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姜黄素诱导的膜动力学中不依赖凋亡的改变。

Apoptosis-independent alterations in membrane dynamics induced by curcumin.

作者信息

Jaruga E, Sokal A, Chrul S, Bartosz G

机构信息

Department of Molecular Biophysics, University of Lodz, Lodz, Poland.

出版信息

Exp Cell Res. 1998 Dec 15;245(2):303-12. doi: 10.1006/excr.1998.4225.

Abstract

Curcumin is a well-known natural compound with antiinflammatory properties. Its antiproliferative effect and ability to modulate apoptotic response are considered essential in cancer therapy. The physicochemical properties of curcumin suggest membranous localization, which prompted an investigation of the mechanisms of membrane disturbances evoked by curcumin. We chose the erythrocyte as a convenient model for studying membrane effects of curcumin and showed its nonspecific, apoptosis-independent way of action. Curcumin was found to expand the cell membrane, inducing echinocytosis. Changes in cell shape were accompanied by transient exposure of phosphatidylserine. Membrane asymmetry was recovered by the action of aminophospholipid translocase, which remained active in the presence of curcumin. Lipids rearrangements and drug partitioning caused changes of lipid fluidity. Such nonspecific effects of curcumin on cellular membranes would produce artifacts of apoptosis measurement, since several methods are based on membrane changes.

摘要

姜黄素是一种具有抗炎特性的著名天然化合物。其抗增殖作用以及调节凋亡反应的能力在癌症治疗中被认为至关重要。姜黄素的物理化学性质表明其定位于细胞膜,这促使人们对姜黄素引起的膜干扰机制进行研究。我们选择红细胞作为研究姜黄素膜效应的便捷模型,并展示了其非特异性、不依赖凋亡的作用方式。发现姜黄素可使细胞膜扩张,诱导棘形红细胞增多。细胞形状的改变伴随着磷脂酰丝氨酸的短暂暴露。膜不对称性通过氨基磷脂转位酶的作用得以恢复,该酶在姜黄素存在的情况下仍保持活性。脂质重排和药物分配导致脂质流动性发生变化。姜黄素对细胞膜的这种非特异性作用会产生凋亡测量的假象,因为有几种方法是基于膜的变化。

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