Li P F, Dietz R, von Harsdorf R
Department of Cardiology, Franz-Volhard-Clinic and Max-Delbrück-Centerfor Molecular Medicine, Humboldt-University Berlin, Germany.
FEBS Lett. 1997 Mar 10;404(2-3):249-52. doi: 10.1016/s0014-5793(97)00093-8.
Apoptosis of vascular smooth muscle cell (VSMC) plays an important role in the genesis of atherosclerosis and restenosis. In order to investigate the role of reactive oxygen species in the induction of VSMC apoptosis, rat VSMCs were treated with glucose oxidase/glucose (GO/G) or diethylmaleate (DEM). The results showed that GO/G and DEM led to VSMC death. Administration of catalase, superoxide dismutase and deferoxamine revealed that H2O2 was the major reactive oxygen species causing cell death, and H2O2O exerted its effect by formation of hydroxyl radical (.OH). GO/G- and DEM-induced VSMC death occurred by apoptosis characterized by "DNA ladders", condensation of nuclei, positive to in situ nick-end labeling and increases in histone-associated DNA fragmentation. This study suggests that H2O2 and its derived form .OH might be related to apoptosis of VSMC in atherosclerosis and restenosis.
血管平滑肌细胞(VSMC)凋亡在动脉粥样硬化和再狭窄的发生过程中起重要作用。为了研究活性氧在诱导VSMC凋亡中的作用,用葡萄糖氧化酶/葡萄糖(GO/G)或马来酸二乙酯(DEM)处理大鼠VSMC。结果显示,GO/G和DEM导致VSMC死亡。给予过氧化氢酶、超氧化物歧化酶和去铁胺表明,H2O2是导致细胞死亡的主要活性氧,且H2O2通过形成羟基自由基(·OH)发挥作用。GO/G和DEM诱导的VSMC死亡通过凋亡发生,其特征为“DNA梯带”、细胞核浓缩、原位缺口末端标记呈阳性以及组蛋白相关DNA片段增加。本研究提示,H2O2及其衍生的·OH可能与动脉粥样硬化和再狭窄中VSMC的凋亡有关。