Sodium butyrate abolishes the degradation of type II collagen in human chondrocytes.

Excessive expression of matrix metalloproteinases (MMPs) induced by pro-inflammatory cytokines such as interleukin-1β (IL-1β) has been associated with destruction of the articular cartilage matrix in chondrocytes from patients with osteoarthritis (OA). Among the MMPs, MMP-1, MMP-3 and MMP-13 participate in the degradation of type II collagen, the main component of the extracellular matrix in articular cartilage. Sodium butyrate is a bacterial metabolite used in the treatment of inflammatory diseases. However, the effects of sodium butyrate on the expression of MMPs and degradation of type II collagen has not been explored. In the current study, for the first time, we aimed to determine whether sodium butyrate influences IL-1β-induced degradation of type II collagen in human chondrocytes in the articular cartilage matrix. Our results indicate that sodium butyrate significantly abrogated IL-1β-induced up-regulation of MMP-1, MMP-3, and MMP-13 at both the gene and protein levels. In addition, treatment with sodium butyrate suppressed expression of the endogenous tissue inhibitors TIMP-1 and TIMP-2. Notably, sodium butyrate attenuated IL-1β-induced degradation of type II collagen. Mechanistically, we found that sodium butyrate abolished the activation of NF-κB by inhibiting phosphorylation of IKK, IκBα, and NF-κB p65. Based on these observations, we conclude that butyrate may have potential as a therapeutic agent for OA.