Abstract
Traumatic arthritis is a common orthopedic surgery disease that seriously affects the health of patients. The expression and role of Galectins in traumatic osteoarthritis remains unclear. SD rats were divided into control group and osteoarthritis model group. Real-time PCR and ELISA were used to analyze Galectins-1 expression. Chondrocytes were isolated and cultured and divided into control group, Galectins-1 siRNA group and Galectins-1 group followed by analysis of proliferation of chondrocytes by MTT assay, cell migration by Transewell chamber, expression of RUNX2 and ADAMTS-4/5 by Real-time PCR, and PI3K/Akt by Western blot. Galectins-1 mRNA and secretion in synovial fluid was significantly reduced in model group compared to control (P < 0.05). Transfection of Galectins-1-pcDNA3.1 plasmid into chondrocytes of osteoarthritic rats significantly increased the expression of Galectins-1, promoted chondrocyte proliferation and cell migration, and downregulated RUNX2 and ADAMTS-4/5 (P < 0.05). Up-regulation of Galectins-1 blocked the expression of PI3K/Akt signaling pathway. Transfection of Galectins-1 siRNA significantly reduced the expression of Galectins-1, inhibited chondrocyte proliferation and cell migration, and upregulated RUNX2 and ADAMTS-4/5 (P < 0.05). Down-regulation of Galectins-1 up-regulated PI3K/Akt signaling pathway. Galectins-1 expression is reduced in joint tissues in rat model of traumatic osteoarthritis. Up-regulation of Galectins-1 expression can promote chondrocyte proliferation and migration by regulating PI3K/Akt signaling pathway, which may reduce chondrocyte damage in rats with traumatic osteoarthritis.
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