Honokiol and Magnolol Inhibit CXCL10 and CXCL11 Production in IL-27-Stimulated Human Oral Epithelial Cells

被引：10
|
作者：
Hosokawa, Yoshitaka [1 ]
Hosokawa, Ikuko [1 ]
Ozaki, Kazumi [2 ]
Matsuo, Takashi [1 ]
机构：
[1] Tokushima Univ, Grad Sch, Inst Biomed Sci, Dept Conservat Dent, 3-18-15 Kuramoto Cho, Tokushima, Tokushima, Japan
[2] Tokushima Univ, Inst Biomed Sci, Dept Oral Hlth Care Promot, Grad Sch, Tokushima, Tokushima, Japan
来源：
INFLAMMATION | 2018年 / 41卷 / 06期
基金：
日本学术振兴会;
关键词：
honokiol; magnolol; anti-inflammatory effect; oral epithelial cells; INFLAMMATORY BONE-RESORPTION; SIGNAL TRANSDUCER; PATHWAY; IL-27; CONSTITUENTS; ACTIVATION; INDUCTION; APOPTOSIS; CANCER;
D O I：
10.1007/s10753-018-0854-z
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Honokiol and magnolol, which are lignans isolated from Magnolia quinquepeta, have some pharmacological effects. However, the anti-inflammatory effects of honokiol and magnolol on periodontal disease are still uncertain. The aim of this study was to examine the effect of honokiol and magnolol on CXC chemokine receptor 3 (CXCR3) ligands, which are related with Th1 cell migration, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Honokiol and magnolol inhibited CXC chemokine ligand (CXCL)10 and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent manner. Moreover, we revealed that honokiol and magnolol could suppress signal transducer and activator of transcription (STAT)3 and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells though STAT1 phosphorylation was not suppressed by honokiol and magnolol treatment. Furthermore, STAT3 and Akt inhibitors could suppress CXCR3 ligand production in TR146 cells. In summary, honokiol and magnolol could reduce CXCR3 ligand production in oral epithelial cell by inhibiting STAT3 and Akt activation.
引用
收藏
页码：2110 / 2115
页数：6
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