塔莫西芬降低胆固醇7倍,并废除了在非脂蛋白E淘汰赛小鼠的脂质病变的发展
J Reckless1, J C Metcalfe, D J Grainger
1Department of Biochemistry, University of Cambridge, UK. jr3@mole.bio.cam.ac.uk
Circulation
|March 18, 1997
概括
塔莫西芬 (TMX) 治疗显著减少了阿波利波蛋白E (apo E) 淘汰赛小鼠的脂质病变,降低了胆固醇和甘油三. 这表明TMX可能通过改变脂蛋白样本和增加TGF-β来提供心血管保护.
科学领域:
- 心血管科学 心血管科学
- 药理学 药理学是指药理学的学科.
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 阿波利波蛋白E (apo E) 淘汰赛小鼠是动脉样硬化症的模型,发展严重的血管脂质病变.
- 这些小鼠的损伤发育独立于食脂肪含量.
研究的目的:
- 为了研究他莫西芬 (TMX) 对ApoE淘汰赛小鼠脂质病变发展的影响.
- 探索 TMX 的心血管作用背后的潜在机制.
主要方法:
- 口服他莫西芬 (TMX) 给ApoE淘汰小鼠.
- 使用油红色O染色对脂质病变发展的测定.
- 对血脂蛋白 (VLDL,LDL,HDL) 概况和甘油三水平的分析.
- 测量主动和潜伏的TGF-β度在大动脉.
主要成果:
- 在正常和高脂肪饮食的小鼠中,TMX消除了脂质病变的发展.
- TMX治疗导致总胆固醇降低了7倍,总甘油三降低了62%.
- 血LDL胆固醇下降了37%,而HDL胆固醇增加了64%.
- TMX显著增加了主动 (87%) 和潜伏加上主动 (24%) TGF-β 的大动脉度.
结论:
- 在apoE淘汰赛小鼠中,TMX抑制了脂质病变的形成.
- 通过TMX进行心血管保护可能与脂质蛋白样本 (增加HDL,减少LDL) 的有利变化有关.
- 由TMX诱导的TGF-β水平升高也被认为是对动脉样硬化的保护机制.
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