摘要
Berberine 被识别通过低密度脂蛋白(LDL ) 的正式就职在人和仓鼠降低浆液胆固醇水平在肝的房间的受体。在阻止动脉粥样硬化评估它的潜力，在在 apolipoprotein 电子 deficient 的动脉粥样硬化开发的 berberine 的效果(apoE ?/?) 老鼠被调查。在 apoE ?/ ？鼠标，在 vivo 导致的 berberine 泡沫房间形成和支持的动脉粥样硬化开发。berberine 导致的泡沫房间形成也在老鼠 RAW264.7 房间，以及在老鼠和人的主要巨噬细胞被观察。由导致 scavenger 受体 A (SR -- 一) 在巨噬细胞的表示， berberine 增加了修改 LDL (DiO-Ac-LDL ) 的举起。导致 Berberine 的 SR -- 表情也在动脉粥样硬化患者在 vivo 并且在房间在巨噬细胞泡沫房间被观察损害。在 RAW264.7 房间的分析显示 berberine 导致了 SR -- 由压制 PTEN 表示的表情，它导致了持续 Akt 激活。我们的结果建议那在减轻动脉粥样硬化评估减少胆固醇的混合物的潜力，它涉及动脉粥样硬化开发的房间上的效果例如巨噬细胞，应该也被考虑。泡沫房间形成的提升能抵销阴沉的浆液胆固醇的有益的效果。
Berberine is identified to lower the serum cholesterol level in human and hamster through the induction of low density lipoproteins （LDL） receptor in hepatic cells. To evaluate its potential in preventing atherosclerosis, the effect of berberine on atherosclerosis development in apolipoprotcin E-deficient （apoE^-/-） mice was investigated. In apoE^-/- mice, berberine induced in rivo foam cell formation and promoted atheroselerosis development. The foam cell formation induced by berberinc was also observed in mouse RAW264.7 cells, as well as in mouse and human primary macrophages. By inducing scavenger receptor A （SR-A） expression in macrophages, berberine increased the uptake of modified LDL （DiO-Ac-LDL）. Bcrberine-induced SR-A expression was also observed in macrophage foam cells in vivo and in the cells at atherosclerotic lesion. Analysis in RAW264.7 cells indicated that berberine induced SR-A expression by suppressing PTEN expression, which led to sustained Akt activation. Our results suggest that to evaluate the potential of a cholesterol-reducing compound in alleviating atherosclerosis, its effect on the ceils involved in atherosclerosis development, such as macrophages, should also be considered. Promotion of foam cell formation could counter-balance the beneficial effect of lowering serum cholesterol.
