Xanthan gum protects temporomandibular chondrocytes from IL‑1β through Pin1/NF‑κB signaling pathway

• Published in: Molecular medicine reports Vol. 22; no. 2; pp. 1129 - 1136
• Main Authors: Yuan, Fang, Xie, Jian-Li, Liu, Ke-Yin, Shan, Jian-Liang, Sun, Yu-Gang, Ying, Wang-Gui
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.08.2020
• Subjects: Adaptor Proteins, Signal Transducing - metabolism; Animals; Cell Survival - drug effects; Cells, Cultured; Chemokine CCL2 - metabolism; Chondrocytes - drug effects; Cytokines - metabolism; Interleukin-1beta - pharmacology; Male; Matrix Metalloproteinases - metabolism; Nitric Oxide Synthase Type II - metabolism; Polysaccharides, Bacterial - pharmacology; Protective Agents - pharmacology; Rats; Rats, Sprague-Dawley; Signal Transduction; Temporomandibular Joint Disorders - chemically induced; Temporomandibular Joint Disorders - drug therapy; Transcription Factor RelA - metabolism
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2020.11233

Temporomandibular disorder (TMD) is a complicated and multi‑factorial disease related to inflammation and cartilage destruction. Intra‑articular injection of xanthan gum (XG) has been demonstrated to protect the joint cartilage and reduce osteoarthritis progression. However, the role and mechanism of XG in TMD is still unclear. In the present study, chondrocytes were isolated from rats and identified by immunofluorescence. Cells were stimulated by XG or interleukin (IL)‑1β. Cell viability was analyzed by MTT assay. Tumor necrosis factor α (TNF‑α) and IL‑6 levels were determined by ELISA. The expression of monocyte chemoattractive protein‑1 (MCP‑1), inducible nitric oxide synthase (iNOS), collagens, matrix metalloproteinases (MMPs), peptidyl‑prolyl isomerase 1 (Pin1) and phosphorylated nuclear factor κB (NF‑κB) p65 (p‑p65) was analyzed by quantitative PCR or western blotting. MMP activity was assessed by gelatin zymography. Compared with the control, XG treatment partially reversed the IL‑1β‑reduced cell viability. In addition, IL‑1β stimulation increased inflammatory cytokine expression, including TNF‑α, IL‑6 secretion, MCP‑1 and iNOS expression, whereas XG treatment reduced the expression of these inflammatory cytokines compared with that of the IL‑1β‑stimulated cells. Additionally, XG increased the expression of collagen, but reduced MMP expression and activity as compared with that in the IL‑1β group. In addition, XG treatment prevented the IL‑1β‑increased Pin1 and p‑p65 expression. These data suggested that XG reduced the expression of inflammatory cytokines and may maintain the balance between collagens and MMPs partially through the Pin1/NF‑κB signaling pathway in IL‑1β‑stimulated temporomandibular chondrocytes. Therefore, XG may be useful in the treatment of TMD.