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首页> 外文OA文献 >The novel compound NO-1886 increases lipoprotein lipase activity with resulting elevation of high density lipoprotein cholesterol, and long-term administration inhibits atherogenesis in the coronary arteries of rats with experimental atherosclerosis.
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The novel compound NO-1886 increases lipoprotein lipase activity with resulting elevation of high density lipoprotein cholesterol, and long-term administration inhibits atherogenesis in the coronary arteries of rats with experimental atherosclerosis.

机译：新型化合物NO-1886可增加脂蛋白脂肪酶的活性，从而导致高密度脂蛋白胆固醇的升高，并且长期给药可抑制实验性动脉粥样硬化大鼠冠状动脉的动脉粥样硬化。

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摘要

We have discovered a novel compound, NO-1886, which possesses a powerful lipoprotein lipase (LPL) activity-increasing action. Administration of NO-1886 increased LPL activity in the postheparin plasma, adipose tissue, and myocardium of rats, and produced a reduction in plasma triglyceride levels with concomitant elevation of HDL cholesterol levels. Administration of NO-1886 increased LPL enzyme mass in postheparin plasma and mRNA activity in epididymal adipose tissue, and it was concluded that the mode of action of this compound is stimulation of tissue LPL synthesis. We also conducted long-term studies to assess the impact of increases in LPL activity and HDL levels on the development of atherosclerotic lesions in rats. Administration of NO-1886 for as long as 90 d significantly decreased the degree of atherosclerotic changes in the coronary arteries of vitamin D2-treated, cholesterol-fed rats. Statistical analysis indicated that increased concentration of HDL is the factor contributing mostly to the prevention of coronary artery sclerosis. In summary, the results of our study indicate that compound NO-1886 increases LPL activity, causing an elevation in HDL levels, and that long-term administration of NO-1886 to rats with experimental atherosclerosis provides significant protection against the development of coronary artery lesions.
机译：我们发现了一种新型化合物NO-1886，它具有强大的脂蛋白脂肪酶（LPL）活性增强功能。 NO-1886的使用增加了大鼠肝素后血浆，脂肪组织和心肌中的LPL活性，并导致血浆甘油三酯水平降低，同时HDL胆固醇水平升高。 NO-1886的使用增加了肝素后血浆中LPL酶的质量，并增加了附睾脂肪组织中的mRNA活性，因此得出结论，该化合物的作用方式是刺激组织LPL的合成。我们还进行了长期研究，以评估LPL活性和HDL水平升高对大鼠动脉粥样硬化病变发展的影响。服用NO-1886长达90天，可显着降低经维生素D2处理，由胆固醇喂养的大鼠的冠状动脉的动脉粥样硬化改变程度。统计分析表明，HDL浓度升高是预防冠状动脉硬化的主要因素。总而言之，我们的研究结果表明，化合物NO-1886可提高LPL活性，从而导致HDL水平升高，并且长期向实验性动脉粥样硬化大鼠施用NO-1886可有效防止冠状动脉病变的发展。

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