Albiflorin alleviation efficacy in osteoarthritis injury using in-vivo and in-vitro models

Objectives Osteoarthritis seriously affects the daily life of people. Albiflorin (AF) has anti-inflammatory and antioxidant functions in various human diseases. This study aimed to clarify the function and mechanism of AF in osteoarthritis. Methods The functions of AF on rat chondrocyte proliferation and apoptosis, inflammatory response, oxidative stress and extracellular matrix (ECM) degradation in rat chondrocytes induced by interleukin-1beta (IL-1 beta) were evaluated by Western blot, immunofluorescence, flow cytometry and enzyme-linked immunosorbent assay. The mechanism of AF on the IL-1 beta induced rat chondrocyte injury was investigated by multiple experiments in vitro. Meanwhile, the AF function in vivo was assessed using haematoxylin-eosin staining, Alcian blue, Safranin O/Fast green staining, immunohistochemical analysis and TUNEL assay. Key findings Functionally, AF accelerated the rat chondrocyte proliferation and repressed cell apoptosis. Meanwhile, AF reduced the inflammatory response, oxidative stress and ECM degradation in rat chondrocytes caused by IL-1 beta. Mechanistically, the receptor activator of the NF-kappaB ligand (RANKL), an activator for the NF-.B signalling pathway, partially reversed the alleviating effect of AF on IL-1 beta-induced chondrocyte injury. Furthermore, the in-vitro results confirmed that AF exerted protective properties against osteoarthritis injury in vivo. Conclusion Albiflorin relieved osteoarthritis injury in rats by inactivating the NF-.B pathway.