摘 要：为研究淫羊藿苷对哮喘幼鼠的免疫调节作用及相关机制，本研究通过卵清蛋白致敏联合雾化激发建立哮喘模型。将幼鼠随机分为对照组（Con组）、模型组（Mod组）、淫羊藿苷低剂量组（Low-Ica组）、淫羊藿苷高剂量组（High-Ica组）、淫羊藿苷高剂量+Janus激酶2（JAK2）激活剂香豆霉素A1（CA1）组（High-Ica+CA1组），每组12只。肺功能检测仪检测幼鼠气道反应性和增强呼吸间歇（Penh）值，苏木精-伊红（HE）染色观察幼鼠肺组织形态变化，酶联免疫吸附分析检测幼鼠血清中免疫球蛋白E（IgE）、白细胞介素-4（IL-4）、IL-17、干扰素-γ（IFN-γ）水平，流式细胞仪检测幼鼠肺泡灌洗液中嗜酸性粒细胞（EOS）凋亡水平，蛋白免疫印迹（WB）检测幼鼠肺组织中JAK2、信号转导与转录活化因子3（STAT3）、磷酸化STAT3（p-STAT3）的蛋白表达水平。结果显示：与Con组相比，Mod组幼鼠Penh值升高（P<0.05），肺组织损伤程度加重，IgE、IL-4、IL-17水平升高（P<0.05），JAK2、p-STAT3蛋白表达水平升高（P<0.05），IFN-γ水平、EOS凋亡百分比降低（P<0.05）；与Mod组相比，Low-Ica组和High-Ica组幼鼠Penh值降低（P<0.05），肺组织损伤程度减轻，IgE、IL-4、IL-17水平降低（P<0.05），JAK2、p-STAT3蛋白表达水平降低（P<0.05），IFN-γ水平、EOS凋亡百分比升高（P<0.05）；JAK2激活剂能逆转High-Ica组的上述变化。上述研究表明，淫羊藿苷可以改善哮喘幼鼠的肺组织损伤，其机制可能与抑制JAK2/STAT3信号通路、促进EOS凋亡、调节1型辅助性T细胞（Th1）/Th2和Th17免疫失衡有关。
关键词：淫羊藿苷；哮喘；免疫调节；Janus激酶2；信号转导与转录活化因子3
中图分类号：R285.5      文献标志码：A     DOI：10.3969/j.issn.1007-7146.2026.04.010

Abstract: To investigate the immunomodulatory effect of icariin on asthmatic young mice and its related mechanism, an asthma model was established by ovalbumin sensitization combined with aerosol challenge in this study. The young mice were randomly divided into the control group (Con group), model group (Mod group), low-dose icariin group (Low-Ica group), high-dose icariin group (High-Ica group), and high-dose icariin + Janus kinase 2 (JAK2) activator coumermycin A1 (CA1) group (High-Ica+CA1 group), with 12 mice in each group. Airway reactivity and enhanced pause (Penh) value were detected by a pulmonary function detector. Morphological changes in lung tissue were observed by hematoxylin and eosin (HE) staining. Serum levels of immunoglobulin E (IgE), interleukin-4 (IL-4), IL-17, and interferon-γ (IFN-γ) were measured by enzyme-linked immunosorbent assay. The apoptosis level of eosinophil (EOS) in bronchoalveolar lavage fluid was detected by flow cytometry. The protein expression levels of JAK2, signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 (p-STAT3) in lung tissue were detected by Western blot (WB). The results showed that compared with the Con group, the Penh value increased (P<0.05), lung tissue injury was aggravated, and the levels of IgE, IL-4, IL-17, and the protein expression levels of JAK2 and p-STAT3 increased (P<0.05), while the level of IFN-γ and the apoptosis percentage of EOS decreased (P<0.05) in the Mod group; compared with the Mod group, the Penh value decreased (P<0.05), lung tissue injury was alleviated, and the levels of IgE, IL-4, IL-17, and the protein expression levels of JAK2 and p-STAT3 decreased (P<0.05), while the level of IFN-γ and the apoptosis percentage of EOS increased (P<0.05) in the Low-Ica group and High-Ica group; the JAK2 activator was found to reverse the aforementioned changes in the High-Ica group. The study indicates that icariin can alleviate lung tissue injury in asthmatic young mice, and its mechanism may be related to the inhibition of the JAK2/STAT3 signaling pathway, promotion of EOS apoptosis, and regulation of T helper 1 cell (Th1)/Th2 and Th17 immune imbalance.
Keywords: icariin; asthma; immunomodulation; Janus kinase 2; signal transducer and activator of transcription 3
（Acta Laser Biology Sinica, 2026, 35(4): 369-375）