Gomisin N Decreases Inflammatory Cytokine Production in Human Periodontal Ligament Cells
Gomisin N Decreases Inflammatory Cytokine Production in Human Periodontal Ligament Cells
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DOI：
10.1007/s10753-016-0482-4
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发表时间：
2017-04-01
期刊：
影响因子：
5.1
通讯作者：
Matsuo, Takashi
中科院分区：
文献类型：
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作者：
Hosokawa, Yoshitaka;Hosokawa, Ikuko;Matsuo, Takashi
Gomisin N是从北五味子中分离得到的一种木脂素，具有一定的药理作用。然而，戈米辛N对牙周病的抗炎作用尚不确定。本研究的目的是检查戈米辛N对肿瘤坏死因子（TNF）-α刺激的人牙周膜细胞（HPDLC）中炎症介质产生的影响。Gomisin N以剂量依赖性方式抑制TNF-α刺激的HPDLC中白细胞介素（IL）-6，IL-8，CC趋化因子配体（CCL）2和CCL 20的产生。此外，我们发现，gomisin N可以抑制细胞外信号调节激酶（ERK）和c-Jun N末端激酶（JNK）的磷酸化在TNF-α刺激的HPDLC，虽然蛋白激酶B（Akt）的磷酸化没有抑制gomisin N的治疗。综上所述，戈米辛N可能通过抑制TNF-α刺激的ERK和JNK通路活化，减少牙周韧带细胞中细胞因子的产生，从而发挥抗炎作用。
Gomisin N, which is a lignan isolated from Schisandra chinensis, has some pharmacological effects. However, the anti-inflammatory effects of gomisin N on periodontal disease are uncertain. The aim of this study was to examine the effect of gomisin N on inflammatory mediator production in tumor necrosis factor (TNF)-alpha-stimulated human periodontal ligament cells (HPDLC). Gomisin N inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 2, and CCL20 production in TNF-alpha-stimulated HPDLC in a dose-dependent manner. Moreover, we revealed that gomisin N could suppress extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase (JNK) phosphorylation in TNF-alpha-stimulated HPDLC though protein kinase B (Akt) phosphorylation was not suppressed by gomisin N treatment. In summary, gomisin N might exert anti-inflammatory effects by attenuating cytokine production in periodontal ligament cells via inhibiting the TNF-alpha-stimulated ERK and JNK pathways activation.