The anti-inflammatory and autophagy-induced effects of baicalin in ankylosing spondylitis hip ligament fibroblasts

Ankylosing spondylitis (AS) is characterised by chronic inflammation that affects the axial skeleton and peripheral joints. Hip involvement occurs in nearly one-third of patients with AS and is considered a poor prognostic sign. Inflammation is also associated with AS progression. Baicalin is a bioactive flavonoid possessing both anti-inflammatory and antioxidant properties, although its activity in AS has not been investigated. The aim of our study was to evaluate the effects of baicalin on AS pathogenesis-related cells and investigate the potential mechanisms. Fibroblasts were isolated from AS patients who met the modified New York criteria and underwent total hip arthroplasty. Flow cytometry was used to identify the fibroblasts. Cytokine expression was evaluated by enzyme-linked immunosorbent assay and real-time polymerase chain reaction, and protein expression was detected using western blotting. Immunofluorescence and transmission electron microscopy were used to assess autophagy. Baicalin effectively inhibited the expression of inflammatory cytokines upregulated by lipopolysaccharides in AS hip ligament fibroblasts. Moreover, the lipopolysaccharide-triggered nuclear factor kappa-B (NF-κB) and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathways were also suppressed by baicalin. Furthermore, baicalin markedly induced autophagy, which suppressed inflammation dose-dependently. The anti-inflammatory activity of baicalin was mediated by the repression of NF-κB and JAK/STAT signalling pathways. Furthermore, the induction of autophagy may contribute to inhibiting inflammation.