| 引用本文: | 丁文文,夏鸿,周静,缪园欣.原花青素对苯肾上腺素诱导的心肌肥大保护机制研究[J].中国现代应用药学,2021,38(15):1820-1825. |
| DING Wenwen,XIA Hong,ZHOU Jing,MIAO Yuanxin.Study on Protective Mechanism of Proanthocyanidins on Phenylephrine-induced Cardiac Hypertrophy[J].Chin J Mod Appl Pharm(中国现代应用药学),2021,38(15):1820-1825. |
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| 摘要: |
| 目的 探讨葡萄籽原花青素（grape seed proanthocyanidins，GSP）对苯肾上腺素（phenylephrine，PE）诱导的乳鼠心肌肥大的保护作用及其机制。方法 采用PE（20 μmol·L-1）刺激48 h建立乳鼠心肌肥大模型，分为正常对照组、模型组和GSP低、中、高剂量组（10，20，50 μmol·L-1）。持续给药48 h后，采用Image J测定心肌细胞面积，Western blotting检测心钠素和β-肌凝蛋白重链的表达。后续实验分组：正常对照组、模型组、GSP阴性对照组、GSP中剂量组，采用荧光探针DCFDA检测活性氧含量，采用试剂盒分别检测细胞内超氧化物歧化酶活性（superoxide dismutase，SOD）、丙二醛含量、上清液乳酸脱氢酶活性，Western blotting检测RhoA蛋白和ROCK活性。结果 与模型组相比，GSP干预能够明显降低心肌细胞面积（P<0.05），减少肥大基因心钠素和β-肌凝蛋白重链的表达（P<0.05），并且降低活性氧荧光含量（P<0.05），升高SOD，明显降低丙二醛以及乳酸脱氢酶活性（P<0.05），明显抑制RhoA蛋白和ROCK活性（P<0.05）。结论 GSP对心肌肥大的保护作用与抑制活性氧、RhoA/ROCK信号通路活化有关。 |
| 关键词: 心肌肥大 原花青素 活性氧 RhoA ROCK |
| DOI：10.13748/j.cnki.issn1007-7693.2021.15.005 |
| 分类号:R285.5 |
| 基金项目:荆楚理工学院校级重点项目（ZD202001）；湖北省教育厅中青年人才项目（Q20204305）；湖北省高等学校优秀中青年科技创新团队项目（T201819） |
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| Study on Protective Mechanism of Proanthocyanidins on Phenylephrine-induced Cardiac Hypertrophy |
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DING Wenwen1, XIA Hong1, ZHOU Jing1, MIAO Yuanxin2
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1.Jingchu University of Technology, School of Medical, Jingmen 448000, China;2.Jingchu University of Technology, School of Biological Engineering, Jingmen 448000, China
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| Abstract: |
| OBJECTIVE To study the protective effect and mechanism of grape seed proanthocyanidins(GSP) on phenylephrine(PE)-induced cardiac hypertrophy in neonatal rats. METHODS A model of neonatal cardiac hypertrophy was established by PE(20 μmol·L-1) stimulation for 48 h, which was divided into normal control group, model group, GSP low, medium, and high dose group(10, 20, 50 μmol·L-1). After 48 h of continuous administration, Image J was used to measure the area of cells, Western blotting was used to detect the expression of atrial natriuretic peptide(ANP) and β-myosin heavy chain(β-MHC). Subsequent experimental groups:normal control group, model group, GSP negative control group, GSP medium dose group, fluorescent probe DCFDA was used to detect reactive oxygen species(ROS) content, kits were used to detect intracellular superoxide dismutase(SOD) activity, malondialdehyde(MDA) content, lactate dehydrogenase(LDH) activity of supernatant, Western blotting was used to detect RhoA protein and ROCK activity. RESULTS Compared with control group, GSP intervention could significantly reduce the area of cardiomyocytes(P<0.05), reduce the expression of hypertrophic genes ANP and β-MHC(P<0.05), and reduce the fluorescence content of ROS(P<0.05), improve SOD activity, reduce MDA content and LDH activity(P<0.05), and significantly inhibit RhoA protein and ROCK activity(P<0.05). CONCLUSION The protective effect of GSP on cardiac hypertrophy is related to the inhibition of ROS and RhoA/ROCK signaling pathway. |
| Key words: cardiac hypertrophy proanthocyanidins reactive oxygen species(ROS) RhoA ROCK |
