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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats
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Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats

机译：心肌细胞凋亡与遗传性癫痫大鼠心肌损伤的关系

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摘要

Many clinical cases have been reported where epilepsy profoundly influenced the pathophysiological function of the heart; however, the underlying mechanisms were not elucidated. We use the tremor (TRM) rat as an animal model of epilepsy to investigate the potential mechanisms of myocardial injury. Cardiac functions were assessed by arrhythmia score, heart rate, heart: body mass ratio, and hemodynamic parameters including left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and maximum rate of left ventricular pressure rise and fall (+dp/dtmax and -dp/dtmax). Catecholamine level was detected by HPLC. Apoptotic index was estimated by TUNEL assay. The expressions of Bcl-2, Bax, caspase-3, extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal protein kinases (JNK), and p38 were evaluated by Western blot. The results indicated that there existed cardiac dysfunction and cardiomyocyte apoptosis, accompanied by increasing catecholamine levels in TRM rats. Further investigation revealed that apoptosis was mediated by reducing Bcl-2, upregulating Bax, and activating caspase-3. Additional experiments demonstrated that P-ERK1/2 was decreased, whereas P-JNK and P-p38 were upregulated. Our results suggest that the sympathetic nervous system activation and cardiomyocyte apoptosis are involved in the myocardial injury of TRM rats. The mechanisms of apoptosis might be associated with the activation of the mitochondria-initiated and the mitogen-activated protein kinase pathways.
机译：已有许多临床案例报道，癫痫病深刻地影响了心脏的病理生理功能。但是，尚未阐明其潜在机制。我们使用震颤（TRM）大鼠作为癫痫的动物模型，以研究心肌损伤的潜在机制。通过心律不齐评分，心率，心体重比和血液动力学参数（包括左心室收缩压（LVSP），左心室舒张末压（LVEDP）和左心室最大压升和下降率（ + dp / dtmax和-dp / dtmax）。通过HPLC检测儿茶酚胺水平。通过TUNEL测定法估计细胞凋亡指数。 Western blot检测Bcl-2，Bax，caspase-3，细胞外信号调节蛋白激酶（ERK），c-Jun NH2末端蛋白激酶（JNK）和p38的表达。结果表明，TRM大鼠存在心脏功能障碍和心肌细胞凋亡，同时儿茶酚胺水平升高。进一步的研究表明，凋亡是通过减少Bcl-2，上调Bax和激活caspase-3介导的。其他实验证明P-ERK1 / 2降低，而P-JNK和P-p38上调。我们的结果表明，交感神经系统的激活和心肌细胞凋亡与TRM大鼠的心肌损伤有关。凋亡的机制可能与线粒体引发的和丝裂原活化的蛋白激酶途径的激活有关。

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