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.