Catalpol attenuates IL-1b induced matrix catabolism, apoptosis and inflammation in rat chondrocytes and inhibits cartilage degeneration

Abstract

Background: Chondrocyte 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, antioxidative, and anti-apoptotic effects in various diseases. However, whether catalpol protects against osteoarthritis has not been investigated. Material/Methods: To assess the role of catalpol in osteoarthritis and the potential mechanism of action, chondrocytes were treated with interleukin (IL)-1b 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. Results: The results showed that catalpol prevented chondrocyte apoptotic level triggered by IL-1b, suppressed the release of catabolic enzymes, and inhibited the degradation of extracellular matrix induced by IL-1b. Catalpol also inhibited the nuclear factor kappa B (NF-kB) pathway, reduced the production of inflammatory cytokines (IL-6, tumor necrosis factor-a) in IL-1b-treated chondrocytes, and partially reversed cartilage degeneration in the knee joint in animal model of osteoarthritis. Conclusions: Our work suggested that catalpol treatment attenuates IL-1b-induced inflammatory response and catabolism in rat chondrocytes by inhibiting the NF-kB pathway, suggesting the therapeutic potential of catalpol for the treatment of osteoarthritis.