Mycoplasma gallisepticum (MG) infection produces a profound inflammatory response in the respiratory tract and evade birds' immune recognition to establish a chronic infection. Previous reports documented that the flavonoid baicalin possess potent anti-inflammatory, and antioxidant activities. However, whether baicalin prevent immune dysfunction is largely unknown. In the present study, the preventive effects of baicalin were determined on oxidative stress generation and apoptosis in the spleen of chickens infected with MG. Histopathological examination showed abnormal morphological changes including cell hyperplasia, lymphocytes depletion, and the red and white pulp of spleen were not clearly visible in the model group. Oxidative stress-related parameters were significantly (P < 0.05) increased in the model group. However, baicalin treatment significantly (P < 0.05) ameliorated oxidative stress and partially alleviated the abnormal morphological changes in the chicken spleen compared to model group. Terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling assay results, mRNA, and protein expression levels of mitochondrial apoptosis-related genes showed that baicalin significantly attenuated apoptosis. Moreover, baicalin restored the mRNA expression of mitochondrial dynamics-related genes and maintain the balance between mitochondrial inner and outer membranes. Intriguingly, the protective effects of baicalin were associated with the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2)/Heme oxygenase-1 (HO-1) pathway and suppression of nuclear factor-kappa B (NF-κB) pathway in the spleen of chicken. In summary, these findings indicated that baicalin promoted mitochondrial dynamics imbalance and effectively prevents oxidative stress and apoptosis in the splenocytes of chickens infected with MG.

中文翻译：

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黄芩苷通过在鸡毒支原体感染期间通过相反的调节 NF-κB 和 Nrf2/HO-1 信号通路恢复鸡脾中的线粒体动力学来改善氧化应激和细胞凋亡。

鸡毒支原体 (MG) 感染会在呼吸道产生严重的炎症反应，并逃避鸟类的免疫识别，从而建立慢性感染。以前的报告记录了黄酮类黄芩苷具有有效的抗炎和抗氧化活性。然而，黄芩苷是否能预防免疫功能障碍在很大程度上是未知的。在本研究中，确定了黄芩苷对感染 MG 的鸡脾脏中氧化应激的产生和细胞凋亡的预防作用。组织病理学检查可见模型组细胞增生、淋巴细胞减少、脾脏红白髓未见明显形态学改变。模型组氧化应激相关参数显着升高（P < 0.05）。然而，与模型组相比，黄芩苷处理显着（P < 0.05）改善了氧化应激并部分缓解了鸡脾脏的异常形态变化。末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记测定结果、线粒体凋亡相关基因的 mRNA 和蛋白表达水平显示黄芩苷显着减弱细胞凋亡。此外，黄芩苷恢复了线粒体动力学相关基因的 mRNA 表达，维持了线粒体内外膜之间的平衡。有趣的是，黄芩苷的保护作用与核因子红细胞2相关因子2（Nrf2）/血红素加氧酶1（HO-1）通路的上调和核因子-κB（NF-κB）通路的抑制有关。鸡的脾脏。总之，