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Effects of ligustrazine on the mitochondrial structure and functions in the process myocardial hypertrophy / 中国中西医结合杂志
Chinese Journal of Integrated Traditional and Western Medicine ; (12): 661-665, 2012.
Article in Chinese | WPRIM | ID: wpr-252539
ABSTRACT
<p><b>OBJECTIVE</b>To explore changes of mitochondrial structure and functions, as well as the protection of ligustrazine in the process of myocardial hypertrophy.</p><p><b>METHODS</b>Neonatal myocardial cells were isolated and cultured with angiotensin II (Ang II) for 72 or 96 h. The total protein content was detected using BCA method. The cell diameter was measured by inverted microscope, by which to reflect the proliferation situation of cardiomyocytes. The mitochondrial membrane potential (MMP) was measured by fluorescence microscope. The mitochondrial monoamine oxidase (MAO) activity was detected by spectrophotometer. The mitochondrial cytochrome oxidase (COX) activity and the mitochondrial damage percentage were detected by microplate reader, by which to reflect the damage of mitochondrial outer membrane's structure and the membranes' function. Also, cells were treated with ligustrazine and losartan and then the pharmacological effects on the mitochondrial structure and functions in the myocardial cells treated with Ang II were observed.</p><p><b>RESULTS</b>At 72 h and 96 h, when compared with the blank group, cells treated with Ang II had increased total protein content (P < 0.01) and enlarged diameter (P < 0.01). Treated with Ang II, the MAO activity and the outer membrane damage percentage of myocardial cells significantly increased (P < 0.01), and mitochondrial COX activity and the mitochondrial MMP significantly decreased (P < 0.01). Compared with the model group at the same time period, ligustrazine significantly reduced myocardial cells' total protein content and myocardial cell diameter, and significantly decreased myocardial cells' MAO activity, increased mitochondrial COX activity, improved the outer membrane damage percentage and inner membrane MMP at 72 and 96 h, all showing statistical difference (P < 0.01, P < 0.05).</p><p><b>CONCLUSIONS</b>During the process of myocardial hypertrophy existed the damage to the mitochondrial structure and functions. Ligustrazine protected the mitochondrial structure and functions of the myocardial cells in reversing Ang II induced myocardial cell hypertrophy.</p>
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Pharmacology / Pyrazines / Cardiomyopathy, Hypertrophic / Angiotensin II / Cells, Cultured / Rats, Sprague-Dawley / Electron Transport Complex IV / Myocytes, Cardiac / Metabolism Limits: Animals Language: Chinese Journal: Chinese Journal of Integrated Traditional and Western Medicine Year: 2012 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Pathology / Pharmacology / Pyrazines / Cardiomyopathy, Hypertrophic / Angiotensin II / Cells, Cultured / Rats, Sprague-Dawley / Electron Transport Complex IV / Myocytes, Cardiac / Metabolism Limits: Animals Language: Chinese Journal: Chinese Journal of Integrated Traditional and Western Medicine Year: 2012 Type: Article