Kogure Kentaro, Nakashima Sawa, Tsuchie Akiko, Tokumura Akira, Fukuzawa Kenji
Faculty of Pharmaceutical Sciences, University of Tokushima, Shomachi-1, Tokushima 770-8505, Japan.
Chem Phys Lipids. 2003 Nov;126(1):29-38. doi: 10.1016/s0009-3084(03)00091-4.
To obtain information about the mechanism of apoptosis induced by oxidized low density lipoproteins (oxLDL) in atherosclerotic plaques, we examined the effects of lysophosphatidylcholine (LPC) and platelet-activating factor (PAF)-like lipids (PAF-LL), which can be derived from oxLDL, on rat vascular smooth muscle cells (VSMC). All the lipids with different structures examined induced apoptosis of VSMC, so we studied the mechanism of induction of apoptosis by LPC. LPC-induced apoptosis was inhibited by alpha-tocopherol (alpha-T) and cholesterol (Chol), but not by other antioxidants such as palmitoyl ascorbic acid and PAF receptor antagonist. The cells temporarily became spherical and highly permeable before induction of apoptosis, and their change in shape was prevented by alpha-T and Chol. From these results, we suggest that the apoptosis induced by oxLDL-derived phospholipids in VSMC is caused by temporary membrane distortion, not through specific receptors.
为了获取有关氧化型低密度脂蛋白（oxLDL）在动脉粥样硬化斑块中诱导细胞凋亡机制的信息，我们研究了可从oxLDL衍生而来的溶血磷脂酰胆碱（LPC）和血小板活化因子样脂质（PAF-LL）对大鼠血管平滑肌细胞（VSMC）的影响。所检测的所有具有不同结构的脂质均诱导了VSMC的凋亡，因此我们研究了LPC诱导细胞凋亡的机制。LPC诱导的细胞凋亡受到α-生育酚（α-T）和胆固醇（Chol）的抑制，但不受其他抗氧化剂如棕榈酰抗坏血酸和PAF受体拮抗剂的抑制。细胞在诱导凋亡之前会暂时变成球形且通透性增强，而它们形状的改变可被α-T和Chol阻止。从这些结果来看，我们认为oxLDL衍生的磷脂在VSMC中诱导的细胞凋亡是由暂时的膜扭曲引起的，而非通过特定受体。
