Li Jingyang, Luo Ronghui, Fu Yunjian, Liu Siyu, Dong Qiaoli, Sun Yamin, Tian Xinyue, Zhu Yi, Wang Peiyi, Guo Ling, Lu Qirong, Ye Chun, Fu Shulin, Qiu Yinsheng
Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan 430023, China.
Biomolecules. 2025 Mar 31;15(4):507. doi: 10.3390/biom15040507.
() 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.
（）可导致宿主发生格拉斯病和全身炎症反应。目前可用的治疗方法疗效有限，且无法在抗炎和抗菌作用之间取得平衡。在本研究中，我们调查了黄芩苷、阿莫西林和丙磺舒对受（此处原文缺失某种病菌或病原体相关信息）攻击的小鼠血液生化参数、血常规指标、存活率、细菌载量和病理组织损伤的影响。黄芩苷、阿莫西林和丙磺舒治疗显著改变了受攻击小鼠的血液生化参数和血常规检测指标，提高了存活率，减轻了细菌载量，并减轻了病理组织损伤。通过流式细胞术检测，黄芩苷、阿莫西林和丙磺舒治疗还增加了CD3、CD3CD4和CD3CD8 T细胞的数量，并通过免疫组织化学恢复了受攻击小鼠血管中CD3、CD4和CD8蛋白表达的强度。这些化合物降低了受攻击小鼠脾脏中白细胞介素1β（IL-1β）、IL-18、肿瘤坏死因子α（TNF-α）和高迁移率族蛋白B1（HMGB1）的表达。此外，黄芩苷、阿莫西林和丙磺舒抑制了受攻击小鼠脾脏中含吡咯结构域蛋白3（NLRP3）炎性小体的激活和细胞凋亡。本研究表明了黄芩苷、阿莫西林和丙磺舒在调节格拉斯病炎症反应中的重要作用。这些发现可能为使用抗生素和抗炎药物联合治疗以控制（此处原文缺失相关病菌或病原体相关信息）感染提供新策略。
