The anacardic 6-pentadecyl salicylic acid induces macrophage activation via the phosphorylation of ERK1/2, JNK, P38 kinases and NF-κB
The anacardic 6-pentadecyl salicylic acid induces macrophage activation via the phosphorylation of ERK1/2, JNK, P38 kinases and NF-κB
复制标题
DOI：
10.1016/j.intimp.2015.08.038
复制
发表时间：
2015-12-01
影响因子：
5.6
通讯作者：
Vega, Libia
中科院分区：
文献类型：
--
作者：
Gnanaprakasam, J. N. Rashida;Estrada-Muniz, Elizabet;Vega, Libia
Amphipterygium adstringens是一种传统上用于治疗牙龈炎、胃溃疡甚至胃癌的植物，但涉及免疫应答调节的机制尚未阐明。6-十五烷基水杨酸（6-pentadecylsalicylic acid，6SA）是A. adstringens。为了评价6 SA的免疫调节能力，我们使用小鼠脾细胞并测定辅助和细胞毒性T细胞、自然杀伤（NK）细胞和F4/80（+）巨噬细胞中转录因子NF-κ B和MAP激酶ERK 1/2、JNK和p38的磷酸化。用6SA处理没有细胞毒性，如通过台盼蓝排斥和四唑盐（MU）测试所测量的。此外，6SA没有改变辅助和细胞毒性T淋巴细胞，NK细胞或巨噬细胞的比例。此外，6SA处理显著增加ERK 1/2、JNK、P38和NF-κ B的磷酸化，主要在巨噬细胞中。在该细胞（腹膜巨噬细胞）中，用6 SA处理增加了一氧化氮（NO）、白细胞介素（IL）-6和肿瘤坏死因子（TNF）-α的分泌，并减少了IL-4和IL-10的分泌，这取决于MARK和NF-κ B磷酸化。此外，6SA还通过磷酸化不同的激酶来增强巨噬细胞的迁移和吞噬活性。这些数据表明，6 SA通过MAP激酶和NF-κ B的磷酸化诱导巨噬细胞中的经典活化途径，从而活化适应性免疫系统。(C)2015 Elsevier B. V.版权所有。
Amphipterygium adstringens is a plant traditionally used to treat gingivitis, gastric ulcer and even gastric cancer but the mechanism involved in the regulation of the immune response is not elucidated yet. The 6-pentadecylsalicylic acid (6SA) is the main anacardic acid found in A. adstringens. In order to evaluate the immune-modulatory abilities of 6SA, we used mouse splenocytes and determined the phosphorylation of the transcription factor NF-kappa B and MAP kinases ERK1/2, JNK and p38 in helper and cytotoxic T cells, natural killer (NK) cells and F4/80(+) macrophages. Treatment with 6SA was not cytotoxic as measured by both trypan blue exclusion and tetrazolium salts (MU) tests. Additionally, 6SA did not alter the proportion of helper and cytotoxic T lymphocytes, NK cells or macrophages. Moreover, 6SA treatment significantly increased the phosphorylation of ERK1/2, JNK, P38 and NF-kappa B mainly in macrophages. In this cells (peritoneal macrophages), treatment with 6SA increased the secretion of nitric oxide (NO), interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha and decreased the secretion of IL-4 and IL-10 depending on MARK and NF-kappa B phosphorylation. In addition, 6SA increased the migration and phagocytic activity of macrophages also depending on the phosphorylation of different kinases. These data suggest that 6SA induces the classical activation pathway in macrophages via the phosphorylation of MAP kinases and NF-kappa B thus activating the adaptive immune system. (C) 2015 Elsevier B.V. All rights reserved.