Liu Hanqun, Wang Zicheng, Qiu Tong, Du Wenxing, Wu Zhe, Chen Sheng, Jiao Wenjie
Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Department of Thoracic Surgery, Peking University People's Hospital, Beijing, Beijing, China.
Front Pharmacol. 2025 Apr 1;16:1562535. doi: 10.3389/fphar.2025.1562535. eCollection 2025.
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.
肺缺血再灌注(I/R)损伤是肺移植中不可避免的并发症,其特征是氧自由基和有毒物质过度产生。右美托咪定(DEX)是一种广泛使用的麻醉剂,已被证明能显著提高谷胱甘肽(GSH)水平,从而防止铜内流。本研究探讨DEX在肺I/R损伤中的保护机制,特别关注铜死亡。利用夹闭大鼠左肺门90分钟后再灌注120分钟建立的I/R模型,我们研究了DEX对肺损伤评分、GSH含量以及铜死亡相关关键蛋白表达的影响。总之,铜死亡与肺部I/R损伤有关,DEX对肺I/R损伤的保护作用部分是通过抑制铜死亡介导的。