Regulation of adenosine triphosphate-sensitive potassium channels suppresses the toxic effects of amyloid-beta peptide (25-35).
Regulation of adenosine triphosphate-sensitive potassium channels suppresses the toxic effects of amyloid-beta peptide (25-35).
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调节三磷酸腺苷敏感钾通道可抑制淀粉样蛋白β肽的毒性作用（25-35）。
DOI：
10.3969/j.issn.1673-5374.2013.01.007
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发表时间：
2013-01-05
影响因子：
6.1
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Kong M;Ba M;Liang H;Shao P;Yu T;Wang Y
本研究以0-20 μM淀粉样蛋白β肽（25-35）处理PC12细胞24小时诱导细胞毒性，发现5-20 μM淀粉样蛋白β肽（25-35）可降低PC12细胞活力，而三磷酸腺苷敏感钾通道激活剂二氮氧化物可抑制淀粉样蛋白β肽（25-35）诱导的PC12细胞活力下降。二氮氧化合物保护PC12细胞免受淀粉样蛋白-β肽（25-35）诱导的线粒体膜电位和细胞内活性氧水平升高的影响。这些保护作用被选择性线粒体三磷酸腺苷敏感钾通道阻滞剂5-羟癸酸逆转。诱导型一氧化氮合酶抑制剂n ω-硝基- l -精氨酸也能保护PC12细胞免受淀粉样蛋白-β肽（25-35）诱导的线粒体膜电位和细胞内活性氧水平升高的影响。然而，过氧化氢酶不能逆转淀粉样蛋白-β肽（25-35）诱导的细胞内活性氧的增加。24小时暴露于淀粉样蛋白-β肽（25-35）不会导致细胞凋亡或坏死，这表明线粒体膜电位和活性氧水平的增加先于细胞死亡。数据表明淀粉样蛋白-β肽（25-35）细胞毒性与三磷酸腺苷敏感钾通道和一氧化氮有关。三磷酸腺苷敏感钾通道的调节可抑制淀粉样蛋白-β肽诱导的PC12细胞毒性（25-35）。
In this study, we treated PC12 cells with 0–20 μM amyloid-β peptide (25–35) for 24 hours to induce cytotoxicity, and found that 5–20 μM amyloid-β peptide (25–35) decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide (25–35). Diazoxide protected PC12 cells against amyloid-β peptide (25–35)-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nω-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide (25–35)-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H2O2-degrading enzyme catalase could not reverse the amyloid-β peptide (25–35)-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-β peptide (25–35) did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide (25–35) cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide (25–35).
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