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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Apurinic/Apyrimidinic endonuclease 1 regulates inflammatory response in macrophages.
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Apurinic/Apyrimidinic endonuclease 1 regulates inflammatory response in macrophages.

机译：Apurinic / Apyrimidinic内切核酸酶1调节巨噬细胞的炎症反应。

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摘要

The multi-functional apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) DNA repair and redox signaling protein has been shown to have a role in cancer growth and survival, however, little has been investigated concerning its role in inflammation. In this study, an APE1 redox-specific inhibitor (E3330) was used in lypopolysaccharide (LPS)-stimulated macrophages (RAW264.7). E3330 clearly suppressed secretion of inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin (IL-6) and IL-12 and inflammatory mediators nitric oxide (NO) as well as prostaglandin E(2) (PGE(2)) from the LPS-stimulated RAW264.7 cells. These data were supported by the down-regulation of the LPS-dependent expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) genes in the RAW264.7 cells. The effects of E3330 were mediated by the inhibition of transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein 1 (AP-1) in the LPS-stimulated macrophages, both known targets of APE1. In conclusion, pharmacological inhibition of APE1 by E3330 suppresses inflammatory response in activated macrophages and can be considered as a novel therapeutic strategy for the inhibition of tumor-associated macrophages.
机译：多功能的嘧啶二酮内切核酸酶1 /氧化还原因子-1（APE1 / Ref-1）DNA修复和氧化还原信号蛋白已被证明在癌症的生长和存活中起作用，然而，关于其在炎症中的作用的研究很少。在这项研究中，APE1氧化还原特异性抑制剂（E3330）用于脂多糖（LPS）刺激的巨噬细胞（RAW264.7）。 E3330明显抑制了炎症细胞因子的分泌，包括肿瘤坏死因子-α（TNF-alpha），白介素（IL-6）和IL-12和炎性介质一氧化氮（NO）以及前列腺素E（2）（PGE（2） ）来自LPS刺激的RAW264.7细胞。这些数据得到了RAW264.7细胞中诱导型一氧化氮合酶（iNOS）和环氧合酶-2（COX-2）基因LPS依赖性表达下调的支持。 E3330的作用是通过抑制LPS刺激的巨噬细胞（这是APE1的靶标）中的转录因子核因子-κB（NF-kappaB）和激活蛋白1（AP-1）介导的。总之，E3330对APE1的药理抑制作用抑制了活化巨噬细胞的炎症反应，可以被认为是抑制肿瘤相关巨噬细胞的一种新型治疗策略。

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