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| 1 | NF-kB and STAT3-key players in liver inflammation and cancer显示文摘 | | 2011 | Cell Research2011，21，1： | 119 |
| 2 | Normal and disease-related biological functions of Twist1 and underlying molecular mechanisms显示文摘这篇文章在开发,基因疾病和癌症考察分子的结构,表达式模式,生理的函数,病理学的角色和 Twist1 的分子的机制。Twist1 是基本 helix-loop-helix 包含域的抄写因素。以便绑 Nde1 电子盒子元素并且激活或镇压形成 homo-dimers 或 hetero-dimers 它的目标基因。在开发期间, Twist1 为中层说明和区别是必要的。人的 Twist1 基因的异质接合的 loss-of-function 变化包括 Saethre-Chotzen 症候群引起几疾病。Twist1 空的老鼠胚胎与打开的头部的神经试管和有缺点的头间充组织死,体节和手足芽。Twist1 在胸被表示,肝,前列腺,胃并且癌症的另外的类型,和它的表示通常与侵略、变形的癌症显型被联系。在癌症房间, Twist1 是由包括 SRC-1 的多重因素的 upregulated, STAT3, MSX2, HIF-1α,连接 integrin 的 kinase 和 NF-κ B。Twist1 显著地提高上皮间充质的转变(EMT ) 和癌症房间移植和侵略,因此支持癌症转移。Twist1 由直接镇压部分地支持 EMT 由招募的 E-cadherin 表示改变的 nucleosome 和为基因压抑并且由 upregulating Bmi1 的 deacetylase 建筑群, AKT2, YB-1,等等。新兴的证据也建议 Twist1 在扩大和癌症干细胞的化学疗法的抵抗起一个作用。Twist1 由支持 Twist1 功能的调节的人的转移和鉴定的机制的进一步的理解可以为开发新策略禁止 EMT 和癌症转移保持诺言。 | Qian Qin Young Xu Tao He Chunlin Qin Jianming Xu | 2012 | Cell Research2012，22，1： | 66 |
| 3 | Constitutive activation of Stat3 signaling pathway in human colorectal carcinoma显示文摘AIM: Signal transducers and activators of transcription (STATs) are a family of transcription factors activated in response to cytokines and growth factors. Constitutive activation of Stat3 has been observed in a growing number of tumor-derived cell lines, as well as tumor specimens from human cancers. The purpose of this study was to investigate the expression of p-Stat3, activated form of Stat3, and its downstream mediators including cyclin D1 and Bcl-XL in colorectal carcinoma (CRC), and to explore the possible mechanism of Stat3 signaling pathway in the tumorigenesis of colorectal carcinoma. METHODS: Tissue samples from 45 patients of primary colorectal carcinoma were selected for studying Stat3 signaling pathway protein expression. Western blot analysis was used to measure the expression of p-Stat3, cyclin D1, and Bcl-xu proteins in colorectal carcinomas. Furthermore, the expression patterns of these proteins were analyzed for their distribution at the cellular level by immunohistochemical staining of the tissues. RESULTS: Protein levels of p-Stat3, cyclin D1, and Bcl-XL were increased in colorectal carcinomas compared with adjacent normal mucosae (P<0.05). Elevated levels of pStat3 were correlated with the nodal metastasis and the stage (P<0.05). Overexpression