Wu Yumiao, Wang Qinqin, Zhu Wanqing, Wang Danyi, Yong Yayun, Li Weiwei, Sun Jichao
Guangxi University of Chinese Medicine, Nanning, 530200, China.
Jiangxi University of Chinese Medicine, Nanchang, 330004, China.
Sci Rep. 2025 Mar 26;15(1):10383. doi: 10.1038/s41598-025-95280-8.
Allergic asthma is an inflammatory condition characterized by the release of pro-inflammatory cytokines and the expansion of mucus-producing cells. This research aimed to evaluate the impact of Kaempferol 3-O-gentiobioside (K3G), extracted from Sauropus spatulifolius Beille leaves, on inflammatory cytokine secretion and mucus overproduction in IL-13-stimulated airway epithelial cells (16HBE cells) and ovalbumin (OVA)-induced allergic asthma mouse models. Studies have found that K3G significantly reduces the release of pro-inflammatory cytokines (IgE, TNF-α, histamine, IL-1β, IL-6, and IL-8) induced by IL-13. It also mitigating the expression of the mucin5AC (MUC5AC). Additionally, K3G also downregulated the expression of NLRP3, TLR4, p-IκBα, and p-P65 proteins. In an OVA-induced mouse asthma model, K3G treatment reduced the secretion of pro-inflammatory cytokines, and inhibited the increase in mucus-secreting cells in a dose-dependent manner. Furthermore, exposure to IL-13 and OVA increased the expression of NOTCH signaling receptors in both 16HBE cells and lung tissues of the mice. K3G treatment effectively targeted NOTCH1 and inhibits activation of the NOTCH pathway. In conclusion, K3G alleviates asthma-related airway alterations by suppressing inflammatory cytokines and excessive mucus secretion via the NOTCH signaling pathway. These results indicate the therapeutic promise of K3G in treating allergic asthma.
过敏性哮喘是一种炎症性疾病，其特征在于促炎细胞因子的释放和产生黏液的细胞的扩增。本研究旨在评估从白饭树叶中提取的山奈酚3-O-龙胆二糖苷（K3G）对白细胞介素-13（IL-13）刺激的气道上皮细胞（16HBE细胞）和卵清蛋白（OVA）诱导的过敏性哮喘小鼠模型中炎性细胞因子分泌和黏液过度产生的影响。研究发现，K3G显著降低IL-13诱导的促炎细胞因子（IgE、TNF-α、组胺、IL-1β、IL-6和IL-8）的释放。它还减轻了黏蛋白5AC（MUC5AC）的表达。此外，K3G还下调了NLRP3、TLR4、p-IκBα和p-P65蛋白的表达。在OVA诱导的小鼠哮喘模型中，K3G治疗降低了促炎细胞因子的分泌，并以剂量依赖性方式抑制了黏液分泌细胞的增加。此外，暴露于IL-13和OVA会增加16HBE细胞和小鼠肺组织中NOTCH信号受体的表达。K3G治疗有效地靶向NOTCH1并抑制NOTCH途径的激活。总之，K3G通过NOTCH信号通路抑制炎性细胞因子和过多黏液分泌，从而减轻哮喘相关的气道改变。这些结果表明K3G在治疗过敏性哮喘方面具有治疗前景。
