Icariin inhibits MMP-1, MMP-3 and MMP-13 expression through MAPK pathways in IL-1β-stimulated SW1353 chondrosarcoma cells

Osteoarthritis (OA) is the most common type of arthritis and is a leading cause of disability worldwide, resulting in pain, reduced quality of life and socioeconomic burden. Current therapies for OA focus on mitigating the symptoms of advanced disease, but novel therapeutic agents are needed to inhibit the processes leading to OA. The present study aimed to investigate the effects of Icariin on matrix metalloproteinase (MMP)-1, MMP-3 and MMP-13 expression in interleukin (IL)-1 beta-stimulated human SW1353 chondrosarcoma cells, and to investigate the possible mechanism underlying the chondroprotective effects of Icariin. In the present study, IL-1 beta was applied on SW1353 chondrosarcoma cells to mimic the microenvironment of osteoarthritis. The cells were treated with Icariin and mitogen-activated protein kinase (MAPK) signaling pathway activators or inhibitors. MMP-1, MMP-3, MMP-13, phosphorylated (P)-p38, P-c-Jun N-terminal kinase (JNK) and P-extracellular signal-regulated kinase (ERK) expression was assessed using reverse transcription-quantitative polymerase chain reaction, ELISA and western blot analysis. The results of the present study demonstrated that Icariin inhibited the expression of MMP-1, MMP-3, MMP-13, P-p38, P-ERK and P-JNK. Furthermore, it was revealed that the inhibition of p38 and ERK contributed to the inhibition of MMP-1 and MMP-3 by Icariin, whereas the inhibition of p38 and JNK contributed to the inhibition of MMP-13. The present results suggested that Icariin may have a chondroprotective effect, exerted through the inhibition of MMP-1, MMP-3 and MMP-13 via MAPK pathways. Therefore, Icariin may have potential as a novel therapeutic strategy for the treatment of osteoarthritis.