摘要： 目的 探讨右美托咪定（DEX）对病理性心肌细胞肥大的保护作用。方法 建立新生乳鼠离体细胞群，共分为6组。对照组（C组）无血清培养24 h，模型组（A组）血管紧张素Ⅱ（Ang Ⅱ）培养24 h，DEX组（AD组）Ang Ⅱ+DEX（5 μmol/L）培养24 h，C’组无血清培养48 h，A’组Ang Ⅱ孵育24 h停药24 h，AD’组DEX+Ang Ⅱ孵育24 h停药24 h。免疫荧光观察细胞形态变化，Western blotting检测心房钠尿肽（ANP）、脑尿钠肽（BNP）和肌球蛋白重链（β-MHC）蛋白表达水平，CCK-8检测细胞活性。结果 与C组比较，A组细胞增大，ANP、BNP和β-MHC表达增加，AD组增大更显著。CCK-8检测显示，与C组比较，A组活性降低，AD组活性明显增加。与C’组比较，A’组肥大相关蛋白表达明显增加，但与A’组比较，AD’组ANP和BNP蛋白表达明显减少，差异均有统计学意义（P < 0.05）。结论 DEX可通过代偿性、类似生理性心肌肥大的作用机制缓解病理性肥大的发生，发挥保护心肌的作用。

右美托咪定对病理性心肌细胞肥大的保护作用

曹雪峰¹, 赵亮², 方波³, 刘旭东⁴, 段凤梅¹, 姬云飞⁴

1. 承德医学院附属医院麻醉科, 河北 承德 067000;
2. 承德医学院基础医学院药理教研室, 河北 承德 067000;
3. 中国医科大学附属第一医院麻醉科, 沈阳 110001;
4. 承德市中心医院麻醉疼痛科, 河北 承德 067000

收稿日期:2023-01-29出版日期:2023-12-30发布日期:2023-12-12
通讯作者:赵亮E-mail:shijianzhengzaifei@163.com
作者简介:曹雪峰(1983-),女,副主任医师,博士研究生
基金资助:国家自然科学基金（81700310）；河北省重点研发计划（22377746D）；承德市科学技术研究与发展计划（201904A099）


关键词: 右美托咪定, 心肌肥大, 血管紧张素, 细胞保护
Abstract: Objective The purpose of this study was to investigate the protective effect of dexmedetomidine (DEX) on pathological cardiomyocyte hypertrophy.Methods An in vitro cell population was established in neonatal rats. The rats were divided into six groups:control group (C) without serum for 24 h, model group (A) with angiotensinⅡ (AngⅡ) for 24 h, dexmedetomidine group (AD) with Ang Ⅱ+DEX (5 μmol/L) for 24 h, C' group with serum-free culture for 48 h, A' group with AngⅡ for 24 h, and AD' group with DEX+AngⅡ for 24 h. The morphological changes of cells were observed by immunofluorescence. The protein expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and myosin heavy chain (β-MHC) were detected by western blot, and the cell activity was detected by CCK-8.Results Compared with group C, the size of cells in group A was larger, and that in group AD was even more significant. Similar observations were found for hypertrophy related proteins. Compared with group C, the expression of ANP, BNP, and β MHC increased in group A, although the increase in AD group was more obvious. CCK-8 detection showed that compared with group C, the activity of group A decreased and that of group AD increased significantly. Compared with the C' group, the expression of hypertrophy-related protein in the A' group was significantly increased, but the expression of ANP and BNP protein in the AD' group was significantly lower than that in the A' group. The differences were statistically significant (P < 0.05).Conclusion Dexmedetomidine can alleviate the occurrence of pathological hypertrophy through compensatory mechanisms similar to physiological myocardial hypertrophy, and may play a role in myocardial protection.
Key words: dexmedetomidine, cardiac hypertrophy, angiotensin Ⅱ, cell protection
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