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信号传导抑制剂,可选择性地抑制TLR-介导的细胞因子和一氧化氮的产生。",{"key":240,"value":241},"相关类别","信号通路\n>>\n自噬\n>>\n自噬\n信号通路\n>>\n免疫及炎症\n>>\nToll样受体(TLR)\n研究领域\n>>\n炎症\u002F免疫",{"key":243,"value":244},"靶点","TLR4[1]",{"key":246,"value":247},"体外研究","在RAW264.7细胞和小鼠腹腔巨噬细胞中,Resatorvid(TAK-242)抑制脂多糖(LPS)诱导的NO,肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-6的产生,IC50为1.1到11 nM。 Resatorvid(TAK-242)还抑制LPS刺激的人外周血单核细胞(PBMCs)中这些细胞因子的产生,IC50值为11至33 nM [1]。",{"key":249,"value":250},"体内研究","Resatorvid(TAK-242)显然降低了两种基因型小鼠的血清抗dsDNA水平。或者,Resatorvid(TAK-242)显着抑制IFN-γ,TNF-α和IL-1β的产生,但它们的浓度仍然远高于NS处理的对应物[2]。 Resatorvid(TAK-242)预应力给药可防止大鼠大脑额叶皮质中潜在有害的炎症和氧化\u002F亚硝化介质的积累。在应激期开始时,Resatorvid(TAK-242)iv给药完全阻断应激暴露后TLR-4 mRNA和蛋白质上调[3]。",{"key":252,"value":253},"细胞实验","将RAW264.7细胞以3×10 6个细胞\u002F孔的密度接种在六孔培养板中并孵育过夜。用补充有1％FCS和10μg\u002F mL卡那霉素的RPMI 1640培养基洗涤后，在存在或不存在Resatorvid（TAK-242）的情况下用5ng \u002F mL LPS和1U \u002F mL IFN-γ刺激细胞（1） -100 nM）指示的时间。除去培养上清液，使用总RNA分离试剂ISOGEN分离总RNA。通过使用TaqMan逆转录试剂将总RNA逆转录成cDNA。使用预先开发的TaqMan测定试剂和Universal PCR master mix在ABI Prism 7700上进行TNF-α和IL-6的定量实时PCR分析。使用比较阈值循环方法进行mRNA的定量。通过刺激获得的最高对照水平（没有Resatorvid（TAK-242））被认为是100％，并且对照组在其他时间点和TAK-242添加组的水平被表示为最高对照水平的百分比。 [1]。",{"key":255,"value":256},"动物实验","C57BL \u002F 6背景（雌性，10周龄）的小鼠[2] 30只ApoE  -  \u002F  - 和30只野生型小鼠在标准光照条件下喂食含有0.25％胆固醇和15％可可脂的高脂肪饮食（12 h亮 - 暗循环）和温度（21±1℃）。矿泉水随意饮用。将两种基因型的小鼠随机分配至LPS或LPS + Resatorvid（TAK-242）或盐水给药。 LPS（2.5mg \u002F kg），LPS（2.5mg \u002F kg）加Resatorvid（TAK-242）（0.3mg \u002F kg）和生理盐水分别通过腹膜内注射给药，每周两次，持续4周。在实验结束时，所有小鼠都接受了安乐死，注射过量戊巴比妥（50mg \u002F kg）。大鼠[3]使用最初重200至225g的雄性远交Wistar Hannover大鼠。在将动物引入塑料限制器后立即（约10秒）立即以0.5mg \u002F kg的剂量在尾静脉中静脉内注射Resatorvid（TAK-242）。该剂量是基于之前的体内研究选择的，该研究报告了其在暴露于缺氧的小胶质细胞中的抗炎\u002F抗氧化和神经保护特性。浓度为0.9％的二甲基亚砜用作载体。",{"key":258,"value":259},"参考文献","[1].\nIi M, et al. A novel cyclohexene derivative, ethyl (6R)-6-[N-(2-Chloro-4-fluorophenyl)sulfamoyl]cyclohex-1-ene-1-carboxylate (TAK-242), selectively inhibits toll-like receptor 4-mediated cytokine production through suppression of intracellular signaling.\n[2].\nNi JQ, et al. Role of toll-like receptor 4 on lupus lung injury and atherosclerosis in LPS-challenge ApoE?\u002F? mice. Clin Dev Immunol. 2013;2013:476856.\n[3].\nGárate I, et al. Toll-like 4 receptor inhibitor TAK-242 decreases neuroinflammation in rat brain frontal cortex after stress. J Neuroinflammation. 2014 Jan 11;11:8.\n[4].\nWang L, et al. Doxorubicin-Induced Systemic Inflammation Is Driven by Upregulation of Toll-Like Receptor TLR4 and Endotoxin Leakage. Cancer Res. 2016 Nov 15;76(22):6631-6642.\n[5].\nShibata A, et al. Toll-like receptor 4 antagonist TAK-242 inhibits autoinflammatory symptoms in DITRA. J Autoimmun. 2017 Jun;80:28-38.\n[6].\nJanda J, et al. Resatorvid-based Pharmacological Antagonism of Cutaneous TLR4 Blocks UV-induced NF-κB and AP-1 Signaling in Keratinocytes and Mouse Skin. Photochem Photobiol. 2016 Nov;92(6):816-825.\n[7].\nKrock E, et al. Low back pain and disc degeneration are decreased following chronic toll-like receptor 4 inhibition in a mouse model. 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