of cyclin D1 was associated with the nodal metastasis (P<0.05). There was also a significant correlation between the expressions of p-Stat3 and cyclin D1 (r=0.382, P<0.05). CONCLUSION: Constitutive activation of Stat3 may play an important role in the tumorigenesis of colorectal carcinoma, and the detailed mechanism of Stat3 signaling pathway in CRC deserves further investigation. | Xiang-TaoMa ShanWang Ying-JiangYe Ru-YuDu Zhi-RongCui MaSomsouk | 2004 | World Journal of Gastroenterology2004，10，11： | 68 |
| 4 | STAT3:慢性炎症介导肿瘤发生和进展的关键节点显示文摘炎症与肿瘤是近年来肿瘤领域的研究热点.在肿瘤发生、发展过程中,白介素6(interleukin-6,IL-6)等炎症因子可将肿瘤细胞与其所处的肿瘤微环境编织成一个炎性网络,而信号传导蛋白和转录激活物(signal transducers and activators of transcription 3,STAT3)正是这一炎性网络中的关键节点,在慢性炎症介导肿瘤形成的过程中发挥重要作用.本文从STAT3的信号通路构成入手,由肿瘤细胞及肿瘤微环境两方面展开,综述了肿瘤发生发展过程中STAT3在肿瘤细胞及各种炎症/免疫细胞中的作用,以及靶向STAT3治疗肿瘤的转化医学研究进展. | 侯嘉杰 孙倍成 | 2014 | 生物化学与生物物理进展2014，41，1： | 54 |
| 5 | Resveratrol provides neuroprotection by regulating the JAK2/STAT3/PI3K/AKT/mTOR pathway after stroke in rats显示文摘Ischemic stroke is a common disease with high mortality and morbidity worldwide.One of the important pathophysiological effects of ischemic stroke is apoptosis.A neuroprotective effect is defined as the inhibition of neuronal apoptosis to rescue or delay the infarction in the surviving ischemic penumbra.Resveratrol is a natural polyphenol that reportedly prevents cerebral ischemia injury by regulating the expression of PI3K/AKT/mTOR.Therefore,this study aimed to elucidate the neuroprotective effect of resveratrol on cerebral ischemia/reperfusion injury and to investigate the signaling pathways and mechanisms through which resveratrol regulates apoptosis in the ischemic penumbra.Rats were subjected to middle cerebral artery occlusion for 2 h followed by 24 h reperfusion.Cerebral infarct volume was measured using 2%TTC staining.TUNEL staining was conducted to evaluate neuronal apoptosis.Western blotting and immunohistochemistry were used to detect the proteins involved in the JAK2/STAT3/PI3K/AKT/mTOR pathway.The results suggested that resveratrol significantly improved neurological function,reduced cerebral infarct volume,decreased neuronal damage,and markedly attenuated neuronal apoptosis;these effects were attenuated by the inhibition of PI3K/AKT with LY294002 and JAK2/STAT3 with AG490.We also found that resveratrol significantly upregulated the expression of p-JAK2,p-STAT3,p-AKT,p-mTOR,and BCL-2 and downregulated