Baicalin Inhibits Inflammatory Responses to Interleukin-1β Stimulation in Human Chondrocytes

A mix of flavonoids comprising baicalin (BA) and catechin showed effective impacts on controlling the progress of knee osteoarthritis (OA). However, little is known about the underlying mechanisms. The influences of BA on the transcriptional levels of a series of proinflammatory genes were measured using real-time reverse transcription and polymerase chain reaction (RT-PCR). The expressions of proteins involved in nuclear factor-kappa B (NF-kappa B) activation were detected by Western blot. The in vitro results were confirmed in a mouse OA model. We found that BA treatment led to remarkable reductions of OA-related proinflammatory gene expressions, including interleukin (IL)-6, tumor necrosis factor (TNF), chemokine (C-X-C motif) ligand 1 (CXCL1), and CXCL10. The transcriptional levels of inducible nitric oxide synthase (iNOS/Nos2), matrix metalloproteinases (MMP)3, and MMP13 were significantly inhibited by BA. We measured the productions of nitrite and prostaglandin E-2 from human chondrocytes and BA was shown to reduce their productions. On the contrary, mRNA levels of aggrecan and collagen-II were enhanced by BA treatment. The inhibitory role of BA on OA may possibly be mediated by NF-kappa B signaling because of comparable decreases of phosphorylated (p)-p65 and p-I kappa B alpha and less p65 translocation in the nucleus after BA treatment. In OA mice model, BA significantly reduced synovitis scores and related gene expressions, including IL-6, TNF, CXCL1, CXCL10, MMP3, MMP13, and Nos2. In conclusion, BA suppresses the inflammatory responses of human chondrocytes to IL-1 beta stimulation, and NF-kappa B signaling may be involved in the mechanisms of BA functions.