Xu Ying, Xu Lili, Jian Xuli, Wang Qianqian, Li Zhen, Ge Hongzhou
Department of Otolaryngology, Qingdao Traditional Chinese Medicine Hospital (Qingdao Hiser Hospital), Qingdao Hiser Hospital Affiliated of Qingdao University, Qingdao, 266033, Shandong, People's Republic of China.
Intravenous Infusion Dispensing Center, Qingdao Traditional Chinese Medicine Hospital (Qingdao Hiser Hospital), Qingdao Hiser Hospital Affiliated of Qingdao University, Qingdao, 266033, Shandong, People's Republic of China.
Immunol Res. 2025 Jan 14;73(1):32. doi: 10.1007/s12026-024-09590-6.
Baicalein, one of the major active flavonoids found in Scutellaria baicalensis, has been revealed to exhibit potent anti-inflammatory properties in allergic airway inflammation. This study aimed to explore the role of baicalein and its relevant mechanism in the treatment of allergic rhinitis (AR). The bioinformatics tools were used to predict the targets of baicalein and AR-related genes. AR mice were induced by ovalbumin (OVA) and treated with lentivirus-encapsulated knockdown of nuclear receptor subfamily 4 group A member 1 (NR4A1) or protein arginine N-methyltransferase 1 (PRMT1) plasmids and baicalein. IL-4/IL-13-induced human nasal mucosal epithelial cells (HNEpC) were transfected with knockdown of NR4A1 or PRMT1 plasmids and baicalein treatment. Baicalein alleviated AR-like symptoms and reduced the levels of immunoglobulin E, histamine, and LTC4 in serum and IL-4, IL-25, and IL-33 concentrations in nasal lavage fluids of mice induced with OVA by increasing NR4A1 expression. NR4A1 blocked the NFκB/p65 pathway by mediating transcriptional repression of PRMT1. Knockdown of PRMT1 overturned the effects of NR4A1 knockdown on IL-4/IL-13-induced HNEpC and OVA-induced mice. Collectively, these findings provide evidence that baicalein activation of NR4A1 mediates transcriptional repression of PRMT1 and relieves AR in mice by blocking the NFκB/p65 pathway.
黄芩素是黄芩中发现的主要活性黄酮类化合物之一，已被证明在过敏性气道炎症中具有强大的抗炎特性。本研究旨在探讨黄芩素在过敏性鼻炎（AR）治疗中的作用及其相关机制。利用生物信息学工具预测黄芩素的靶点和AR相关基因。用卵清蛋白（OVA）诱导AR小鼠，并用慢病毒包裹的核受体亚家族4 A组成员1（NR4A1）或蛋白质精氨酸N-甲基转移酶1（PRMT1）质粒及黄芩素进行处理。用NR4A1或PRMT1质粒敲低并进行黄芩素处理转染白细胞介素-4/白细胞介素-13诱导的人鼻黏膜上皮细胞（HNEpC）。黄芩素通过增加NR4A1表达减轻AR样症状，并降低OVA诱导的小鼠血清中免疫球蛋白E、组胺和白三烯C4的水平以及鼻灌洗液中白细胞介素-4、白细胞介素-25和白细胞介素-33的浓度。NR4A1通过介导PRMT1的转录抑制来阻断NFκB/p65通路。敲低PRMT1可逆转NR4A1敲低对白细胞介素-4/白细胞介素-13诱导的HNEpC和OVA诱导的小鼠的影响。总的来说，这些发现提供了证据，表明黄芩素激活NR4A1介导PRMT1的转录抑制，并通过阻断NFκB/p65通路减轻小鼠的AR。