expression of cleaved caspase-3 and BAX,which was partially reversed by LY294002 and AG490.These results suggested that resveratrol provides a neuroprotective effect against cerebral ischemia/reperfusion injury,which is partially mediated by the activation of JAK2/STAT3 and PI3K/AKT/mTOR.Resveratrol may indirectly upregulate the PI3K/AKT/mTOR pathway by activating JAK2/STAT3. | Yongying Hou Ke Wang Weijun Wan Yue Cheng Xia Pu Xiufeng Ye | 2018 | Genes & Diseases2018，5，3： | 60 |
| 6 | NF-κB and STAT3 signaling pathways collaboratively link infl ammation to cancer显示文摘Although links between cancer and inflammation were fi rstly proposed in the nineteenth century,the molecular mechanism has not yet been clearly understood.Epidemiological studies have identified chronic infections and infl ammation as major risk factors for various types of cancer.NF-κB transcription factors and the signaling pathways are central coordinators in innate and adaptive immune responses.STAT3 regulates the expression of a variety of genes in response to cellular stimuli,and thus plays a key role in cell growth and apoptosis.Recently,roles of NF-κB and STAT3 in colon,gastric and liver cancers have been extensively investigated.The activation and interaction between STAT3 and NF-κB play vital roles in control of the communication between cancer cells and infl ammatory cells.NF-κB and STAT3 are two major factors controlling the ability of pre-neoplastic and malignant cells to resist apoptosis-based tumor-surveillance and regulating tumor angiogenesis and invasiveness.Understanding the molecular mechanisms of NF-κB and STAT3 cooperation in cancer will offer opportunities for the design of new chemo-preventive and chemotherapeutic approaches. | Yihui Fan Renfang Mao Jianhua Yang | 2013 | Protein & Cell2013，4，3： | 52 |
| 7 | 半夏泻心汤对胃癌前病变大鼠胃黏膜组织中的NF-κB/STAT3信号通路的影响研究显示文摘[目的]通过检测大鼠胃黏膜组织中的NF-κB/STAT3信号通路中等相关指标,揭示半夏泻心汤对胃癌前病变(PLGC)大鼠的影响及防治作用机制。[方法]130只清洁级雄性SD大鼠,采用改良MNNG+复合法造模PLGC大鼠110只,分为模型组:PLGC大鼠20只;模型中药组:造模同时中药干预10只;空白组:正常喂养20只。中药干预阶段,剩余模型大鼠随机分为模型对照组10只、半夏泻心汤高、中、低剂量组分别为12、12、10只。观察检测各组大鼠胃黏膜组织中的NF-κB、STAT3、IL-1β、TNF-α、Bcl-2、C-MYC、p21情况。[结果]中药干预后,NF-κB:模型中药组比模型组表达低,高剂量组、中剂量组及低剂量组均比模型对照组表达低,高剂量组、中剂量组明显;STAT3:模型中药组比模型组表达低,高剂量组、中剂量组及低剂量组均比模型对照组表达低,高剂量组、中剂量组、低剂量组间差异无统计学意义;IL-1β:模型中药组比模型组表达低,高剂量组、中剂量组及低剂量组均比模型对照组表达低,中剂量组明显。TNF-α:模型中药组比模型组表达低,高剂量组、中剂量组及低剂量组均比模型对照组表达低,低剂量组明显。Bcl-2:模型中药组比模型组表达低,高剂量组、中剂量组比模型对照组表达低,高剂量组明显;C-MYC:模型中药组比模型组表达低,高剂量组、中剂量组比模型对照组表达低,高剂量组明显;p21:模型中药组比模型组表达高,高剂量组、中剂量组比模型对照组表达高,高剂量组明显。[结论]中药半夏泻心汤通过抑制PLGC大鼠胃黏膜组织NF-κB/STAT3信号通路中的炎性因子、癌因子,促进抑癌因子的表达,从而影响阻断PLGC的发生发展。 | 李慧臻 刘琳 王兴章 刘华一 杨岩 赵双梅 张淑坤 李棣华 | 2017 | 中国中西医结合消化杂志2017，25，4： | 42 |
