用。对于白念珠菌MAPK信号通路的作用及相关调控机制的了解，可以为寻找新的药物作用靶点，治疗念珠菌病提供帮助。

简介：Objective:Theaimofthepresentstudywastoanalyzetheprognosticfactorsinpatientswithhepatoblastoma(HB)inoursinglecenterandtoevaluateperiostin(POSTN)expressioninHBanditsassociationwithclinicopathologicalvariables.Inaddition,theunderlyingmechanismofhowPOSTNpromotesHBprogressionwasdiscussed.Methods:POSTNexpressionwasinvestigatedinHBtumorsbyimmunohistochemistry(IHC),immunofluorescence(IF)andWesternblot(WB).TheassociationamongPOSTNexpression,clinicopathologicalfeaturesandoverallsurvival(OS)wasalsoevaluated.ThemigrationandadhesionabilityofHBcellsweremeasuredusingchemotaxisandcell-matrixadhesionassays,respectively.Epithelial-mesenchymaltransition(EMT)-associatedmarkersandactivationoftheERKpathwayweredetectedbyWB.Results:HBpatientshadpoorprognosiswhichdisplayedlymphnodemetastasis,vascularinvasion,POSTNandvimentinexpression.POSTNexpressionwasalsoassociatedwithlymphnodemetastasis.Furthermore,overexpressedPOSTNpromotedmigrationandtheadhesiveabilityofHBcellsinvitro.Inaddition,wedemonstratedthatPOSTNactivatedtheMAPK/ERKpathway,upregulatedtheexpressionofSnailanddecreasedtheexpressionofOVOL2.Finally,POSTNpromotedtheexpressionofEMT-associatedmarkers.Conclusions:POSTNmightmodulateEMTviatheERKsignalingpathway,therebypromotingcellularmigrationandinvasion.OurstudyalsosuggeststhatPOSTNmayserveasatherapeuticbiomarkerinHBpatients.

简介：摘要小窝蛋白-1是肺组织细胞膜上的一个特殊结构，在应力及高氧损伤的调控方面起着十分关键的作用；丝裂原活化蛋白激酶(mitogen-activatedproteinkinase，MAPK)是哺乳动物细胞中重要的信号转导通路，其中p38MAPK通路在细胞生长、细胞应激、炎症和凋亡等多种病生理过程中起关键作用，引起医学界的广泛关注，本文就p38MAPK信号通路及其与小窝蛋白的相关性做一综述，旨在对小窝蛋白-1在急性肺损伤中的作用进行进一步研究。

简介：ERK1/2andp38MAPK途径的激活参与了HGF介导的WB细胞的增殖调控,ERK、p38MAPK途径参与HGF介导的WB细胞在增殖调控,ERK、p38MAPK、PI3K/Akt等信号途径可以被多种细胞生长因子激活

简介：总结分析针刺对p38MAPK信号通路的影响，为进一步研究针刺疗效寻找理论依据。以“针灸＋p38MAPK”为关键词检索中国知网（CNKI）全文期刊与学位论文数据库及美国公共卫生检索系统（PubMed）数据库，共纳入中文文献19篇，英文文献7篇。通过阅读文献，发现p38MAPK信号通路在介导生长抑制信号、前凋亡信号和炎性反应等方面有着重要作用。针刺可通过p38MAPK途径实现对疾病的调控，尤其在心脑血管、肺疾病及镇痛方面效果较为显著，为针刺治疗疾病的理论基础提供了科学依据。

