Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
Neurotoxicology. 2013 May;36:63-71. doi: 10.1016/j.neuro.2013.03.004. Epub 2013 Mar 18.
Parkinson's disease (PD) is characterized by the selective loss of dopaminergic nigrostriatal neurons, which leads to disabling motor disturbances. Sulforaphane (SFN), found in cruciferous vegetables, is a potent indirect antioxidant and recent advances have shown its neuroprotective activity in various experimental models of neurodegeneration. This study was undertaken to examine the effects of SFN on behavioral changes and dopaminergic neurotoxicity in mice exposed to 6-hydroxydopamine (6-OHDA). For this purpose, mice were treated with SFN (5mg/kg twice a week) for four weeks after the unilateral intrastriatal injection of 6-OHDA. The increase in 6-OHDA-induced rotations and deficits in motor coordination were ameliorated significantly by SFN treatment. In addition, SFN protected 6-OHDA-induced apoptosis via blocking DNA fragmentation and caspase-3 activation. These results were further supported by immunohistochemical findings in the substantia nigra that showed that SFN protected neurons from neurotoxic effects of 6-OHDA. The neuroprotective effect of SFN may be attributed to its ability to enhance glutathione levels and its dependent enzymes (glutathione-S-transferase and glutathione reductase) and to modulate neuronal survival pathways, such as ERK1/2, in the brain of mice. These results suggest that SFN may potentially be effective in slowing down the progression of idiopathic PD by the modulation of oxidative stress and apoptotic machinery.
帕金森病（PD）的特征是多巴胺能黑质纹状体神经元的选择性丧失，导致运动障碍。存在于十字花科蔬菜中的萝卜硫素（SFN）是一种有效的间接抗氧化剂，最近的研究表明其在各种神经退行性变的实验模型中具有神经保护活性。本研究旨在研究 SFN 对暴露于 6-羟基多巴胺（6-OHDA）的小鼠行为变化和多巴胺能神经毒性的影响。为此，在单侧纹状体注射 6-OHDA 后，用 SFN（每周两次，5mg/kg）处理小鼠 4 周。SFN 治疗显著改善了 6-OHDA 诱导的旋转增加和运动协调缺陷。此外，SFN 通过阻断 DNA 片段化和半胱天冬酶-3 激活来保护 6-OHDA 诱导的细胞凋亡。这些结果在黑质中的免疫组织化学发现中得到进一步支持，表明 SFN 可保护神经元免受 6-OHDA 的神经毒性影响。SFN 的神经保护作用可能归因于其增强谷胱甘肽水平及其依赖的酶（谷胱甘肽-S-转移酶和谷胱甘肽还原酶）的能力，并调节神经元存活途径，如 ERK1/2，在小鼠的大脑中。这些结果表明，SFN 通过调节氧化应激和细胞凋亡机制，可能有效减缓特发性 PD 的进展。
