Baicalin, Amoxicillin, and Probenecid Provide Protection in Mice Against Challenge.

() causes Glässer's disease and systemic inflammatory responses in the host. The currently available therapies have limited efficacy and fail to achieve a balance between anti-inflammatory and antibacterial effects. In this study, we investigated the effects of baicalin, amoxicillin, and probenecid on blood biochemical parameters, routine blood indicators, survival rate, bacterial burden, and pathological tissue damage in -challenged mice. Treatment with baicalin, amoxicillin, and probenecid significantly modified the blood biochemical parameters and routine blood test indicators, increased the survival rate, attenuated the bacterial burden, and alleviated pathological tissue damage in -challenged mice. Treatment with baicalin, amoxicillin, and probenecid also increased the number of CD3, CD3CD4, and CD3CD8 T cells as measured by flow cytometry, and restored the intensity of the CD3, CD4, and CD8 protein expression in the blood vessels of -challenged mice by immunohistochemistry. These compounds reduced interleukin 1β (IL-1β), IL-18, tumor necrosis factor alpha (TNF-α), and high mobility group box 1 protein (HMGB1) expression in the spleen of -challenged mice. Furthermore, baicalin, amoxicillin, and probenecid inhibited activation of the family pyrin domain containing 3 (NLRP3) inflammasome and apoptosis in the spleen of -challenged mice. This study showed the important roles of baicalin, amoxicillin, and probenecid in the modulation of the inflammatory response of Glässer's disease. The findings might provide new strategies for combination therapy using antibiotics and anti-inflammatory drugs to control infection.