Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study

Lung ischemia-reperfusion (I/R) injury represents an inevitable complication in lung transplantation, characterized by the excessive production of oxygen free radicals and toxic substances. Dexmedetomidine (DEX), a widely used anesthetic agent, has been shown to significantly elevate glutathione (GSH) levels, thereby conferring protection against copper influx. This study investigates the protective mechanisms of DEX in lung I/R injury, with a particular focus on cuproptosis. Utilizing a rat I/R model established by clamping the left hilum of lung for 90 min followed by 120 min of reperfusion, we examined the effects of DEX on lung injury scores, GSH content, and the expression of key proteins involved in cuproptosis. In conclusion, cuproptosis is implicated in pulmonary I/R injury, and the protective effect of DEX against lung I/R injury is partly mediated by inhibition of cuproptosis.

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Journal
Frontiers in Pharmacology
Published
2025-04-01
DOI
https://doi.org/10.3389/fphar.2025.1562535
Primary Topic
Nitric Oxide and Endothelin Effects
Type
article
Field-Weighted Citation Impact
0.00

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article

Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study

Hanqun Liu, Zhe Wu, Wenjie Jiao, Sheng Chen et al.
Frontiers in Pharmacology
Nitric Oxide and Endothelin Effects
article

Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study

Hanqun Liu, Zhe Wu, Wenjie Jiao, Sheng Chen, Wenxing Du, Zicheng Wang, Tong Qiu
article en

Abstract

Lung ischemia-reperfusion (I/R) injury represents an inevitable complication in lung transplantation, characterized by the excessive production of oxygen free radicals and toxic substances. Dexmedetomidine (DEX), a widely used anesthetic agent, has been shown to significantly elevate glutathione (GSH) levels, thereby conferring protection against copper influx. This study investigates the protective mechanisms of DEX in lung I/R injury, with a particular focus on cuproptosis. Utilizing a rat I/R model established by clamping the left hilum of lung for 90 min followed by 120 min of reperfusion, we examined the effects of DEX on lung injury scores, GSH content, and the expression of key proteins involved in cuproptosis. In conclusion, cuproptosis is implicated in pulmonary I/R injury, and the protective effect of DEX against lung I/R injury is partly mediated by inhibition of cuproptosis.

Frontiers in PharmacologyVol. 16
Qingdao University (CN), Peking University (CN), Affiliated Hospital of Qingdao University (CN), Peking University People's Hospital (CN)
National Natural Science Foundation of China, Natural Science Foundation of Shandong Province, Postdoctoral Innovation Project of Shandong Province
Good health and well-being
Openalex Percentile: Top 92%
Nitric Oxide and Endothelin Effects
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Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study — Hanqun Liu, Zhe Wu, et al. · Frontiers in Pharmacology (2025) | TGRS Research Map | TGRS