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BAY x 1005可减轻载脂蛋白E/低密度脂蛋白受体双敲除小鼠的动脉粥样硬化。

BAY x 1005 attenuates atherosclerosis in apoE/LDLR - double knockout mice.

作者信息

Jawień J, Gajda M, Olszanecki R, Korbut R

机构信息

Chair of Pharmacology, Jagiellonian University School of Medicine, Cracow, Poland.

出版信息

J Physiol Pharmacol. 2007 Sep;58(3):583-8.

Abstract

Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, wanted to find out if other FLAP inhibitor - BAYx1005 given at a dose of 1.88 mg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model BAYx1005 inhibited atherogenesis, measured both by "en face" method (23.84 +/- 2.7% vs. 15.16 +/- 1.4%) and "cross-section" method (497236 +/- 31516 microm(2) vs. 278107 +/- 21824 microm(2)). This is the first report that shows the effect of BAYx1005 on atherogenesis in gene-targeted mice.

摘要

最近,我们已经表明,MK-886——一种5-脂氧合酶激活蛋白(FLAP)抑制剂,可抑制载脂蛋白E/低密度脂蛋白受体双敲除小鼠的动脉粥样硬化。因此,我们想弄清楚,在16周内每天以每100毫克体重1.88毫克的剂量给予另一种FLAP抑制剂——BAYx1005,是否也能减轻动脉粥样硬化的发生。在载脂蛋白E/低密度脂蛋白受体双敲除(apoE/LDLR-DKO)小鼠模型中,BAYx1005抑制了动脉粥样硬化的发生,这通过“正面”方法(23.84±2.7%对15.16±1.4%)和“横截面”方法(497236±31516平方微米对278107±21824平方微米)来衡量。这是第一份显示BAYx1005对基因靶向小鼠动脉粥样硬化发生影响的报告。

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