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Dexmedetomidine postconditioning suppresses myocardial ischemia/reperfusion injury by activating the SIRT1/mTOR axis.

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机构： [1]Guangzhou First People’s Hospital, School of Medicine, South China University of Technology, Guangzhou 510405, Guangdong, P.R. China [2]Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, P.R. China [3]The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, P.R. China [4]The First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, P.R. China [5]Department of Anesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, P.R. China

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Myocardial ischemia/reperfusion (MI/R) triggers a complicated chain of inflammatory reactions. Dexmedetomidine (Dex) has been reported to be important in myocardial disorders. We evaluated the role of Dex in MI/R injury via the silent information regulator factor 2-related enzyme 1 (SIRT1)/mammalian target of rapamycin (mTOR) signaling pathway. First, Dex was immediately injected into rat models of MI/R injury during reperfusion. After Evans Blue-triphenyl tetrazolium chloride (TTC) and Hematoxylin-Eosin (H-E) staining, MI/R injury was observed. The extracted serum and myocardial tissues were used to detect oxidative stress and the inflammatory response. Western blot analysis was performed to evaluate MI/R autophagy and the levels of proteins associated with the SIRT1/mTOR axis. The effects of the combination of Dex and SIRT1 inhibitor EX527 on MI/R injury and autophagy were evaluated. Finally, the mechanism of Dex was tested, and autophagy levels and the levels of proteins associated with the SIRT1/mTOR signaling pathway were assessed in MI/R rats. The results of the present study suggested that Dex relieved MI/R injury, reduced cardiomyocyte apoptosis, oxidative stress and inflammatory reactions, up-regulated the SIRT1/mTOR axis and decreased overautophagy in MI/R rats. SIRT1 inhibitor EX527 attenuated the protective effects of Dex. Our study demonstrated that Dex alleviated MI/R injury by activating the SIRT1/mTOR axis. This investigation may offer new insight into the treatment of MI/R injury. © 2020 The Author(s).

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出版当年[2019]版：

大类 | 3 区生物

小类 | 4 区生化与分子生物学 4 区细胞生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 3 区生化与分子生物学 4 区细胞生物学

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第一作者机构： [1]Guangzhou First People’s Hospital, School of Medicine, South China University of Technology, Guangzhou 510405, Guangdong, P.R. China

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