Catalpol Attenuates IL-1β Induced Matrix Catabolism, Apoptosis and Inflammation in Rat Chondrocytes and Inhibits Cartilage Degeneration.

Abstract

BackgroundChondrocyte dysfunction and apoptosis are 2 major features during the progression of osteoarthritis. Catalpol, an iridoid glycoside isolated from the root of Rehmannia, is a valuable medication with anti-inflammatory, anti-oxidative, and anti-apoptotic effects in various diseases. However, whether catalpol protects against osteoarthritis has not been investigated.Material/MethodsTo assess the role of catalpol in osteoarthritis and the potential mechanism of action, chondrocytes were treated with interleukin (IL)-1β and various concentrations of catalpol. Catabolic metabolism, apoptotic level and relative signaling pathway were measured by western blot, real-time polymerase chain reaction and immunofluorescence staining. Meanwhile, we assess the cartilage degeneration in an experimental rat model using Safranin O fast green staining and cartilage was graded according to the Osteoarthritis Research Society International (OARSI) system.ResultsThe results showed that catalpol prevented chondrocyte apoptotic level triggered by IL-1β, suppressed the release of catabolic enzymes, and inhibited the degradation of extracellular matrix induced by IL-1β. Catalpol also inhibited the nuclear factor kappa B (NF-κB) pathway, reduced the production of inflammatory cytokines (IL-6, tumor necrosis factor-α) in IL-1β-treated chondrocytes, and partially reversed cartilage degeneration in the knee joint in animal model of osteoarthritis.ConclusionsOur work suggested that catalpol treatment attenuates IL-1β-induced inflammatory response and catabolism in rat chondrocytes by inhibiting the NF-κB pathway, suggesting the therapeutic potential of catalpol for the treatment of osteoarthritis.