Acute lung injury (ALI) is a major cause of sepsis-induced acute respiratory failure. Emodin has been considered to play a protective role for acute lung edema in cecal ligation and puncture (CLP)-induced sepsis model. In this study we aimed to investigate whether emodin could improve CLP-induced lung sepsis via regulating aquaporin (AQP) and tight junction (TJ), inflammatory factors, and pulmonary apoptosis. The results showed that sepsis-induced pulmonary pathological changes were significantly improved after emodin treatment. Emodin was found to upregulate AQP and TJ expression in the CLP model. Meanwhile, inflammatory cytokine release and pulmonary apoptosis was remarkably reduced after emodin treatment in lung sepsis. Our data demonstrated that emodin could suppresse inflammation, restore pulmonary epithelial barrier and reduce mortality in CLP-induced ALI, suggesting the potential therapeutic application of emodin in sepsis.

急性肺损伤（ALI）是脓毒症引起的急性呼吸衰竭的主要原因。大黄素被认为对盲肠结扎穿刺（CLP）诱导的脓毒症模型中的急性肺水肿具有保护作用。在本研究中，我们旨在探讨大黄素是否可以通过调节水通道蛋白（AQP）和紧密连接（TJ）、炎症因子和肺细胞凋亡来改善CLP诱导的肺脓毒症。结果显示，脓毒症引起的肺部病理变化经大黄素治疗后明显改善。发现大黄素在 CLP 模型中上调 AQP 和 TJ 表达。同时，大黄素治疗肺脓毒症后，炎症细胞因子释放和肺细胞凋亡显着减少。我们的数据表明，大黄素可以抑制炎症、恢复肺上皮屏障并降低 CLP 诱导的 ALI 的死亡率，表明大黄素在脓毒症中的潜在治疗应用。