| 8 | 三七化学成分分析及其抗炎机制的网络药理学探讨显示文摘目的利用超高效液相色谱与四极杆飞行时间质谱联用(ultra performance liquid chromatography quadrupole-time-offlight hybrid mass spectrometry,UPLC-Q-TOF-MS)分析三七的主要化学成分,运用网络药理学研究三七抗炎的多成分、多靶标、多途径作用机制。方法通过UPLC-Q-TOF-MS分析三七的主要化学成分,使用DAVID数据库进行基因本体论(Gene Ontology,GO)分析和京都基因与基因组百科全书(Kyoto Encyclopedia of Genesand Genomes,KEGG)通路分析,并运用Cytoscape 3.6.1软件绘制网络互作图,Image GP工具绘制GO气泡图。结果研究得到人参皂苷Rh1、人参皂苷Rg1、月桂酸单甘油酯(monolaurin)等22个关键抗炎作用的活性成分和表皮生长因子受体(EGFR)、信号传导蛋白和转录激活物3(STAT3)、丝裂原活化蛋白激酶-14(MAPK14)等31个关键靶点。GO、KEGG通路富集分析发现,三七可能主要通过人参皂苷Rh1、人参皂苷Rg1、月桂酸单甘油酯、β-胡萝卜苷(β-daucosterol)和人参环氧炔醇(panaxydol)等活性成分,作用于EGFR、STAT3、MAPK14、白介素-2(IL-2)等靶点,调节癌症信号通路(Pathways in cancer)、细胞因子受体相互作用(Cytokine-cytokine receptor interaction)、突触细胞黏附分子(CAMs)等信号通路发挥抗炎作用。结论三七抗炎体现了多成分、多靶点、多途径的特点,为进一步开展三七抗炎作用药效物质基础和作用机制研究提供了新的思路和方法。 | 庞会婷 罗朵生 郭姣 | 2020 | 中草药2020，51，21： | 47 |
| 9 | MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines显示文摘迷走神经神经能通过“一条胆碱能的反煽动性的小径”控制煽动性的反应,它被 α 调停; 7-nicotinic 醋胆素受体(α 7nAChR ) 在巨噬细胞上。然而,连接 α 的细胞内部的机制; 7nAChR 激活和支持 inflammatory cytokine 生产遗体不好理解。在这研究,我们发现 miR-124 是由在暴露 LPS 的房间和老鼠的胆碱能的收缩筋的 upregulated。利用 miR-124 模仿并且 siRNA 击倒,我们证明 miR-124 是为胆碱能的反煽动性的行动的一个批评调停人。而且,我们的数据显示 miR-124 由指向信号变换器和抄写 3 的使活跃之物(STAT3 ) 到减少 IL-6 生产和 TNF-α 调制导致 LPS 的 cytokine 生产;变换酶(不作声) 减少 TNF-α版本。这些结果也显示 miR-124 是为煽动性的疾病的处理的一个潜在的治疗学的目标。 | Yang Sun Qi Li Huan Gui Dong-Ping Xu Yi-LiYang Ding-Feng Su Xia Liu | 2013 | Cell Research2013，23，11： | 35 |
| 10 | 骨关节炎发病机制的研究进展显示文摘骨关节炎(osteoarthritis,OA)是一种以关节软骨变性和丢失及关节边缘和软骨下骨骨质再生为病理特征的慢性关节疾病。常见部位膝、髋、肘和收的小关节等。OA的病因尚不明确,但具有相似的生物学、形态学和临床特征。OA主要累及关节软骨、软骨下骨、关节囊及韧带、滑膜和周围肌肉。多见于中老年人,女性多于男性。随着老龄化社会的到来,OA患者数量将逐渐升高。到2020年老年人为发达国家人口总数的1/4,65岁以上的老年人所患慢性病一半为OA。我国大于60岁骨关节炎患者约1.3亿人,约占人口总数的30%。OA是影响人类健康最常见的关节疾患之一。骨关节炎严重威胁人类的健康和生活,一直是骨科科学研究的重要课题。虽然在OA的早期治疗和抑制其发展方向的投入较大,但在过去20年里,药物治疗方面也未取得长足的进步。尽管对关节软骨的生理、生化以及软骨细胞的代谢有了一定的了解,但OA的病因、发病机制至今尚不十分明确。因此对其早期诊断与治疗缺乏明确的针对性。骨关节炎的发病机制是由多种因素所致,包括基因遗传性;生物力学因素;软骨营养、代谢异常;软骨细胞凋亡等。现从关节软骨的结构、细胞因子学说、自由基学说、miRNA、STAT3等方面对骨关节炎的发病机制进行综述。 | 石晓明 于占革 | 2013 | 中华临床医师杂志(电子版)2013，7，24： | 40 |
