Here, we aimed to investigate the role of Xanthatin in asthma and its underlying mechanism. BALB/c mice were treated with ovalbumin (OVA) to establis a mouse model of asthma. Our results showed that OVA injection significantly increased inflammatory cell infiltration and goblet cell hyperplasia in lung issues, while Xanthatin treatment and STAT3 inhibitor C188-9 administration relieved these symptoms. Moreover, OVA-induced OVA-specific immunoglobulin E level in serum and the number of total cell, macrophages, lymphocytes, neutrophils, and eosinophils in bronchoalveolar lavage fluid (BALF) were markedly reduced by Xanthatin treatment and signal transducer and activator of transcription 3 (STAT3) inhibition. Additionally, Xanthatin treatment and STAT3 inhibition was also significantly decreased the levels of inflammatory cytokines in BALF in asthmatic mice. We further demonstrated that the STAT3/nuclear factor-kappaB (NF-κB) pathway was blocked by Xanthatin in asthmatic mice. Overall, we conclude that Xanthatin attenuates airway inflammation in asthmatic mice through blocking the STAT3/NFκB signaling pathway, indicating the potential of Xanthatin as a useful therapeutic agent for asthma.

在这里，我们旨在研究黄原素在哮喘中的作用及其潜在机制。BALB/c 小鼠用卵清蛋白 (OVA) 处理以建立哮喘小鼠模型。我们的结果表明，OVA 注射显着增加了肺部疾病中的炎性细胞浸润和杯状细胞增生，而黄原素治疗和 STAT3 抑制剂 C188-9 给药可缓解这些症状。此外，OVA 诱导的血清中 OVA 特异性免疫球蛋白 E 水平以及支气管肺泡灌洗液 (BALF) 中的总细胞、巨噬细胞、淋巴细胞、中性粒细胞和嗜酸性粒细胞的数量通过黄原素处理和信号转导和转录激活剂 3 显着降低。 STAT3) 抑制。此外，黄原素处理和 STAT3 抑制也显着降低了哮喘小鼠 BALF 中炎性细胞因子的水平。我们进一步证明 STAT3/核因子-κB (NF-κB) 通路在哮喘小鼠中被黄原素阻断。总的来说，我们得出结论，黄原素通过阻断 STAT3/NFκB 信号通路减轻哮喘小鼠的气道炎症，表明黄原素作为哮喘治疗剂的潜力。