高氧
未折叠蛋白反应
细胞凋亡
肺
内质网
切碎
半胱氨酸蛋白酶12
药理学
ATF6
医学
信号转导
化学
半胱氨酸蛋白酶
内科学
程序性细胞死亡
生物化学
作者
Meina Huang,Jinhui Wang,Meili Zhai,Jiqiang Liu,Yongjie Zhu,Yang Zhang,Jing Zhao,Huiquan Wang,Jinglai Sun,Hongbin Yu,Chong Liu
标识
DOI:10.1016/j.bbadis.2023.166885
摘要
Perioperative hyperoxia therapy is of great significance to save the lives of patients, but little is known about the possible mechanisms that induce hyperoxia-induced acute lung injury (HALI) and the measures for clinical prevention and treatment. In this experiment, the models were established with a feeding chamber with automatic regulation of oxygen concentration. The results showed that with the increase in inhaled oxygen concentration and the prolongation of exposure time, the severity of lung injury also increases significantly, reaching the diagnostic indication of HALI after 48 h of inhaling 95 % oxygen concentration. Subsequently, according to the dynamic changes of apoptosis in lung specimens, and the expression changes in Sig-1R-regulated ER stress pathway proteins (Sig-1R, GRP78, p-PERK, ATF6, IRE1, Caspase-12, ATF4, CHOP, Caspase-3 and p-JNK), it was confirmed that the Sig-1R-regulated ER stress signaling pathway was involved in the occurrence of HALI. To explore the preventive and therapeutic effects of routine clinical medication on HALI during the perioperative period, our research group selected dexmedetomidine (Dex) with lung protection. The experimental results revealed that Dex partially reversed the changes in the expression levels of Sig-1R-regulated ER stress pathway proteins. These results preliminarily confirmed that Dex may inhibit apoptosis induced by high oxygen concentration through the Sig-1R-regulated ER stress signaling pathway, thus playing a protective role in HALI.
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