| 11 | Stat3及其靶基因产物与结直肠癌恶性程度关系的研究显示文摘背景与目的:转录信号转导子与激活子3(signal transducers and activatorsof transcription 3,Stat3)通路受细胞因子与生长因子的刺激而活化,参与调节细胞的增殖、分化与凋亡。Stat3因可以介导细胞的恶性转化而被确认为是癌基因。本研究分析Stat3及其靶基因产物cyclin D1与Bcl-x_L在结直肠癌组织与细胞中的表达情况,探讨Stat3及其靶基因产物在结直肠癌发病机制中的作用。方法:用Western blot检测45例结直肠癌组织、癌旁肠粘膜以及结肠癌细胞系SW480和HCT116中Stat3(p-stat3)及其靶基因产物cyclin D1和Bcl一x_L蛋白表达,用免疫组织化学染色进行细 胞内定位,同时对结直肠癌组织中p-Stat3、cyclin D1及Bcl-x_L表达情况与不同临床病理特征进行统计学分析。结果:结直肠癌组织中p-Stat3、cyclin D1及Bcl-x_L蛋白表达率分别为57.8%、64.4%及68.9%,癌旁肠粘膜表达率分别为42.2%、35.6%及31.1%;其蛋白表达水平(A值)分别为114263±53 598、58 321±24 872、71 032±43 425;癌旁肠粘膜分别为55 971±28 762、22 563±11 160、37 281±14 622(P<0.05)。p-Stat3表达水平与结直肠癌临床分期及淋巴结转移有关(P=0.026,0.018),cyclin D1与淋巴结转移有关(P=0.041)。p-Stat3与cyclin D1在结直肠癌组织中表达情况呈? | 马向涛 王杉 叶颖江 社如昱 崔志荣 | 2003 | 癌症2003，22，11： | 31 |
| 12 | GRIM-19的功能及与肿瘤的相关性显示文摘GRIM-19最初被认为定位于细胞核,后来发现在线粒体中也有表达。GRIM-19还是线粒体中NADH脱氢酶1复合物的基本亚单位,在线粒体Ⅰ型呼吸过程中至关重要。在病毒感染导致细胞癌变的过程中,GRIM-19很可能是病毒癌基因结合的靶点,目前认为,GRIM-19参与和细胞的增殖、凋亡的调控过程,其表达降低或位点突变可以导致细胞的异常增殖和恶性转化。在肿瘤的形成及凋亡抑制中发挥着重要的作用。 | 周颖 凌斌 | 2008 | 医学分子生物学杂志2008，5，3： | 30 |
| 13 | JAK2/STAT3/SOCS3信号通路与肿瘤转移显示文摘肿瘤转移与多种细胞信号通路作用有关,其中与JAK2/STAT3/SOCS3通路关系尤为密切,JAK2/STAT3信号通路的激活参与了肿瘤发生、发展、侵袭和转移等多个环节。细胞因子信号转导抑制蛋白3(suppressors of cytokine signaling 3,SOCS3)负性调控JAK2/STAT3通路,进而抑制肿瘤的增殖和生长;信号转导与转录激活因子3(signal transducer and activator of transcription 3,STAT3)信号通路的激活促成了肿瘤炎性微环境的形成,参与了肿瘤血管生成、上皮间质转化和细胞外基质降解等多个环节,在肿瘤的侵袭和转移过程中发挥重要作用。本文着重对JAK2/STAT3/SOCS3信号通路与肿瘤转移的关系进行综述,针对JAK2/STAT3/SOCS3细胞信号动态网络在肿瘤中作用机制研究和药物设计为肿瘤治疗提供了新方向。 | 蒋树龙 花宝金 | 2014 | 中国肿瘤生物治疗杂志2014，21，6： | 29 |
| 14 | 清金化痰颗粒对COPD急性期(痰热郁肺型)大鼠肺组织STAT1,STAT3的调控作用显示文摘目的:研究清金化痰颗粒对慢性阻塞性肺疾病(COPD)急性期(痰热郁肺型)大鼠肺组织中信号转导与转录激活因子1,3(STAT1,STAT3)的调控作用。方法:采用烟熏+脂多糖(LPS)气管注射方法建立COPD痰热郁肺证大鼠模型(正常组除外),随机分为正常组,模型组,罗红霉素组(0.031 5 g·kg^(-1)),清金化痰颗粒低、高剂量组(9.4,37.6 g·kg-1),每组8只。每日ig给药1次,连续给药2周。观察各组大鼠的一般行为活动和病理学变化特点,采用大鼠肺功能检测仪测定各组大鼠相关肺功能指标:0.3 s用力肺活量(FEV0.3),用力肺活量(FVC),FEV0.3/FVC,肺活量(VC),采用实时荧光定量聚合酶链式反应(Real-time PCR)法测定肺组织白细胞介素-6(IL-6),STAT1及STAT3 mRNA表达,免疫组化法检测肺组织IL-6,STAT1及STAT3蛋白表达。结果:与正常组比较,模型组肺组织中IL-6,STAT1及STAT3 mRNA表达显著升高(P<0.01);与模型组比较,罗红霉素组、清金化痰颗粒低、高剂量组均能显著降低大鼠肺组织IL-6,STAT1及STAT3 mRNA表达(P<0.01),罗红霉素组和清金化痰高剂量组减低更明显,二者之间无明显差异。各组大鼠肺组织中IL-6,STAT1及STAT3蛋白的表达中,与正常组比较,模型大鼠肺组织中的IL-6,STAT1及STAT3平均积分吸光度IA值显著升高(P<0.01);与正常组比较,模型组大鼠肺功能参数FEV0.3,FVC,FEV0.3/FVC,VC值均降低(P<0.01);与模型组比较,各给药组肺功能参数FEV0.3,FVC,VC值均有升高(P<0.01,P<0.05);与模型组比较,罗红霉素组、清金化痰颗粒低、高剂量组能显著降低大鼠肺组织IL-6,STAT1及STAT3平均IA值(P<0.01),罗红霉素组和清金化痰颗粒高剂量组减低更明显,二者之间差异无统计学意义。结论:清金化痰颗粒可下调JAK/STAT信号通路中STAT1,STAT3的过度表达和持续活化,来抑制IL-6的水平的升高,减轻气道炎症,抑制COPD急性发作与加重。 | 许光兰 赵媚 钟云青 陈平 李娇 黄志健 | 2017 | 中国实验方剂学杂志2017，23，2： | 29 |
