To analyze the role of E3 ubiquitin ligase constitutive photomorphogenetic protein 1(COP-1) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and preliminarily explore its mechanism of action.

All of 48 male C57 mice were randomly divided into 4 groups: COP-1 knockout: COP-1^{+ /-}-PBS (KOPBS group), COP-1^{+ /-}-LPS (KOLPL group); Non-knockout COP-1: WT-PBS (WTPBS group), WT-LPS (WTLPS group), 12 in each group. Among them, the LPS group was given LPS 10 mg/kg intratracheally to model acute lung injury, while the PBS group was treated with an equal volume of PBS for the same time. 24 hours after modeling, lung tissue was taken, HE stained to observe morphological changes in lung tissue, wet/dry weight ratio (W/D) was measured, ELISA was used to measure tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), myeloperoxidase (MPO) activity in lung tissue and bronchoalveolar lavage fluid (BALF).

Morphological observations showed that infiltration of inflammatory cells, congestion, and edema in the KOLPS group lung tissue were more significant compared to the WT-LPS group, KOPBS group lung tissue, and the WTPBS group. Compared to the WTPBS group and KOPBS group, WTLPS group and KOLPS group, the level of inflammatory factors, MPO activity in lung tissue, and lung W/D ratio were significantly increased (P<0.05).

The knockout of E3 ubiquitin ligase COP-1 can aggravate LPS-induced acute lung injury in mice, the therapeutic effect of COP-1 in pneumonia needs further exploration.