| 右美托咪定对心肌收缩蛋白表达的影响 |
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| 引用本文： | 陈效安,谷蕾,梁素梅,韩娟萍. 右美托咪定对心肌收缩蛋白表达的影响[J]. 心脏杂志, 2021, 33(4): 415-420. DOI: 10.12125/j.chj.202012083 |
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| 作者姓名： | 陈效安 谷蕾 梁素梅 韩娟萍 |
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| 作者单位： | 西安国际医学中心医院心脏内科，陕西 西安 710100 |
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| 摘 要： | 目的 研究右美托咪定(DEX)对心肌细胞收缩相关蛋白表达的影响及其分子机制。 方法 在50 ml/L浓度氧环境下培养H9C2细胞，建立心肌低氧损伤模型。实验分为对照组、低氧组、低氧+DEX (0.01 μmol/ml、1 μmol/ml、100 μmol/ml)组。除对照组培养在正常细胞环境中外，其余四组培养在低氧环境下，且其中三组按要求添加相应浓度的DEX。细胞存活率和细胞凋亡水平分别采用MTT法和流式细胞仪进行检测，采用ELISA试剂盒检测细胞培养液中心肌酶谱蛋白cTnI、LDH和CK-MB的漏出量，Western blot法检测H9C2细胞中titin、β-MHC、PI3K、Akt、p-PI3K、p-Akt蛋白表达。 结果 低氧条件成功诱导心肌细胞缺氧损伤。低氧组细胞较对照组存活率低、凋亡增加、细胞培养液中cTnI、LDH和CK-MB蛋白水平增加；低氧+ DEX (0.01 μmol/ml、1 μmol/ml、100 μmol/ml)组较低氧组，细胞存活率增加、凋亡减少，cTnI、LDH和CK-MB蛋白水平降低，p-PI3K和p-Akt蛋白表达增加，β-MHC和titin蛋白表达降低，且随着DEX剂量增加，变化更显著。 结论 在低氧损伤心肌细胞中，DEX能抑制收缩相关蛋白表达，可能与PI3K/Akt信号通路有关，是否与激活PI3K/Akt信号通络相关，还有待进一步研究。
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| 关 键 词： | 心肌细胞 缺氧损伤 右美托咪定 PI3K/Akt |
| 收稿时间： | 2020-12-25 |
Effect of dexmedetomidine on the expression of contraction related proteins in cardiomyocytes |
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| Affiliation: | Department of Cardiology, Xi'an International Medical Center Hospital, Xi'an 710100, Shaanxi, China |
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| Abstract: | AIM To study the effect of dexmedetomidine (DEX) on the expression of contractile protein and its molecular mechanism after hypoxia injury. METHODS H9C2 cells were cultured under 50 ml/L oxygen concentration to establish hypoxic injury. The experiment was divided into control group, hypoxia group, hypoxia + DEX (0.01 μmol/ml, 1 μmol/ml, 100 μmol/ml) group. In addition to the control group in normal cell environment, the remaining four groups were cultured in hypoxia environment, and three groups were added with corresponding concentrations of DEX as required. MTT method was used to measure cell survival rate, flow cytometry was used to detect apoptosis level, ELISA was used to detect cTnI, LDH and CK-MB levels in culture medium, the expression of titin, β-MHC, PI3K, Akt, p-PI3K, p-Akt protein in H9C2 cells were detected by Western blot. RESULTS Myocardial cell injury was induced successfully, compared with the normal control group, the cell survival rate was decreased, apoptosis was increased, and the level of zymogram protein in the center of the culture medium increased; compared with the hypoxic culture group, the cell survival rate, apoptosis and myocardial zymogram protein level of the hypoxic + dexmedetomidine groups were increased; Western blot showed that the expression of p-PI3K and p-Akt were increased, while the expression of titin and β-MHC were decreased, and all this is in a dose-dependent manner. CONCLUSION Dexmedetomidine regulates the expression of contractile protein in hypoxic myocardial cells, which may be related to the PI3K/Akt signaling pathway. Whether it is associated with activation of PI3K/Akt signaling, further research is needed. |
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