| 15 | 针灸联合自血疗法治疗慢性荨麻疹(血虚风燥型)效果及对UAS评分、外周血T淋巴细胞STAT3 mRNA表达水平的影响显示文摘目的:探讨针灸联合自血疗法对血虚风燥型慢性荨麻疹患者的治疗效果及荨麻疹活动性评分(UAS)、外周血T淋巴细胞信号转导与转录激活因子3(STAT3)mRNA表达水平的影响。方法:将94例血虚风燥型慢性荨麻疹患者随机分为对照组与观察组,每组47例,对照组采用自血疗法治疗,观察组加用针灸疗法,评估两组疗效及中医症状、体征积分的改善情况,采用UAS评分评定患者治疗前后荨麻疹风团数量及瘙痒程度的变化,并于治疗前后留取外周血,测定患者外周血T淋巴亚群(CD3^+、CD4^+、CD8^+、CD4^+/CD8^+)及STAT3 mRNA表达水平的变化。结果:①治疗4周,两组瘙痒程度、皮损分布、风团大小、皮损红斑、皮损数量等中医症状及体征积分积分均降低(P<0.05),观察组各积分均低于对照组(P<0.05);②观察组总有效率高于对照组(P<0.05);③治疗4周,两组UAS表各维度评分及总分均降低(P<0.05),观察组UAS评分低于对照组(P<0.05);④治疗4周,两组CD4^+上升,CD8^+降低,CD4^+/CD8^+上升及外周血T淋巴细胞STAT3 mRNA水平降低(P<0.05),观察组CD4^+、CD4^+/CD8^+、STAT3 mRNA水平低于对照组,CD8^+水平高于对照组(P<0.05)。结论:针灸联合自血疗法治疗血虚风燥型慢性荨麻疹可改善患者症状及体征,提高治疗效果,降低UAS评分,改善其免疫功能,下调外周血T淋巴细胞STAT3 mRNA表达水平。 | 邹宇 吕欣桐 唐清体 | 2019 | 中华中医药学刊2019，37，7： | 30 |
| 16 | 基于STAT3/NF-kB/IL-6通路研究加味黄芩汤治疗溃疡性结肠炎的作用机制显示文摘目的探讨加味黄芩汤对溃疡性结肠炎的治疗效果及对STAT3/NF-kB/IL-6通路的调控作用。方法将48只小鼠随机分为空白组、模型组、阳性药物组(柳氮磺吡啶)、中药低剂量组、中药中剂量组、中药高剂量组,8只/组,按照3%DSS造模法对除空白组以外的5组小鼠进行溃疡性结肠炎造模,造模7 d后,空白组和模型组以生理盐水灌胃,药物治疗组以相应的药物灌胃,灌胃量均为10 ml/kg,共持续1周。治疗结束后,使用颈椎脱臼法处死小鼠,测量结肠长度,通过HE染色法观察各组小鼠结肠组织形态变化及结肠组织病理学评分变化,通过RT-qPCR法和Western blot法检测各组小鼠结肠组织STAT3、NF-kB、IL-6 mRNA及蛋白表达水平变化。结果与空白组相比,模型组、阳性药物组及中药各剂量组小鼠结肠长度明显缩短(P<0.05),结肠组织病理评分均明显升高(P<0.05);与模型组相比,阳性药物组及中药各剂量组小鼠结肠长度明显延长(P<0.05),结肠组织病理评分均明显降低(P<0.05);与阳性药物组相比,中药高剂量组小鼠结肠长度明显延长(P<0.05),结肠组织病理评分均明显降低(P<0.05),中药中剂量组结肠长度及结肠组织病理评分均无明显差异(P>0.05)、中药低剂量组结肠长度明显缩短(P<0.05),结肠组织病理评分均明显增加(P<0.05);与中药高剂量组相比,中药中、低剂量组小鼠结肠长度均明显缩短(P<0.05),结肠组织病理评分均明显增加(P<0.05);与中药中剂量组相比,中药低剂量组小鼠结肠长度均明显缩短(P<0.05),结肠组织病理评分均明显增加(P<0.05)。与空白组相比,模型组结肠组织STAT3、NF-kB、IL-6 mRNA及蛋白表达水平明显升高(P<0.01),与模型组相比,阳性药物组及中药各剂量组结肠组织STAT3、NF-kB、IL-6 mRNA及蛋白表达水平明显降低(P<0.01),其中中药高剂量组结肠组织STAT3、NF-kB、IL-6 mRNA及蛋白表达水平明显低于阳性药物组及中药中、低剂量组(P<0.05)。而中药中剂量组结肠组织STAT3、NF-kB、IL-6 mRNA及蛋白表达水平与阳性药物组无明显差异(P>0.05),但明显低于中药低剂量组(P<0.05)。结论加味黄芩汤对溃疡性结肠炎具有一定的改善作用,其作用机制可能与通过影响STAT3/NF-kB/IL-6通路下调结肠组织STAT3、NF-kB、IL-6表达有关。 | 王康 缪志伟 董筠 叶柏 | 2020 | 南方医科大学学报2020，40，2： | 30 |
| 17 | Hydrodynamic Gene Delivery of Interleukin-22 Protects the Mouse Liver from Concanavalin A-, Carbon Tetrachloride-,and Fas Ligand-Induced Injury via Activation of STAT3显示文摘Interleukin-22 (IL-22) is a recently identified T cell-derived cytokine whose biological significance remains obscure. Previously, we have shown that IL-22 plays a protective role in T cell-mediated hepatitis induced by Concanavalin A (Con A), acting as a survival factor for hepatocytes. In the present paper, we demonstrate that hydrodynamic gene delivery of IL-22 cDNA driven either by a liver-specific albumin promoter or a human