简介：新生／格特隐球菌是一种双相担子类病原真菌。隐球菌性脑膜炎是最常见的隐球菌病，致残率和死亡率极高。和宿主环境有效交流对隐球菌的生存至关重要。隐球菌利用复杂的信号系统来感应外界环境的变化并调控繁殖、发展和毒力。已知多种信号通路参与新生隐球菌对宿主环境的应答，调控新生隐球菌毒力。MAPK通路（mitogen—activatedproteinkinase）是其中最重要的信号通路之一，包括高渗透性甘油促分裂原激酶信号转导通路（highosmolarityglycerolmitogenactivatedproteinkinasesignalingtransductionpathway，HOG．MAPK）、蛋白激酶C信号转导通路（proteinkinaseCmitogenactivatedproteinkinasesignalingtransductionpathway，PKC—MAPK）及Stel2转录基因通路（sterilel2transcriptorsmitogenactivatedproteinkinasesignalingtransductionpathway，Stel2-MAPK）。对这些传导通路各个环节的了解，不仅有助于阐明MAPK通路的作用机制及其对毒力调控的作用，而且可以为寻找新的药物靶点、治疗新生隐球菌病提供帮助。

简介：信号转导（signaltransduction）指细胞外因子与膜或核受体结合，引发细胞内的一系列生物化学反应，蛋白与蛋白相互作用，直至细胞生理反应所需基因表达开始的过程。

简介：目的探讨自由基清除剂依达拉奉对大鼠脑缺血后丝裂原激活的蛋白激酶（MAPK）表达的影响。方法大脑中动脉阻断法制备大鼠脑缺血再灌注模型,缺血60min后再灌注23h,术前30min及再灌注2h时尾静脉注射依达拉奉1.0mg.kg-1或0.9%氯化钠注射液2ml.kg-1。观察大鼠脑缺血后神经功能缺损症状,TTC染色法检测梗死体积,Fluoro-JadeC法检测细胞死亡,采用免疫印迹法检测MAPK家族三个主要成员：蛋白激酶P38（P38MAPK）,细胞外信号调节激酶（ERK1/2）和c-jun氨基末端激酶（JNK）的表达。结果依达拉奉改善大鼠脑缺血再灌注23h后神经功能缺损症状,减少梗死体积和细胞死亡（P〈0.05）;大鼠脑缺血后MAPK家族被激活（P〈0.01）,依达拉奉能显著降低P38MAPK和JNK的激活,但对ERK1/2的表达无明显影响。结论依达拉奉可能能够通过抑制脑缺血后细胞内P38MAPK和JNK信号传导通路,减轻大鼠脑缺血损伤。

简介：AbstractObjective:The objective of this study was to investigate the expression levels of microRNA-141-5p(miRNA-141-5p), MAPK1 and neutrophil elastase in patients with and without preeclampsia (PE), and the relationship between miRNA-141-5p and MAPK1 with respect to the secretion of elastase by neutrophils in patients with PE.Methods:Thirty patients with PE and 30 healthy pregnant (HP) women were recruited from The Second Hospital of Shanxi Medical University, Taiyuan, China, between February 2017 and July 2018. Neutrophils were isolated from 8 mL peripheral blood samples and cultured. We recorded neutrophil count and morphology during culture. Apoptosis was detected by flow cytometry in different groups at 0, 24, and 48 h. The expression levels of elastase were detected in neutrophils by enzyme-linked immunosorbent assay, whereas the expression levels of miRNA-141-5p in peripheral blood neutrophils were detected by real-time polymerase chain reaction. We used TargetScanHuman Release 7.2 to analyze the target genes of miRNA-141-5p. The expression of MAPK1 in peripheral blood neutrophils was detected by western blotting. Data were analyzed by SPSS version 21.0 software, and comparisons between groups were carried out with the Student t test.Results:There was no significant difference between the PE and HP groups (P > 0.050) with regard to age or body mass index. The weight of newborns in the PE group (2846.00 ± 600.00 g) was significantly lower than that in the HP group (3055.00 ± 230.68 g). The number of neutrophilic granulocytes(NGs) in blood samples from the PE group was significantly higher than that in the HP group (P = 0.003). There was no significant difference between the groups with regard to morphology. Apoptosis in the PE group was delayed when compared with the HP group at different time points. The P value of apoptosis in the PE and HP groups were respectively 0.790, < 0.001 and 0.030 at 0 h, 24 h and 48 h. The expression levels of miRNA-141-5p in the PE group were significantly lower than those in the HP group (P < 0.050). The expression levels of MAPK1 in neutrophils from the PE group were significantly higher than those in the HP group (P < 0.050) by western blot. The expression levels of elastase in neutrophils from the PE group were significantly higher than those in the HP group (P < 0.050). Furthermore, the number of NGs in peripheral blood from the PE group was higher than that of the HP group; however, the levels of apoptosis were lower. The expression levels of miRNA-141-5p in NGs decreased, the expression of MAPK1 increased, and the secretion of neutrophil elastase in the NG medium increased in the PE group than those in the HP group.Conclusion:Collectively, our analysis suggested that miRNA-141-5p may be involved in the pathogenesis of PE by regulating the MAPK1 signaling pathway to activate neutrophils and increase the secretion of elastase.

