Baicalin Attenuates Mycoplasma gallisepticum-Induced Inflammation via Inhibition of the TLR2-NF-κB Pathway in Chicken and DF-1 Cells.

Previous reports demonstrated that baicalin possesses potential anti-inflammatory properties. The present study was conducted to determine the effects of baicalin against inflammatory responses in chicken and DF-1 cells infected with Mycoplasma gallisepticum (MG).

An MG infection model was developed in chickens to study the anti-inflammatory mechanism of baicalin. Baicalin was mixed in water at a dose of 450 mg/kg per day, and the treatment is continued for 7 consecutive days. Samples were taken at 1, 4, and 7 days post treatment.

By using transmission electron microscopy, ultrastructure of lung and tracheal cells has been examined. It can be seen that the cilia cells in the MG-infected group have pyknosis, degeneration, and necrosis. In the lung tissues, alveolar type-I epithelial cells were severely damaged. In the baicalin-treated group, cilia were swollen, mushroom-shaped edema bubbles formed on the apex, and fused together. Alveolar type I epithelial cells injury was significantly reduced. Compared to MG-infection group, the levels of proinflammatory cytokines IL-1β and TNF-α were significantly decreased (P < 0.01). The corresponding proteins TLR2 and P-p65 decreased in the baicalin-treated group after 1 (p > 0.05), 4 (p < 0.05), and 7 days (p < 0.05), respectively.

The results showed that baicalin can interfere with inflammatory injury by suppressing the release of inflammatory cytokines IL-1β and TNF-α during MG infection both in vivo and in vitro. Meanwhile, baicalin suppressed TLR2-NFκB signaling pathway by inhibiting the phosphorylation of p65 and IκB, thereby affecting the expression of inflammatory factors. The results suggested that baicalin acts as a potential anti-inflammatory agent against MG infection in chicken and DF-1 cells.