Abstract—Acute lung injury (ALI) is characterized by a series of inflammatory reactions and serves as the main cause of mortality in intensive care unit patients. Although great progress has been made in understanding the pathophysiology of ALI, there are no effective treatments in clinic. Recently, we have synthesized a selenium-containing compound, which possesses obvious anti-inflammatory activity. The aim of the present study is to evaluate the protective effects of the selenium-containing compound 34# in LPS-induced ALI in mice as well as its underlying mechanism. Compound 34# was found to inhibit LPS-induced macrophage inflammatory cytokine release. These effects were observed to be produced via suppression of the MAPK/AP-1 pathway. Compound 34# was also noted to attenuate the LPS-induced lung inflammation in mice with ALI. The corresponding results suggested that compound 34# possesses remarkable protective effects on LPS-induced ALI. Furthermore, the MAPK/AP-1 pathway may prove to be the underlying mechanism. Accordingly, compound 34# may serve as a potential candidate for the prevention of ALI.

摘要：急性肺损伤（ALI）以一系列炎症反应为特征，是重症监护病房患者死亡的主要原因。尽管在了解 ALI 的病理生理学方面取得了很大进展，但临床上尚无有效的治疗方法。最近，我们合成了一种具有明显抗炎活性的含硒化合物。本研究旨在评估含硒化合物34#对LPS诱导的小鼠ALI的保护作用及其潜在机制。发现化合物34#可抑制 LPS 诱导的巨噬细胞炎性细胞因子释放。观察到这些效果是通过MAPK/AP-1 通路的抑制。还注意到化合物34#可减轻 ALI 小鼠中 LPS 诱导的肺部炎症。相应的结果表明化合物34#对LPS诱导的ALI具有显着的保护作用。此外，MAPK/AP-1 通路可能被证明是潜在的机制。因此，化合物34#可作为预防 ALI 的潜在候选者。