| 高 蕤,陈思宇,胡 云,木开达斯·马合木提,戴晓雯.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[J].,2024,(11):2027-2031 |
| 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 |
| The Effects of Dexmedetomidine on Autophagy in Myocardial Tissues of Rats with Myocardial Ischemia-reperfusion and SIRT1/mTOR Pathway Proteins |
| 投稿时间：2023-12-06 修订日期：2023-12-31 |
| DOI：10.13241/j.cnki.pmb.2024.11.005 |
| 中文关键词: 心肌缺血再灌注 自噬 右美托咪定 NAD-依赖性去乙酰化酶 雷帕霉素靶蛋白 信号通路 炎症 |
| 英文关键词: Myocardial ischemia-reperfusion Autophagy Dexmedetomidine NAD-dependent deacetylase Rapamycin target protein Signal pathway Inflammation |
| 基金项目:新疆维吾尔自治区自然科学基金面上项目（2019D01C324） |
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| 中文摘要: |
| 摘要 目的：探讨右美托咪定对心肌缺血再灌注大鼠心肌组织自噬和NAD-依赖性去乙酰化酶（SIRT1）/雷帕霉素靶蛋白（mTOR）通路蛋白的影响。方法：选择45只SPF级雄性SD大鼠8周龄（平均体重220 g），随机分为假手术组、模型组和右美托咪定组，每组各15只；模型组和右美托咪定组复制心肌缺血再灌注模型，右美托咪定组造模前输注盐酸右美托咪定注射液，其他两组输注等量生理盐水。再灌注前和再灌注结束24h后检测血清心肌损伤标志物肌酸激酶同工酶（CK-MB）和肌钙蛋白I（cTnI），炎症因子白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α），处死大鼠后TTC染色计算心肌梗死面积百分比，qRT-PCR和Western blot法检测自噬相关蛋白微管相关蛋白1A/1B-轻链3（LC3）II/I、Beclin-1和P62蛋白，SIRT1和mTOR的表达量。结果：再灌注前模型组和右美托咪定组CK-MB、cTnI、IL-6和TNF-α水平明显高于假手术组，右美托咪定组低于模型组（P＜0.05）；再灌注后模型组CK-MB、cTnI、IL-6和TNF-α水平高于再灌注前，右美托咪定组低于再灌注前，且右美托咪定组显著低于模型组（P＜0.05）。模型组和右美托咪定组心肌梗死面积百分比、LC3 II/I、Beclin-1和P62蛋白、SIRT1和mTOR的表达量高于假手术组，但右美托咪定组显著低于模型组（P＜0.05）。结论：心肌缺血再灌注后可能进一步增加心肌损伤和炎症反应，右美托咪定预处理能够部分减轻心肌损伤、炎症反应、心肌梗死和自噬程度，可能与抑制SIRT1/ mTOR信号通路活性有关。 |
| 英文摘要: |
| ABSTRACT Objective: 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. Methods: 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. Results: 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). Conclusion: 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 pathway activity. |
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