Aramaki Y, Takano S, Tsuchiya S
School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan.
Arch Biochem Biophys. 2001 Aug 15;392(2):245-50. doi: 10.1006/abbi.2001.2458.
To clarify the mechanism of apoptosis of the macrophage-like cell line RAW264.7 induced by cationic liposomes, we focused on the mitochondria and investigated the changes in mitochondrial membrane potential and the release of cytochrome c following treatment of cationic liposomes composed of stearylamine (SA-liposomes). SA-liposomes induced mitochondrial membrane depolarization and also the release of cytochrome c from mitochondria. Caspase-3 was also activated by SA-liposome treatment. Pretreatment of cells with N-acetylcysteine, a scavenger of reactive oxygen species (ROS), conferred resistance to the induction of the membrane depolarization, cytochrome c release, and caspase-3 activation by SA-liposomes. These results indicated that SA-liposomes caused the apoptosis in RAW264.7 cells through the mitochondrial pathway, and ROS generation was required for this phenomenon.
为阐明阳离子脂质体诱导巨噬细胞样细胞系RAW264.7凋亡的机制，我们聚焦于线粒体，研究了由硬脂胺组成的阳离子脂质体（SA-脂质体）处理后线粒体膜电位的变化以及细胞色素c的释放。SA-脂质体诱导线粒体膜去极化，并促使细胞色素c从线粒体释放。SA-脂质体处理还激活了半胱天冬酶-3。用活性氧（ROS）清除剂N-乙酰半胱氨酸预处理细胞，可使细胞对SA-脂质体诱导的膜去极化、细胞色素c释放及半胱天冬酶-3激活产生抗性。这些结果表明，SA-脂质体通过线粒体途径导致RAW264.7细胞凋亡，且该现象需要ROS的产生。
