ALI is a grave medical ailment that manifests as abrupt inflammation of the lungs and diminished oxygen levels. It poses a considerable challenge to the medical fraternity, with elevated rates of morbidity and mortality. Our research endeavors to investigate the potential of hibifolin, a flavonoid glucuronide, imbued with potent antioxidant properties, and its molecular mechanism to combat LPS‐induced ALI in mice. The study utilized ICR mice to create an ALI model induced by LPS. Prior to LPS administration, hibifolin was given at 10, 30, or 50 mg/kg, or dexamethasone was given at 1 mg/kg to assess its preventative impact. Changes in lung tissue, pulmonary edema, and lipid peroxidation were analyzed using H&E stain assay, lung wet/dry ratio assay, and MDA formation assay, respectively. Activity assay kits were used to measure MPO activity and antioxidative enzymes (SOD, CAT, GPx) activity in the lungs. Western blot assay was used to determine the phosphorylation of Nrf‐2 and AMPK2 in the lungs. Hibifolin demonstrated a concentration‐dependent improvement in LPS‐induced histopathologic pulmonary changes. This treatment notably mitigated pulmonary edema, lipid peroxidation, and MPO activity in ALI mice. Additionally, hibifolin successfully restored antioxidative enzyme activity in the lungs of ALI mice. Moreover, hibifolin effectively promoted Nrf‐2 phosphorylation and reinstated AMPK2 phosphorylation in the lungs of ALI mice. The results indicate that hibifolin could effectively alleviate the pathophysiological impact of LPS‐induced ALI. This is likely due to its antioxidative properties, which help to restore antioxidative enzyme activity and activate the AMPK2/Nrf2 pathway. These findings are valuable in terms of enhancing our knowledge of ALI treatment and pave the way for further investigation into hibifolin as a potential therapeutic option for lung injuries.

中文翻译：

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Hibifolin 通过抗氧化酶和 AMPK2/Nrf-2 通路保护 LPS 诱导的急性肺损伤中的促炎反应和氧化应激

ALI 是一种严重的医学疾病，表现为肺部突然发炎和氧气水平降低。它给医学界带来了相当大的挑战，发病率和死亡率很高。我们的研究致力于研究 hibifolin（一种黄酮类葡萄糖醛酸苷，具有有效的抗氧化特性）的潜力，及其对抗 LPS 诱导的小鼠 ALI 的分子机制。该研究利用 ICR 小鼠创建了 LPS 诱导的 ALI 模型。在LPS给药之前，给予10、30或50 mg/kg的hibifolin，或以1 mg/kg的剂量给予地塞米松，以评估其预防作用。分别使用H&E染色测定、肺湿/干比测定和MDA形成测定来分析肺组织、肺水肿和脂质过氧化的变化。使用活性测定试剂盒测量肺部 MPO 活性和抗氧化酶（SOD、CAT、GPx）活性。 Western blot检测用于测定肺中Nrf-2和AMPK2的磷酸化。 Hibifolin 对 LPS 诱导的肺部组织病理学变化具有浓度依赖性改善作用。这种治疗显着减轻了 ALI 小鼠的肺水肿、脂质过氧化和 MPO 活性。此外，hibifolin 成功恢复了 ALI 小鼠肺部的抗氧化酶活性。此外，hibifolin 有效促进 ALI 小鼠肺部的 Nrf-2 磷酸化并恢复 AMPK2 磷酸化。结果表明，hibifolin 可以有效减轻 LPS 诱导的 ALI 的病理生理影响。这可能是由于其抗氧化特性，有助于恢复抗氧化酶活性并激活 AMPK2/Nrf2 通路。这些发现对于增强我们对 ALI 治疗的了解非常有价值，并为进一步研究 hibifolin 作为肺损伤的潜在治疗选择铺平了道路。