抑制基米林合成可以降低阿波利波蛋白E-Knockout小鼠中的腺体生成
Tae-Sik Park1, Robert L Panek, Sandra Bak Mueller
1Cardiovascular Pharmacology, Pfizer Global Research and Development, Ann Arbor, Mich 48105, USA.
Circulation
|November 17, 2004
概括
在小鼠中抑制脊髓髓蛋白 (SM) 合成可减少动脉样硬化. 这种方法降低了胆固醇和甘油三水平,同时增加了HDL胆固醇,为心脏病提供了潜在的治疗策略.
科学领域:
- 生物化学 生物化学
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 血甲基胺 (SM) 水平与冠状动脉疾病风险相关,独立于胆固醇.
- 斯芬哥米林 (SM) 是通过一种涉及胺棕转移酶的途径合成的.
- 抑制SM合成可能提供抗atherogenic效果.
研究的目的:
- 为了研究抑制SM合成的抗atherogenic效应.
- 为了评估胺棕基转移酶抑制剂myriocin对apolipoprotein E (apoE) - knockout小鼠动脉样硬化的影响.
主要方法:
- 在12周的时间里,Apolipoprotein E (apoE) 失败的小鼠被食西方饮食,并补充了myriocin.
- 测量包括血和组织脂水平,脂质配置和脂质蛋白分布.
- 动脉样硬化病变的发展通过对大动脉的油红色O染色来评估.
主要成果:
- 肌素治疗显著降低了基米林 (SM) 和氨酸的血和组织水平.
- 抑制de novo脂生物合成导致总胆固醇和甘油三水平降低.
- 咪里奥辛的使用导致大动脉和大动脉根部的动脉样性损伤覆盖率降低.
结论:
- 抑制新的SM生物合成有效降低血胆固醇和甘油三水平.
- 这种途径的调节导致HDL胆固醇的增加.
- 阻断SM合成证明了在apoE-knockout小鼠中对动脉样硬化病变发展的预防作用.
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