Traumatic arthritis is one of the most common diseases in orthopedics. LGR4 is involved in bone formation and bone development. However, the role of LGR4 in synovial cells of rats with traumatic osteoarthritis has not been reported.
Sprague Dawley (SD) rats were randomly divided into the control group and model group. The Real Time-Polymerase Chain Reaction (RT-PCR), Western blot, and Enzyme-Linked Immunosorbent Assay (ELISA) were used to analyze the expression of LGR4 in synovial tissue and synovial fluid. Synovial cells were isolated and cultured, followed by transfection of LGR4-pcDNA3.1 plasmid into cells. Cell proliferation was analyzed by MTT and EdU assay, and the Caspase-3 activity was assessed using the Caspase-3 activity kit. The secretion of the inflammatory factors interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) was detected by ELISA. NF-κB signaling pathway changes were evaluated by the Western blot.
In the model group, LGR4 mRNA expression in synovial tissue was significantly decreased, and the secretion of LGR4 in the synovial fluid was significantly decreased compared with the control group (p<0.05). LGR4 protein expression in the synovial membrane in the model group tissue was reduced. The transfection of LGR4-pcDNA3.1 plasmid into synovial cells promoted the LGR4 expression, inhibited the proliferation of synoviocytes, increased the Caspase-3 activity, the secretion of IL-1, TNF-α, and IL-6, as well as the decreased expression of NF-κB with a statistical significance, compared with the control group (p<0.05).
LGR4 expression is reduced in the rat model of traumatic osteoarthritis. The upregulation of LGR4 expression can inhibit the secretion of the inflammatory factors and inhibit the proliferation of the synovial cells by regulating NF-κB signaling pathway, which may alleviate the development of the joint inflammation.