Yu Yan, Wang Shuoren, Nie Bo, Sun Yikun, Yan Yanfang, Zhu Lingqun
Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Traditional Chinese Medicine, Beijing 100700, China.
Zhongguo Zhong Yao Za Zhi. 2012 Apr;37(7):979-84.
To study pathological and therapeutical problems concerning myocardial cell mitochondria changes during myocardial cell hypertrophy by culturing rat primary myocardial cells.
Primary myocardial cells were seperated and cultured together with angiotensin II (Ang II) for 72 or 96 hours. The total protein content with the BCA method and the photography and measurement of cell diameter with inverted microscope reflected myocardial cell proliferation. The mitochondrial membrane potential (Delta Psi m) with fluorescence microscope, the mitochondrial single amine oxidase (MAO) activity with spectrophotometer, the mitochondrial cytochrome oxidase (COX) activity and the injury percentage of mitochondrial outer membrane with microplate reader and the contents of ATP, ADP, AMP with high performance liquid chromatography reflected the injury and energy metabolism of myocardial cell mitochondrial structure and function when being cultured together with Ang II. On that basis, cells were treated with Astragali Radix injection and valsartan for observing pharmacological effects on mitochondrial structure and function in restructured myocardial cells.
In 72 h and 96 h, compare with the control group, the model group showed significantly increased total protein content and enlarged myocardial cell diameter. During the course of proliferation, the myocardial cell MAO activity and the injury percentage of mitochondrial outer membrane were significantly increased, with significant decrease in mitochondrial COX activity, mitochondrial Delta Psi m and the content of ATP, ADP and rise in the content of AMP. Astragali Radix injection and valsartan reduced myocardial cell total protein content and cell diameter caused by Ang II, decreased myocardial cell MAO activity, significantly increased mitochondrial COX activity and the content of ATP and ADP, and decreased the content of AMP.
During the process of myocardial hypertrophy, the injury of mitochondrial structure and function and the changes in myocardial cell energy metabolism injury occurred after the injury of mitochondria. Astragali Radix injection and valsartan can reverse myocardial cell mitochondrial structure and function during myocardial cell hypertrophy caused by Ang II. Reversion of myocardial cell hypertrophy and restructuring of myocardial cells helps improve energy metabolism of the myocardial cells.
通过培养大鼠原代心肌细胞，研究心肌细胞肥大过程中心肌细胞线粒体变化的病理及治疗问题。
分离原代心肌细胞并与血管紧张素II（Ang II）共同培养72或96小时。采用BCA法测定总蛋白含量，并用倒置显微镜拍摄和测量细胞直径以反映心肌细胞增殖情况。用荧光显微镜检测线粒体膜电位（ΔΨm），用分光光度计检测线粒体单胺氧化酶（MAO）活性，用酶标仪检测线粒体细胞色素氧化酶（COX）活性及线粒体外膜损伤率，用高效液相色谱法检测ATP、ADP、AMP含量，以反映与Ang II共同培养时心肌细胞线粒体结构和功能的损伤及能量代谢情况。在此基础上，用黄芪注射液和缬沙坦处理细胞，观察其对重构心肌细胞线粒体结构和功能的药理作用。
在72小时和96小时时，与对照组相比，模型组总蛋白含量显著增加，心肌细胞直径增大。在增殖过程中，心肌细胞MAO活性及线粒体外膜损伤率显著增加，线粒体COX活性、线粒体ΔΨm及ATP、ADP含量显著降低，AMP含量升高。黄芪注射液和缬沙坦可降低Ang II所致的心肌细胞总蛋白含量和细胞直径，降低心肌细胞MAO活性，显著提高线粒体COX活性及ATP、ADP含量，降低AMP含量。
在心肌肥大过程中，线粒体结构和功能损伤及心肌细胞能量代谢损伤在心肌细胞损伤之后发生。黄芪注射液和缬沙坦可逆转Ang II所致心肌细胞肥大过程中心肌细胞线粒体的结构和功能。逆转心肌细胞肥大和重构心肌细胞有助于改善心肌细胞的能量代谢。
