BACKGROUND Cold stress, which may lead to local and systemic injury, is reported to be related to the immune system, especially the complement system. At present, the lack of effective treatment is a critical issue. Amentoflavone (AF), which can inhibit cold stress-induced inflammation in lung by multiple mechanisms, is the main therapeutic ingredient in plants of the genus Selaginella. RESULTS In the current study, we found that cold could induce lung inflammation related to the complement system and its downstream pathways. AF treatment significantly inhibited lung inflammation from cold exposure. We presented evidence that AF can bind to complement component 3 (C3) to regulate inflammation-related pathways involving Lck/Yes novel tyrosine kinase (Lyn), protein kinase B (Akt), nuclear factor-κB (NF-κB) and immune factors. Moreover, 30 mg/kg of AF caused significantly greater improvement than 15 mg/kg in reducing the level of C3 in lung tissue. CONCLUSIONS AF can protect lung tissue from cold exposure. The protective effect may be achieved by inhibition of C3 and negative regulation of the B cell receptor (BCR)/NF-κB signaling pathways and high mobility group box 1 (HMGB1), which ultimately ameliorates the inflammatory response.

中文翻译：

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甲黄酮通过抑制C3 / BCR /NF-κB途径改善了冷应激诱导的肺部炎症。

背景技术据报道，可能导致局部和全身性损伤的冷应激与免疫系统特别是补体系统有关。目前，缺乏有效的治疗是一个关键问题。可以通过多种机制抑制冷应激诱导的肺部炎症的黄酮（AF）是卷柏属植物中的主要治疗成分。结果在当前研究中，我们发现感冒可以诱发与补体系统及其下游途径有关的肺部炎症。AF治疗可显着抑制冷暴露引起的肺部炎症。我们提供的证据表明，房颤可以结合补体成分3（C3）来调节涉及Lck /是的新型酪氨酸激酶（Lyn），蛋白激酶B（Akt），核因子-κB（NF-κB）和免疫因子的炎症相关途径。而且，与降低15 mg / kg的肺组织中C3水平相比，30 mg / kg的AF引起的改善明显大于15 mg / kg。结论AF可保护肺组织免受冷暴露。保护作用可通过抑制C3以及负调节B细胞受体（BCR）/NF-κB信号通路和高迁移率族1（HMGB1）来实现，从而最终改善炎症反应。