Ibuprofen attenuates interleukin-1β-induced inflammation and actin reorganization via modulation of RhoA signaling in rabbit chondrocytes

Ibuprofen, a medication in the nonsteroidal anti-inflammatory drug class, is widely used for treating inflammatory diseases such as osteoarthritis. It has been shown in recent years that ibuprofen has a strong effect on Ras homolog gene family, member A (RhoA) inhibition in multiple cell types. Our previous finding also demonstrated that interleukin-1 beta (IL-1 beta) increases filamentous actin (F-actin) of chondrocytes via RhoA pathway. Therefore, we hypothesized that ibuprofen may suppress the IL-1 beta-induced F-actin upregulation in chondrocytes by inhibiting RhoA pathway. To this end, in this study, articular chondrocytes from New Zealand White rabbits were pretreated with 500 mu M ibuprofen for 2 h, then with 10 ng/ml IL-1 beta for 24 h. Results showed that pretreatment with ibuprofen inhibited the IL-1 beta-induced nitric oxide (NO) and prostaglandin E2 (PGE(2)) production, protected the chondrocyte phenotype from IL-1 beta stimulation, and inhibited the IL-1 beta-induced actin remodeling via RhoA signaling modulation. In conclusion, ibuprofen showed not only anti-inflammatory function, but also RhoA inhibition in articular chondrocytes.