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诺米林抑制白细胞介素-1β刺激的人牙周膜细胞中的炎症反应。

Nobiletin Inhibits Inflammatory Reaction in Interleukin-1β-Stimulated Human Periodontal Ligament Cells.

作者信息

Hosokawa Yoshitaka, Hosokawa Ikuko, Ozaki Kazumi, Matsuo Takashi

机构信息

Department of Conservative Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, Japan.

Department of Oral Health Care Promotion, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, Japan.

出版信息

Pharmaceutics. 2021 May 7;13(5):667. doi: 10.3390/pharmaceutics13050667.

DOI:10.3390/pharmaceutics13050667
PMID:34066937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8148442/
Abstract

The immune response in periodontal lesions is involved in the progression of periodontal disease. Therefore, it is important to find a bioactive substance that has anti-inflammatory effects in periodontal lesions. This study aimed to examine if nobiletin, which is found in the peel of citrus fruits, could inhibit inflammatory responses in interleukin (IL)-1β-stimulated human periodontal ligament cells (HPDLCs). The release of cytokines (IL-6, IL-8, CXCL10, CCL20, and CCL2) and matrix metalloproteinases (MMP-1 and MMP-3) was assessed by ELISA. The expression of cell adhesion molecules (ICAM-1and VCAM-1) and the activation of signal transduction pathways (nuclear factor (NF)-κB, mitogen-activated protein kinases (MAPKs) and protein kinase B (Akt)) in HPDLCs were detected by Western blot analysis. Our experiments revealed that nobiletin decreased the expression of inflammatory cytokines, cell adhesion molecules, and MMPs in IL-1β-stimulated HPDLCs. Moreover, we revealed that nobiletin treatment could suppress the activation of the NF-κB, MAPKs, and Akt pathways. These findings indicate that nobiletin could inhibit inflammatory reactions in IL-1β-stimulated HPDLCs by inhibiting multiple signal transduction pathways, including NF-κB, MAPKs, and Akt.

摘要

牙周病变中的免疫反应参与了牙周疾病的进展。因此,找到一种在牙周病变中具有抗炎作用的生物活性物质很重要。本研究旨在检验柑橘类水果果皮中含有的川陈皮素是否能抑制白细胞介素(IL)-1β刺激的人牙周膜细胞(HPDLCs)中的炎症反应。通过酶联免疫吸附测定(ELISA)评估细胞因子(IL-6、IL-8、CXCL10、CCL20和CCL2)和基质金属蛋白酶(MMP-1和MMP-3)的释放。通过蛋白质免疫印迹分析检测HPDLCs中细胞黏附分子(ICAM-1和VCAM-1)的表达以及信号转导通路(核因子(NF)-κB、丝裂原活化蛋白激酶(MAPKs)和蛋白激酶B(Akt))的激活情况。我们的实验表明,川陈皮素可降低IL-1β刺激的HPDLCs中炎症细胞因子、细胞黏附分子和基质金属蛋白酶的表达。此外,我们发现川陈皮素处理可抑制NF-κB、MAPKs和Akt通路的激活。这些发现表明,川陈皮素可通过抑制包括NF-κB、MAPKs和Akt在内的多种信号转导通路,抑制IL-1β刺激的HPDLCs中的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/c71876aedee3/pharmaceutics-13-00667-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/c893c875754d/pharmaceutics-13-00667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/b38fd97a42b8/pharmaceutics-13-00667-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/25022c9b47a5/pharmaceutics-13-00667-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/540edfd2cdb4/pharmaceutics-13-00667-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/5fa3ac3ff7f1/pharmaceutics-13-00667-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/c71876aedee3/pharmaceutics-13-00667-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/c893c875754d/pharmaceutics-13-00667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/b38fd97a42b8/pharmaceutics-13-00667-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/25022c9b47a5/pharmaceutics-13-00667-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/540edfd2cdb4/pharmaceutics-13-00667-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/5fa3ac3ff7f1/pharmaceutics-13-00667-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/8148442/c71876aedee3/pharmaceutics-13-00667-g006.jpg

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