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简介：目的:观察半夏泻心汤体外抑制巨噬细胞分泌炎症因子的作用及对MAPK炎症信号通路的影响,以探讨其治疗胃炎的可能机制。方法:取小鼠8只,提取小鼠腹腔巨噬细胞,原代培养;用家兔制备半夏泻心汤含药血清和对照血清。小鼠腹腔巨噬细胞分为空白对照组、脂多糖(LPS)组、地塞米松组及半夏泻心汤5%含药血清组、10%含药血清组和20%含药血清组,各组分别给予对照血清、LPS、地塞米松和各浓度含药血清。作用6h后收集细胞,用qRT-PCR方法检测细胞内IL-1β、IL-8和TNF-α的mRNA相对表达量;作用24h后,用ELISA方法检测细胞培养上清中炎症因子IL-1β、IL-8和TNF-α的蛋白含量。收集20%含药血清作用30min、60min和2h后的细胞,用Westernblot方法检测细胞外调节蛋白激酶(ERK)和P38的磷酸化水平。结果:qRTPCR结果显示,与不含药血清对照组比较,LPS能明显促进小鼠腹腔巨噬细胞IL-1β、IL-8和TNF-α的mRNA表达(P<0.01);与LPS组比较,地塞米松能明显抑制小鼠腹腔巨噬细胞IL-1β、IL-8和TNF-α的mRNA表达(P<0.01);5%含药血清能明显抑制巨噬细胞TNF-α的mRNA表达(P<0.01),10%和20%含药血清均能明显抑制IL-1β、IL-8和TNF-α的mRNA表达(P<0.01)。ELISA结果显示,5%含药血清能明显抑制小鼠腹腔巨噬细胞IL-1β的分泌(P<0.01),10%、20%含药血清能明显抑制小鼠腹腔巨噬细胞IL-1β、IL-8和TNF-α的分泌(P<0.05,P<0.01)。Westernblot结果显示,半夏泻心汤含药血清作用30min、60min均能抑制小鼠腹腔巨噬细胞MAPK信号通路中P38磷酸化水平(P<0.05、P<0.01);含药血清作用2h能抑制巨噬细胞的ERK和P38的磷酸化水平(P<0.01)。结论:半夏泻心汤可能通过调节巨噬细胞内MAPK炎症信号通路中ERK、P38的磷酸化水平,抑制巨噬细胞分泌炎症因子IL-1β、IL-8和TNF-α而起到治疗胃炎的作用。

简介：摘要硫化氢作为一种新兴气体信号分子，参与人体许多病理及生理过程，具有非常重要的细胞保护功能，可以调节巨噬细胞的增殖和凋亡。故对其深入的研究有很大意义。目前，根据国内外相关研究对其在巨噬细胞MAPK信号通路中的作用作一综述。

简介：WereportedinthismanuscriptthatTGF-β1inducesapoptosisinAML12murinehepatocytes,whichisassociatedwiththeactivationofp38MAPKsignalingpathway.SB202190,aspecificinhibitorofp38MAPK,stronglyinhibitedtheTGF-β1-inducedapoptosisandPAI-1promoteractivity.TreatmentofcellswithTGF-β1activatesp38.Furthermore,over-expressionofdominantnegativemutantp38alsoreducedtheTGF-β1-inducedapoptosis.Thedataindicatethattheactivationofp38isinvolvedinTGF-β1-mediatedgeneexpressionandapoptosis.