cytomegalovirus (CMV) promoter results in IL-22 protein expression, STAT3 activation, and expression of several anti-apoptotic proteins, including Bcl-xL, Bcl-2, and Mcl-1 in the liver. Immunohistochemical analysis reveals that IL-22 protein expression is mainly detected in the cytoplasm of hepatocytes. Overexpression of IL-22 by hydrodynamic gene delivery significantly protects against liver injury, necrosis, and apoptosis induced by administration of Con A, carbon tetrachloride (CCl4), or the Fas agonist Jo-2 mAb. Western blot analyses show that overexpression of IL-22 significantly enhances activation of STAT3 and expression of Bcl-xL, Bcl-2,and Mcl-1 proteins in liver injury induced by Con A. In conclusion, hydrodynamic gene delivery of IL-22 protects against liver injury induced by a variety of toxins, suggesting the therapeutic potential of IL-22 in treating human liver disease. Cellular & Molecular Immunology. 2004;1(1):43-49. | HongnaPan FengHong SvetlanaRadaeva BinGao | 2004 | Cellular & Molecular Immunology2004，1，1： | 30 |
| 18 | The AIM2 inflammasome is a central regulator of intestinal homeostasis through the IL-18/IL-22/STAT3 pathway显示文摘Inflammasomes 为维持肠的动态平衡是重要的,并且 dysbiosis 贡献煽动性的肠疾病(IBD ) 的病理并且为 colorectal 癌症增加风险。Inflammasome 缺点贡献长期的肠的发炎并且在老鼠增加危险性到大肠炎。然而,在黑瘤 2 不在的 inflammasome 传感器(AIM2 ) 通过 DNA 依赖的蛋白质 kinase 和 Akt 小径以一种 inflammasome 独立的方式免于 colorectal 癌症。然而,在 IBD 和 colorectal 癌症的早阶段的 AIM2 inflammasome 的角色留下不清楚。这里,我们证明 AIM2 inflammasome 在肠有一个保护的角色。在稳定的状态期间, Aim2 删除导致 IL-18 分泌物的损失,在肠的上皮的房间和 STAT3 依赖的抗菌剂肽(安培) 的作为结果的损失的 IL-22 有约束力的蛋白质(IL-22BP ) 的抑制 Reg3β并且 Reg3γ,它支持连接 dysbiosis 的大肠炎。在葡聚糖硫酸盐期间导致钠的大肠炎,不正常的 IL-18/在 Aim2 −/− 老鼠的 IL-22BP 小径支持过多的 IL-22 生产和提高的 STAT3 激活。Aim2 −/− 鼠标进一步在提高的 Reg3b 和 Reg3g 表示造成的大肠炎的分辨率期间展出持续 STAT3 和 Akt 激活。这恋职的机制支持肠的地窟房间的增长并且多半在 Aim2 −/− 老鼠的危险性贡献最近描述的增加到 colorectal 癌症。一起,我们的结果在通过 IL-18/ 的规定阻止 dysbiosis 和肠的发炎为 AIM2 inflammasome 表明一个中央角色; IL-22BP/ IL-22 和 STAT3 小径和精选安培的表示。 | Rojo A Ratsimandresy Mohanalaxmi Indramohan Andrea Dorfleutner Christian Stehlik | 2017 | Cellular & Molecular Immunology2017，14，1： | 27 |
