Remifentanil repairs cartilage damage and reduces the degradation of cartilage matrix in post-traumatic osteoarthritis, and inhibits IL-1β-induced apoptosis of articular chondrocytes via inhibition of PI3K/AKT/NF-κB phosphorylation.

Abstract

BackgroundRemifentanil (RFT) is an opioid analgesic with a unique pharmacokinetic profile, and plays an important role in the intra- and post-operative periods. Post-traumatic osteoarthritis (PTO) is a particular type of osteoarthritis (OA) that occurs secondary to a traumatic injury. In the present study, we investigated the effects of RFT both in vivo and in vitro.MethodsIn vivo, 50 Sprague Dawley (SD) rats (7 weeks old) were randomly divided into five groups. Four groups of rats received RFT (0.2, 0.5, and 1 µg) or vehicle (PTO group), while the remaining group served as the control. A PTO model in rats was established using the Hulth method. The cartilage damage, articular cartilage formation, and the degradation of cartilage matrix were evaluated. The effects of RFT on cell proliferation, apoptosis, and nuclear factor (NF)-κB phosphorylation were also examined.ResultsThe results indicated that RFT improved cartilage damage, enhanced articular cartilage formation, and inhibited the degradation of cartilage matrix in PTO model rats. Compared with the control group, the protein levels of Osterix (OSX), Collagen type I alpha 1 (COL1A1), and osteocalcin (OC) were down-regulated in PTO model rats. RFT also inhibited the interleukin-1β (IL-1β)-induced apoptosis of chondrocytes in vitro. Furthermore, the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/NF-κB pathway was inhibited both in vitro and in vitro.ConclusionsRFT has significant potential as a therapeutic intervention to ameliorate PTO and provides a foundation for further clinical studies.