首页> 外文OA文献 >Melatonin Attenuates The Tlr4-mediated Inflammatory Response Through Myd88- And Trif-dependent Signaling Pathways In An In Vivo Model Of Ovarian Cancer.
【2h】

Melatonin Attenuates The Tlr4-mediated Inflammatory Response Through Myd88- And Trif-dependent Signaling Pathways In An In Vivo Model Of Ovarian Cancer.

机译:褪黑素在卵巢癌体内模型中通过Myd88和Trif依赖性信号通路减弱Tlr4介导的炎症反应。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Toll-like receptors (TLRs) are effector molecules expressed on the surface of ovarian cancer (OC) cells, but the functions of the TLR2/TLR4 signaling pathways in these cells remain unclear. Melatonin (mel) acts as an anti-inflammatory factor and has been reported to modulate TLRs in some aggressive tumor cell types. Therefore, we investigated OC and the effect of long-term mel therapy on the signaling pathways mediated by TLR2 and TLR4 via myeloid differentiation factor 88 (MyD88) and toll-like receptor-associated activator of interferon (TRIF) in an ethanol-preferring rat model. To induce OC, the left ovary of animals either consuming 10% (v/v) ethanol or not was injected directly under the bursa with a single dose of 100 μg of 7,12-dimethylbenz(a)anthracene (DMBA) dissolved in 10 μL of sesame oil. The right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of mel (200 μg/100 g b.w./day) for 60 days. Although mel therapy was unable to reduce TLR2 levels, it was able to suppress the OC-associated increase in the levels of the following proteins: TLR4, MyD88, nuclear factor kappa B (NFkB p65), inhibitor of NFkB alpha (IkBα), IkB kinase alpha (IKK-α), TNF receptor-associated factor 6 (TRAF6), TRIF, interferon regulatory factor 3 (IRF3), interferon β (IFN-β), tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6. In addition, mel significantly attenuated the expression of IkBα, NFkB p65, TRIF and IRF-3, which are involved in TLR4-mediated signaling in OC during ethanol intake. Collectively, our results suggest that mel attenuates the TLR4-induced MyD88- and TRIF-dependent signaling pathways in ethanol-preferring rats with OC.
机译:Toll样受体(TLR)是在卵巢癌(OC)细胞表面表达的效应分子,但这些细胞中TLR2 / TLR4信号通路的功能仍不清楚。褪黑激素(mel)起着抗炎因子的作用,据报道在某些侵袭性肿瘤细胞类型中它会调节TLRs。因此,我们研究了乙醇偏爱大鼠的OC和长期mel治疗对TLR2和TLR4通过髓样分化因子88(MyD88)和Toll样受体相关干扰素激活剂(TRIF)介导的信号通路的影响。模型。为了诱导OC,将食用10%(v / v)乙醇或不食用10%(v / v)乙醇的动物的左卵巢直接注射到法氏囊下方,将100μg的7,12-二甲基苯并蒽(DMBA)溶于10 μL香油。右侧卵巢用作假手术对照。形成OC后,一半的动物接受腹膜内注射。每天注入mel(200μg/ 100 g b.w./天)60天。尽管梅尔疗法无法降低TLR2的水平,但它能够抑制OC相关的以下蛋白水平的升高:TLR4,MyD88,核因子κB(NFkB p65),NFkB alpha抑制剂(IkBα),IkB激酶α(IKK-α),TNF受体相关因子6(TRAF6),TRIF,干扰素调节因子3(IRF3),干扰素β(IFN-β),肿瘤坏死因子α(TNF-α)和白介素(IL )-6。此外,mel显着减弱了IkBα,NFkB p65,TRIF和IRF-3的表达,它们在乙醇摄入过程中参与了OC中TLR4介导的信号传导。总的来说,我们的研究结果表明,mel在乙醇偏爱的OC大鼠中减弱了TLR4诱导的MyD88和TRIF依赖性信号通路。

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号