Magnolol Inhibits Tumor Necrosis Factor-α-Induced ICAM-1 Expression via Suppressing NF-κB And MAPK Signaling Pathways in Human Lung Epithelial Cells
Magnolol Inhibits Tumor Necrosis Factor-α-Induced ICAM-1 Expression via Suppressing NF-κB And MAPK Signaling Pathways in Human Lung Epithelial Cells
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DOI：
10.1007/s10753-014-9928-8
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发表时间：
2014-12-01
期刊：
影响因子：
5.1
通讯作者：
Liu Gentao
中科院分区：
文献类型：
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作者：
Wu Chunlian;Wang Heyong;Liu Gentao
厚朴酚是从厚朴的根和树皮中提取的传统中药。它长期以来一直被用于治疗焦虑，咳嗽，头痛和过敏，以及各种炎症。肺部炎症是哮喘和慢性阻塞性肺疾病发病机制中的关键事件。本研究旨在观察厚朴酚对肿瘤坏死因子（TNF）-α诱导的人肺上皮细胞细胞间粘附分子-1（ICAM-1）表达上调、核因子（NF）-κ B（B）和丝裂原活化蛋白激酶（MAPK）信号通路激活以及人巨噬细胞样U937细胞与A549细胞粘附的影响。将A549细胞与25和50 μ mol/l的厚朴酚孵育。然后，使用20 ng/ml TNF-α来激活细胞。厚朴酚对人肺上皮细胞A549的生长有明显的抑制作用，且呈剂量和时间依赖性。厚朴酚抑制U937细胞与TNF-α诱导的A549细胞的粘附。在培养的人肺上皮A549细胞中，厚朴酚降低TNF-α诱导的ICAM-1上调。厚朴酚通过抑制NF-κ B、p38、细胞外信号调节激酶（ERK）1/2和应激活化蛋白激酶（SAPK）/c-Jun N末端激酶（JNK）的磷酸化，抑制TNF-α诱导的A549细胞中NF-κ B和丝裂原活化蛋白激酶（MAPK）信号通路的激活。这些发现支持了厚朴酚通过抑制ICAM-1和NF-κ B和MAPK信号通路抑制肺上皮A549细胞的炎症过程的假设。总之，这些结果表明，厚朴酚提供了显着的潜力，作为一种治疗肺部炎症性疾病，包括哮喘，败血症，慢性阻塞性肺病的治疗。
Magnolol is a traditional Chinese medicine from the root and bark of Magnolia officinalis. It has long been used to treat anxiety, cough, headache and allergies, as well as a variety of inflammations. Lung inflammation is a key event in the pathogenesis of asthma and chronic obstructive pulmonary disease. The present study sought to examine the effects of magnolol on tumor necrosis factor (TNF)-alpha-induced upregulation of intercellular adhesion molecule-1 (ICAM-1), activation of the nuclear factor (NF)-kappa B and mitogen-activated protein kinase (MAPK) signaling pathway in cultured human pulmonary epithelial cells, and adhesion of human macrophage-like U937 cells to A549 cells. A549 cells were incubated with magnolol at 25 and 50 mu mol/l. Then, 20 ng/ml TNF-alpha was used to activate the cells. Magnolol inhibited the growth of human pulmonary epithelial A549 cells in a dose- and time-dependent manner. Magnolol suppressed the adhesion of U937 cells to TNF-alpha-induced A549 cells. In cultured human pulmonary epithelial A549 cells, magnolol decreased TNF-alpha-induced upregulation of ICAM-1. Magnolol repressed TNF-alpha-induced activation of NF-kappa B and mitogen-activated protein kinase (MAPK) signaling pathways in A549 cells by inhibiting phosphorylation of NF-kappa B, p38, extracellular signal-regulated kinase (ERK) 1/2, and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK). These findings support the hypothesis that magnolol inhibits the inflammatory process in lung epithelial A549 cells by suppressing the ICAM-1 and NF-kappa B and MAPK signaling pathways. Taken together, these results indicate that magnolol offers significant potential as a therapeutic treatment for inflammatory diseases of the lungs including asthma, sepsis, and chronic obstructive pulmonary disease.