Molecular immunology · 2025
Dexmedetomidine improve lung inflammation by regulating autophagy and apoptosis of CD4+ T cell via AMPK/mTOR signaling.
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Luo Renjie, Wang Zhao, Xu Fang, Xie Ke
Аннотация
OBJECTIVES: To investigate the protective effect and potential mechanism of dexmedetomidine (Dex) in acute lung injury (ALI).
MATERIALS AND METHODS: C57BL/6 mice and EL-4 cells were used for in vivo and in vitro studies, respectively. Cecal ligation and puncture (CLP) method was used to prepare an acute lung injury model. After dexmedetomidine intervention, tissue and cell samples were collected to evaluate and measure the severity of lung damage, the proportion of Treg cells, the expression of autophagy-related protein levels and AMPK/mTOR pathways.
RESULTS: Dex reduced lung damage, and IL-17a, MPO positive cells in the lung, decreased the levels of pro-inflammatory cytokines, and restrain autophagy and apoptosis via the activation of the AMPK/mTOR pathway and increase of the proportion of Tregs.
CONCLUSIONS: Dex can inhibit the levels of autophagy and apoptosis, increase the proportion of Treg cells, and reduce CLP induced acute lung injury through regulating AKMP/MTOR pathway.
MATERIALS AND METHODS: C57BL/6 mice and EL-4 cells were used for in vivo and in vitro studies, respectively. Cecal ligation and puncture (CLP) method was used to prepare an acute lung injury model. After dexmedetomidine intervention, tissue and cell samples were collected to evaluate and measure the severity of lung damage, the proportion of Treg cells, the expression of autophagy-related protein levels and AMPK/mTOR pathways.
RESULTS: Dex reduced lung damage, and IL-17a, MPO positive cells in the lung, decreased the levels of pro-inflammatory cytokines, and restrain autophagy and apoptosis via the activation of the AMPK/mTOR pathway and increase of the proportion of Tregs.
CONCLUSIONS: Dex can inhibit the levels of autophagy and apoptosis, increase the proportion of Treg cells, and reduce CLP induced acute lung injury through regulating AKMP/MTOR pathway.