Glucose suppresses IL-1β-induced MMP-1 expression through the FAK, MEK, ERK and AP-1 signaling pathways

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/111630

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題名:	Glucose suppresses IL-1β-induced MMP-1 expression through the FAK, MEK, ERK and AP-1 signaling pathways
作者:	TJ, Wu;TJ, Wu;CY, Lin;CY, Lin;CH, Tsai;CH, Tsai;黃元勵;HUANG, YUAN-LI;CH, Tang;CH, Tang
貢獻者:	生物科技學系
日期:	2018-10
上傳時間:	2018-12-24 08:12:04 (UTC+0)
摘要:	Osteoarthritis (OA) commonly affects the synovial joint and is characterized by degradation of articular cartilage. Increased matrix metalloproteinase (MMP) activity plays a major role in this degradation. Dextrose (D‐glucose) prolotherapy has shown promising activity in the treatment of different musculoskeletal disorders, including OA. However, little is known about the role of glucose on MMP inhibition in OA therapy. We found that stimulating chondrocytes with the proinflammatory cytokine interleukin‐1β (IL‐1β) increased the expression of MMP‐1, MMP‐3, and MMP‐13. Glucose reduced this increase in MMP‐1 expression, but had no effect upon MMP‐3 or MMP‐13 expression. Analyses using a focal adhesion kinase (FAK) inhibitor, MEK inhibitors (U0126 and PD98059), an ERK inhibitor, AP‐1 inhibitors (curcumin and tanshinone), or siRNAs demonstrated that the FAK, MEK, ERK, and AP‐1 pathways mediate IL‐1β‐induced increases in MMP‐1 expression. Glucose antagonized IL‐1β‐promoted phosphorylation of FAK, MEK, ERK, and c‐Jun. Thus, glucose decreased IL‐1β‐induced MMP‐1 expression through the FAK, MEK, ERK, and AP‐1 signaling cascades. These findings may provide a better understanding of the mechanisms of prolotherapy on inhibiting MMP expression.
關聯:	ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY
顯示於類別:	[生物科技學系] 期刊論文

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