• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文OA文献 >HDAC 3-selective inhibitor RGFP966 demonstrates anti-inflammatory properties in RAW 264.7 macrophages and mouse precision-cut lung slices by attenuating NF-κB p65 transcriptional activity
【2h】

HDAC 3-selective inhibitor RGFP966 demonstrates anti-inflammatory properties in RAW 264.7 macrophages and mouse precision-cut lung slices by attenuating NF-κB p65 transcriptional activity

机译：HDAC 3-选择性抑制剂RGFP966通过减弱NF-κBp65转录活性在RAW 264.7巨噬细胞和小鼠精密切肺切片中显示出抗炎特性

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。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The increasing number of patients suffering from chronic obstructive pulmonary disease (COPD) represents a major and increasing health problem. Therefore, novel therapeutic approaches are needed. Class I HDACs 1, 2 and 3 play key roles in the regulation of inflammatory gene expression with a particular pro-inflammatory role for HDAC 3. HDAC 3 has been reported to be an important player in inflammation by deacetylating NF-κB p65, which has been implicated in the pathology of COPD. Here, we applied the pharmacological HDAC 3-selective inhibitor RGFP966, which attenuated pro-inflammatory gene expression in models for inflammatory lung diseases. Consistent with this, a robust decrease of the transcriptional activity of NF-κB p65 was observed. HDAC 3 inhibition affected neither the acetylation status of NF-κB p65 nor histone H3 or histone H4. This indicates that HDAC 3 inhibition does not inhibit NF-κB p65 transcriptional activity by affecting its deacetylation but rather by inhibiting enzymatic activity of HDAC 3. Taken together, our findings indicate that pharmacological HDAC 3-selective inhibition by inhibitors such as RGFP966 may provide a novel and effective approach towards development of therapeutics for inflammatory lung diseases.
机译：患有慢性阻塞性肺疾病（COPD）的患者数量不断增加，这代表了一个主要且日益严重的健康问题。因此，需要新颖的治疗方法。 I类HDAC 1、2和3在调节炎症基因表达中起关键作用，对HDAC 3具有特殊的促炎作用。据报道，HDAC 3通过使NF-κBp65脱乙酰化而在炎症中起重要作用。与COPD的病理学有关。在这里，我们应用了药理学上的HDAC 3选择性抑制剂RGFP966，它在炎症性肺疾病模型中减弱了促炎基因的表达。与此相一致，观察到NF-κBp65的转录活性强烈降低。 HDAC 3抑制既不影响NF-κBp65的乙酰化状态，也不影响组蛋白H3或组蛋白H4。这表明，HDAC 3的抑制不会通过影响其去乙酰化而抑制NF-κBp65的转录活性，而是通过抑制HDAC 3的酶促活性。综上所述，我们的发现表明，诸如RGFP966之类的抑制剂对HDAC 3的药理学选择性抑制可能提供开发发炎性肺疾病治疗药物的新颖有效方法。

著录项

相似文献

  • 外文文献
  • 中文文献
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