INHIBITION OF NF-KAPPA-B BY SODIUM-SALICYLATE AND ASPIRIN
INHIBITION OF NF-KAPPA-B BY SODIUM-SALICYLATE AND ASPIRIN
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DOI：
10.1126/science.8052854
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发表时间：
1994-08-12
期刊：
影响因子：
56.9
通讯作者：
GHOSH, S
中科院分区：
文献类型：
--
作者：
KOPP, E;GHOSH, S
转录因子核因子 kappa B (NF-kappa B) 对于参与炎症和感染的多种细胞和病毒基因的诱导表达至关重要，包括白介素 1 (IL-1)、IL-6 和粘附分子。抗炎药物水杨酸钠和阿司匹林抑制了NF-κB的激活，这进一步解释了这些药物的作用机制。这种抑制作用阻止了 NF-κ B 抑制剂 Iκ B 的降解，因此 NF-κ B 保留在细胞质中。水杨酸钠和阿司匹林还抑制转染 T 细胞中 Ig kappa 增强子和人类免疫缺陷病毒 (HIV) 长末端重复序列 (LTR) 的 NF-kappa B 依赖性转录。
The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.