右美托咪定对心肌缺血再灌注大鼠心肌组织自噬 和 SIRT1/mTOR 通路蛋白的影响.

To explore the efftects of dexmedetomidine on autophagy in myocardial tissues of myocardial ischemia-reperfusion rats and NAD dependent deacetylase (SIRT1)/rapamycin target protein (mTOR) pathway proteins. 45 SPF grade male SD rats of 8 weeks old (mean weight 220 g) were randomly divided into sham-surgery group, model group, and dexmedetomidine group, with 15 rats in each group; the model group and dexmedetomidine group were used to replicate myocardial ischemia-reperfusion model. The dexmedetomidine group was infused with dexmedetomidine hydrochloride injection before modeling, while the other two groups were infused with equal amount of physiological saline. Serum myocardial injury markers creatine kinase isoenzyme (CK-MB) and troponin I (cTnI), inflammatory factors interleukin-6 (IL-6), and tumor necrosis factor - α (TNF-α) were detected before and 24 hours after reperfusion; after euthanizing rats, TTC staining was used to calculate the percentage of myocardial infarction area. qRT-PCR and Western blot were used to detect autophagy related proteins microtubule associated protein 1A/1B light chain 3 (LC3) II/I, beclin-1, and P62 proteins, SIRT1 and mTOR, too. CK-MB, cTnI, IL-6, and TNF-α levels in the model group and dexmedetomidine group before reperfusion were significantly higher than sham-surgery group, and the dexmedetomidine group was lower than model group (P<0.05); CK-MB, cTnI, IL-6, and TNF-α levels in the model group after reperfusion were higher than before reperfusion, while the dexmedetomidine group was lower than before reperfusion, what's more, the dexmedetomidine group was significantly lower than model group (P<0.05). The percentage of myocardial infarction area, expression levels of LC3 II/I, beclin-1 and P62 proteins, SIRT1 and mTOR in the model group and dexmedetomidine group were higher than those in the sham-surgery group, but the dexmedetomidine group was significantly lower than the model group (P<0.05). Myocardial ischemia-reperfusion may furtherly increase myocardial injury and inflammatory response. Pretreatment with dexmedetomidine can partially alleviate myocardial injury, inflammatory response, myocardial infarction, and autophagy, which may be related to the inhibition of SIRT1/mTOR signaling [ABSTRACT FROM AUTHOR]