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-1β) were evaluated by Western blot, immunofluorescence, flow cytometry and enzyme-linked immunosorbent assay. The mechanism of AF on the IL-1β 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-1β. Mechanistically, the receptor activator of the NF-kappaB ligand (RANKL), an activator for the NF-κB signalling pathway, partially reversed the alleviating effect of AF on IL-1β-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-κB pathway.