Abstract
Synovial inflammation plays an important role in the pathogenesis and progress of osteoarthritis (OA). There is an urgent need to find safe and effective drugs that can reduce the inflammation and regulate the pathogenesis of cytokines of the OA disease. Here, we investigated the effect of icariin, the major pharmacological active component of herb Epimedium on human osteoarthritis fibroblast-like synoviocytes (OA–FLSs). The OA–FLSs were isolated from patients with osteoarthritis and cultured in vitro with different concentrations of icariin. Then, cell viability, proliferation, and migration were investigated; MMP14, GRP78, and IL-1β gene expression levels were detected via qRT-PCR. Icariin showed low cytotoxicity to OA–FLSs at a concentration of under 10 μM and decreased the proliferation of the cells at concentrations of 1 and 10 μM. Icariin inhibited cell migration with concentrations ranging from 0.1 to 1 μM. Also, the expression of three cytokines for the pathogenesis of OA which include IL-1β, MMP14 and GRP78 was decreased by the various concentrations of icariin. These preliminary results imply that icariin might be an effective compound for the treatment of OA disease.
Highlights
Osteoarthritis (OA) is a chronic joint bone disease characterized by the progressive damage of joint structure including articular cartilage and subchondral bone which always leads to the dysfunction and disability of arthritis [1]
It has been demonstrated that the proliferation of osteoarthritis fibroblast-like synoviocytes (OA–fibroblast-like synoviocytes (FLSs)) could have an effect on both the morphology and proliferation of cartilage cells [12], and the proliferation and migration of OA–FLSs increase the number of cells with many inflammatory cytokines which may lead to hypertrophy and hyperplasia
The results show that no cytotoxic effects of icariin at 0.1, 0.5, 1 μM concentration were observed in the OA–FLSs
Summary
Osteoarthritis (OA) is a chronic joint bone disease characterized by the progressive damage of joint structure including articular cartilage and subchondral bone which always leads to the dysfunction and disability of arthritis [1]. FLSs provide nutrients for articular cartilage and protect the joint structures and the adjacent musculoskeletal tissues. Previous research data indicate that FLSs play an important role in OA cartilage degradation by producing inflammatory and catabolic mediators [9,10,11]. It has been demonstrated that the proliferation of OA–FLSs could have an effect on both the morphology and proliferation of cartilage cells [12], and the proliferation and migration of OA–FLSs increase the number of cells with many inflammatory cytokines which may lead to hypertrophy and hyperplasia. Hypertrophy is one of the typical pathological processes of the OA disease
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