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Apurinic/Apyrimidinic Endonuclease 1 Regulates Inflammatory Response in Macrophages

机译：apurinic / Apyrimidinic核酸内切酶1调节巨噬细胞的炎症反应。

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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-α (TNF-α), interleukin (IL-6) and IL-12 and inflammatory mediators nitric oxide (NO) as well as prostaglandin E2 (PGE2) 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-κB (NF-κB) 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：多功能嘧啶二烯内切核酸酶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）用于经脂多糖（LPS）刺激的巨噬细胞（RAW264.7）。 E3330明显抑制了LPS刺激的炎症细胞因子的分泌，包括肿瘤坏死因子-α（TNF-α），白介素（IL-6）和IL-12以及炎性介质一氧化氮（NO）和前列腺素E2（PGE2）。 RAW264.7细胞。这些数据得到了RAW264.7细胞中LPS依赖性诱导型一氧化氮合酶（iNOS）和环氧合酶2（COX-2）基因表达的下调的支持。 E3330的作用是通过抑制LPS刺激的巨噬细胞（两者都是APE1的靶标）中的转录因子核因子-κB（NF-κB）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，可以被认为是一种抑制肿瘤相关巨噬细胞的新型治疗策略。

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