【自发性高血压合并实验性糖尿病大鼠心肌病理重构:线粒体功能障碍的作用】。

Iu M Kolesnyk, M. I. Kolesnyk, A. V. Abramov
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引用次数: 1

摘要

研究了正常血压Wistar大鼠和自发性高血压大鼠(合并和不合并实验性糖尿病)心肌中心肌营养因子-1、膜联蛋白V、titin和I型胶原蛋白的表达。研究了Ca(2+)诱导的线粒体通透性过渡孔。自发性高血压合并糖尿病大鼠心肌营养因子-1、膜联蛋白V和I型胶原含量均高于正常血压组和合并糖尿病大鼠。与无糖尿病的自发性高血压大鼠相比,高血压和糖尿病动物的心脏titin水平降低了27%。自发性高血压糖尿病大鼠心肌中心肌营养因子-1、膜联蛋白V、titin和I型胶原表达的变化与线粒体孔对Ca2+的敏感性升高有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pathological remodeling of myocardium in spontaneous hypertensive rats with experimental diabetes mellitus: the role of mitochondrial dysfunction].
The expression of cardiotrophin-1, annexin V, titin and type I collagen was investigated in myocardium of normotensive Wistar rats and spontaneous hypertensive rats with and without experimental diabetes. The Ca(2+)-induced mitochondrial permeability transition pore was assessed in mitochondria isolated from rat hearts. The contents of cardiotrophin-1, annexin V and type I collagen in spontaneous hypertensive rats with diabetes were higher compared with that detected in the groups of normotensive rats and rats with diabetes. The cardiac titin level was 27% lower in animals with hypertension and diabetes compared to spontaneous hypertensive rats without diabetes. The changes of cardiotrophin-1, annexin V, titin and type I collagen expression were associated with higher sensitivity of mitochondrial pore to Ca2+ in myocardium of spontaneous hypertensive rats with diabetes.
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