| 19 | Inhibition of STAT3 expression by siRNA suppresses growth and induces apoptosis in laryngeal cancer cells显示文摘Aim: To determine the inhibitory effect of the synthetic STAT3 siRNA on the expression of STAT3 gene in human laryngeal cancer cell lines Hep2 and to investigate the effect of STAT3 siRNA on growth and apoptosis in Hep2 cells. Methods: A pair of DNA templates coding siRNA against STAT3-mRNA was synthesized to reconstruct plasmid of pSilencer1.0-U6 siRNA-STAT3. Hep2 cells were transfected with RPMI-1640 media (untreated), plasmid (empty), and STAT3 siRNA, respectively. Northern blot and Western blot analysis of STAT3 and pTyr-STAT3 expression in Hep2 cells and Western blot analysis of Bcl-2 expression in the Hep2 cell was performed 72 h after transfection. MTT, flow cytometry, and AO/EB assay were used for determination of cells proliferation and apoptosis in Hep2 cells. Results: pTyr-STAT3 was markedly expressed in untreated Hep2 cells and the vector-treated Hep2 cells, whereas pTyr-STAT3 expression was significantly reduced in STAT3 siRNA-transfected Hep2 cells, indicating that STAT3 siRNA inhibited the activity of STAT3. Transfection of Hep2 cells with STAT3 siRNA significantly inhibited STAT3 expression at both mRNA and protein level in Hep2 cells and the inhibition was characterized by time-dependent transfection. Treatment of Hep2 cells with STAT3 siRNA resulted in dose-dependent growth inhibition of Hep2, this significantly increased apoptotic cell rate, and decreased Bcl-2 expression level in Hep2 cells. STAT3 siRNA had an effect on induction of either early or late stage apoptosis. Conclusion: This study demonstrates that STAT3 siRNA effectively inhibits STAT3 gene expression in Hep2 cells leading to growth suppression and induction of apoptosis in Hep2 cells. The use of siRNA technique may provide a novel therapeutic approach to treat laryngeal cancer and other malignant tumors expressing constitutively activated STAT3. | Li-fangGAO De-qiXU Lian-jiWEN Xing-yiZHANG Yue-tingSHAO Xue-jianZHAO | 2005 | Acta Pharmacologica Sinica2005，26，3： | 24 |
| 20 | 黄芩苷对肝癌细胞SMMC-7721 JAK-STAT信号通路STAT3的影响显示文摘目的:探讨黄芩苷对肝癌细胞SMMC-7721JAK-STAT信号通路STAT3的影响.方法:将肝癌细胞SMMC-7721分为4组:对照组、黄芩苷组、AG490组、黄芩苷+AG490组.应用RT-PCR法检测各组肝癌细胞SMMC-7721中STAT3mRNA表达,Westernblot法检测肝癌细胞SMMC-7721中STAT3、P-STAT3蛋白表达.结果:黄芩苷可以下调肝癌细胞SMMC-7721STAT3mRNA表达,与对照组比较明显下降(0.505±0.111vs0.697±0.145,P<0.05);并可以降低STAT3蛋白的表达量(0.879±0.012vs1.087±0.015,P<0.05);还可以抑制STAT3向活化形式P-STAT3转化,与对照组比较P-STAT3表达明显下降(0.983±0.085vs1.103±0.074,P<0.05),而与AG490联合应用后P-STAT3蛋白表达量较单用黄芩苷下降明显(0.756±0.103vs0.983±0.085,P<0.05).结论:黄芩苷能下调STAT3mRNA表达水平,降低STAT3蛋白表达,还可以抑制STAT3向活化形式P-STAT3转化,与AG490有协同作用.黄芩苷可能通过抑制JAK-STAT信号通路发挥抗肿瘤作用. | 郭昱 霍瑞静 姚金锋 | 2011 | 世界华人消化杂志2011，19，22： | 22 |
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