Role of Link N in modulating inflammatory conditions

Mu Chen Yang, Ding-Han Wang, Juin Hong Cherng, Wan-Chun Li, Po Yen Lin, Wun Eng Hsu, Ming-Lun Hsu*

*此作品的通信作者

研究成果: Article同行評審

2 引文 斯高帕斯(Scopus)

摘要

Aims: To elucidate the role of Link N in regulating inflammatory molecules from human mesenchymal stem cells (hMSCs) under interleukin (IL)-1β stimulation in vitro and under Complete Freund's Adjuvant (CFA)-induced arthritis of the temporomandibular joint (TMJ) in vivo. Methods: In vitro analysis of inflammatory cytokines and epithelial-mesenchymal transition (EMT) genes in hMSCs treated with Link N, IL-1β, and co-stimulation of IL-1β and Link N was undertaken using Luminex multiplex assays and real-time polymerase chain reaction, respectively. To determine the impact of Link N in ameliorating TMJ tissue homeostasis in arthritic conditions, histologic changes in CFA-induced arthritic TMJ tissues followed by application of Link N were examined. All data were analyzed using one-way analysis of variance with Bonferroni post hoc test. Results: Increased levels of IL-6; interferon gamma-inducible protein-10; and regulated upon activation, normal T cell expressed, and secreted (RANTES) were detected in response to IL-1β treatment, but these levels were significantly decreased in the co-stimulation group. In contrast, secreted IL-4, IL-10, and transforming growth factor β1-β3 proteins, as well as intracellular erb-b2 receptor tyrosine kinase 3 and Nodal homolog genes, were increased significantly in the co-stimulation group compared to the IL-1β group. Histologic analysis showed significant recovery for rat condyle thickness in the Link N-treated group when compared to the CFA-induced arthritis group. Conclusion: These findings indicate that Link N could modulate inflammation and EMT in vitro and repair arthritis-mediated TMJ disruption in vivo. Link N could be a potential therapeutic agent for TMJ disorder patients.

原文English
頁(從 - 到)114-122
頁數9
期刊Journal of Oral and Facial Pain and Headache
33
發行號1
DOIs
出版狀態Published - 22 3月 2019

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