新型水溶性富勒烯C60(葡萄糖胺)6强制表达BCL-2和BCL-xL,减少肾缺血/再灌注引起的氧化应激

C. Chien, Chau‐Fong Chen, S. Hsu, L. Chiang, M. Lai
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引用次数: 10

摘要

缺血/再灌注引起的氧化应激,尤其是活性氧诱导的细胞凋亡可导致器官功能障碍。C60(glucosamine)6是一种具有较强自由基清除活性的水溶性富勒烯,研究其对肾缺血/再灌注诱导的细胞凋亡形成和超氧化物生成的影响。C60(葡萄糖胺)6预处理,而不是后处理,显著减少肾缺血/再灌注诱导的细胞凋亡和超氧化物的产生,从而改善肾脏血流动力学效应。大鼠肾bcl-2和bcl-xL在C60(葡萄糖胺)6预处理、后处理和未处理组均明显上调。而在C60(葡萄糖胺)6预处理组,bcl-2和bcl-xL的强迫表达明显升高。我们的研究结果表明,新型水溶性富勒烯C60(葡萄糖胺)6强制表达bcl-2和bcl-xL可以减轻肾缺血/再灌注引起的氧化应激。
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FORCED EXPRESSION OF BCL-2 AND BCL-xL BY NOVEL WATER-SOLUBLE FULLERENE, C60(GLUCOSAMINE)6, REDUCES RENAL ISCHEMIA/REPERFUSION-INDUCED OXIDATIVE STRESS
Apoptosis induced by oxidative stress, especially reactive oxygen species, resulting from ischemia/reperfusion would lead to organ dysfunction. C60(glucosamine)6, a water-soluble fullerene with strong free radical scavenging activity, was applied to evaluate its effect on renal ischemia/reperfusion-induced apoptosis formation and superoxide generation. C60(glucosamine)6 pretreatment, but not posttreatment, significantly reduced renal ischemia/reperfusion-induced apoptosis and superoxide generation and, consequently, ameliorated renal hemodynamic effects. Up-regulation in bcl-2 and bcl-xL of the rat kidney was evident in C60(glucosamine)6 pretreated, posttreated, and nontreated groups. However, exaggerated forced expression of bcl-2 and bcl-xL was found in the C60(glucosamine)6 pretreated group. Our results conclude that forced expression of bcl-2 and bcl-xL by the novel water-soluble fullerene, C60(glucosamine)6, can reduce renal ischemia/ reperfusion-induced oxidative stress.
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