Background. Sepsis mortality and morbidity are aggravated by acute lung injury (ALI) or acute respiratory distress syndrome. Published studies have discovered that hyperoside (HYP) has an anti-inflammatory and therapeutic effect in many diseases. However, whether HYP treatment can attenuate sepsis-induced ALI is still obscure. Methods. In this study, a cecal ligation and puncture (CLP)-induced sepsis mouse model was constructed. The mouse lungs were harvested and assessed using proteomics, immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assay for pro-inflammatory cytokines. Human lung microvascular endothelial cells (HLMVECs) were induced with lipopolysaccharide (LPS) for the in vitro model. Results. The results showed that HYP treatment attenuated sepsis-induced ALI through an increased survival rate, decreased inflammatory factor expression, and lung tissue apoptosis. At the same time, HYP pretreatment restored angiogenesis in CLP-induced mouse lung tissues. Proteomics detection showed that Atg13 played a vital role in HYP-mediated protection against sepsis-induced ALI. The in vitro experiment showed HYP treatment attenuated LPS-induced HLMVEC damage by regulating Atg13-mediated autophagy. Inhibiting autophagy or silencing Atg13 reversed the protective effect of HYP against sepsis-induced ALI. Conclusion. Taken together, we conclude that HYP attenuated sepsis-induced ALI by regulating autophagy and inhibiting inflammation.

中文翻译：

---

金丝桃苷通过自噬调节和炎症抑制减轻脓毒症引起的急性肺损伤 (ALI)

背景。急性肺损伤（ALI）或急性呼吸窘迫综合征会加剧脓毒症的死亡率和发病率。已发表的研究发现金丝桃苷（HYP）对多种疾病具有抗炎和治疗作用。然而，HYP 治疗是否可以减轻脓毒症引起的 ALI 仍不清楚。方法。本研究构建了盲肠结扎穿刺（CLP）诱导的脓毒症小鼠模型。收获小鼠肺并使用蛋白质组学、免疫组织化学、免疫荧光和酶联免疫吸附测定来评估促炎细胞因子。用脂多糖（LPS）诱导人肺微血管内皮细胞（HLMVEC）用于体外模型。结果。结果表明，HYP 治疗通过提高存活率、减少炎症因子表达和肺组织凋亡来减轻脓毒症引起的 ALI。同时，HYP 预处理恢复了 CLP 诱导的小鼠肺组织中的血管生成。蛋白质组学检测表明，Atg13 在 HYP 介导的针对脓毒症引起的 ALI 的保护中发挥着至关重要的作用。体外实验表明，HYP 治疗通过调节 Atg13 介导的自噬减轻了 LPS 诱导的 HLMVEC 损伤。抑制自噬或沉默 Atg13 可逆转 HYP 对脓毒症引起的 ALI 的保护作用。结论。综上所述，我们得出结论，HYP 通过调节自噬和抑制炎症来减轻脓毒症诱导的 ALI。