Fu Shulin, Luo Ronghui, Li Jingyang, Fu Yunjian, Dong Qiaoli, Liu Siyu, Sun Yamin, Guo Ling, Hu Jin, Qiu Yinsheng
Wuhan Engineering and Technology Research Center of Animal Disease-Resistant Nutrition, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China.
Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan 430023, China.
Biomolecules. 2025 May 15;15(5):722. doi: 10.3390/biom15050722.
() causes vascular inflammation in piglets, resulting in vascular damage. However, the mechanism causing vascular inflammation remains unclear. Baicalin possesses an anti-inflammatory function. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) has been implicated in immunosuppression. CD163, a scavenger receptor expressed on macrophages that acts as a decoy receptor for TWEAK, plays a crucial role in the regulation of autophagy and inflammation. This research investigated the efficacy of baicalin in reducing immunosuppression elicited by through the regulation of CD163/TWEAK-mediated autophagy. The data demonstrated that altered routine blood indicators and biochemical parameters, increased cytokine production, and induced blood vessel tissue damage. reduced the CD3+ T cell proportion, CD3+CD4+ T cell proportion, and CD3+CD8+ T cell proportion in piglet blood. The proteomic analysis revealed that CD163 was differentially expressed in the blood vessels of challenged piglets. Baicalin was found to regulate CD163/TWEAK axis expression, inhibit Notch/Wnt signaling pathway activation, promote autophagy, and reduce NLRP3/Caspase 1 signaling pathway activation. Baicalin also decreased cytokine production and alleviated pathological tissue damage in the blood vessels of -challenged piglets. Taken together, this study indicates that baicalin alleviates -induced immunosuppression and might promote CD163/TWEAK-mediated autophagy. This finding suggests that baicalin could serve as a potential therapeutic agent to control and related vascular inflammation.
（）导致仔猪血管炎症，进而造成血管损伤。然而，引发血管炎症的机制仍不清楚。黄芩苷具有抗炎功能。肿瘤坏死因子样凋亡弱诱导剂（TWEAK）与免疫抑制有关。CD163是巨噬细胞上表达的一种清道夫受体，作为TWEAK的诱饵受体，在自噬和炎症调节中起关键作用。本研究通过调节CD163/TWEAK介导的自噬，探讨黄芩苷在减轻（）引起的免疫抑制方面的功效。数据表明，（）改变了常规血液指标和生化参数，增加了细胞因子的产生，并导致血管组织损伤。（）降低了仔猪血液中CD3 + T细胞比例、CD3 + CD4 + T细胞比例和CD3 + CD8 + T细胞比例。蛋白质组学分析显示，CD163在受攻击仔猪的血管中差异表达。发现黄芩苷可调节CD163/TWEAK轴表达，抑制Notch/Wnt信号通路激活，促进自噬，并减少NLRP3/Caspase 1信号通路激活。黄芩苷还减少了细胞因子的产生，并减轻了受（）攻击仔猪血管中的病理组织损伤。综上所述，本研究表明黄芩苷可减轻（）诱导的免疫抑制，并可能促进CD163/TWEAK介导的自噬。这一发现表明，黄芩苷可能作为一种潜在的治疗药物来控制（）及相关血管炎症。
