Institute of Brain Science and Brain Research Center, National Yang-Ming University, Taipei, Taiwan.
Ann N Y Acad Sci. 2010 Jul;1201:8-12. doi: 10.1111/j.1749-6632.2010.05628.x.
3-Nitropropionic acid (3-NP) is an irreversible inhibitor of mitochondrial succinate dehydrogenase that has been used to explore the molecular mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration for Huntington's disease (HD). Brain-derived neurotrophic factor (BDNF) is a neurotrophin that may regulate neuronal survival and differentiation. Experimental evidence derived from both clinical as well as basic research suggests a close association between BDNF deficiency and HD pathogenesis. In this review, we focus on recent progress in the molecular mechanisms responsible for the BDNF-mediated neuroprotective effects against mitochondrial dysfunction induced by 3-NP. Delineation of BDNF-mediated neuroprotective actions against 3-NP toxicity may add in the development of therapeutic intervention for HD where mitochondrial dysfunction is known to play a crucial role in pathogenesis of this devastating disease.
3-硝基丙酸（3-NP）是一种不可逆的线粒体琥珀酸脱氢酶抑制剂，已被用于探索与亨廷顿病（HD）中线粒体功能障碍和神经退行性变相关的细胞死亡的分子机制。脑源性神经营养因子（BDNF）是一种神经营养因子，可能调节神经元的存活和分化。来自临床和基础研究的实验证据表明，BDNF 缺乏与 HD 发病机制密切相关。在这篇综述中，我们专注于 3-NP 诱导的线粒体功能障碍中 BDNF 介导的神经保护作用的分子机制的最新进展。阐明 BDNF 介导的神经保护作用对抗 3-NP 毒性可能有助于开发治疗 HD 的干预措施，因为已知线粒体功能障碍在这种毁灭性疾病的发病机制中起着关键作用。
