Acute lung injury (ALI) is a difficult condition to manage, especially when it is complicated by bacterial sepsis. Hibifolin, a flavonoid glycoside, has anti‐inflammatory properties that make it a potential treatment for ALI. However, more research is needed to determine its effectiveness in LPS‐induced ALI. In this study, male ICR mice were treated with hibifolin before LPS‐induced ALI. Protein content and neutrophil count in bronchoalveolar lavage (BAL) fluid were measured by BCA assay and Giemsa staining method, respectively. The levels of proinflammatory cytokines and adhesive molecules were detected by ELISA assay. The expression of NFκB p65 phosphorylation, IκB degradation, and Akt phosphorylation was assessed by western blot assay. Hibifolin pre‐treatment significantly reduced pulmonary vascular barrier dysfunction and neutrophil infiltration into the BAL fluid in LPS‐induced ALI mice. In addition, LPS‐induced expression of proinflammatory cytokines (IL‐1β, IL‐6, TNF‐α) and adhesive molecules (ICAM‐1, VCAM‐1) within the BAL fluid were markedly reduced by hibifolin in LPS‐induced ALI mice. More, hibifolin inhibited LPS‐induced phosphorylation of NFκB p65, degradation of IκB, and phosphorylation of Akt in lungs with ALI mice. In conclusion, hibifolin shows promise in improving the pathophysiological features and proinflammatory responses of LPS‐induced ALI in mice through the NFκB pathway and its upstream factor, Akt phosphorylation.

中文翻译：

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Hibifolin 通过 Akt 磷酸化和 NFκB 通路对脂多糖诱导的急性肺损伤的保护作用


急性肺损伤（ALI）是一种很难治疗的疾病，尤其是当它并发细菌性败血症时。 Hibifolin 是一种黄酮苷，具有抗炎特性，使其成为 ALI 的潜在治疗方法。然而，需要更多的研究来确定其在 LPS 诱导的 ALI 中的有效性。在这项研究中，雄性 ICR 小鼠在 LPS 诱导的 ALI 之前接受了 hibifolin 治疗。分别采用BCA法和吉姆萨染色法测定支气管肺泡灌洗（BAL）液中的蛋白质含量和中性粒细胞计数。采用ELISA法检测促炎细胞因子和粘附分子的水平。通过蛋白质印迹法评估 NFκB p65 磷酸化、IκB 降解和 Akt 磷酸化的表达。 Hibifolin 预处理可显着减少 LPS 诱导的 ALI 小鼠的肺血管屏障功能障碍和 BAL 液中的中性粒细胞浸润。此外，在 LPS 诱导的 ALI 小鼠中，抑制素可显着降低 BAL 液中 LPS 诱导的促炎细胞因子（IL-1β、IL-6、TNF-α）和粘附分子（ICAM-1、VCAM-1）的表达。 。此外，在 ALI 小鼠肺中，hibifolin 可抑制 LPS 诱导的 NFκB p65 磷酸化、IκB 降解和 Akt 磷酸化。总之，hibifolin 通过 NFκB 通路及其上游因子 Akt 磷酸化有望改善 LPS 诱导的小鼠 ALI 的病理生理学特征和促炎症反应。