ABSTRACT This research was designed to investigate if antioxidant sulforaphane (SFN) alleviates methamphetamine (METH)-induced neurotoxicity by activation of the Nrf2-mediated pathway. Oxidative damage, apoptosis and mitochondrial membrane potential were evaluated in PC12 cells or the prefrontal cortex of SD rats post METH treatment with/without SFN. In addition, knockdown of Nrf2 expression in PC12 cells was used to further study the underlying mechanism. The results showed that METH exposure induced increased oxidative damage and apoptosis accompanied by decreased expressions of Nrf2, HO-1 and GCS in PC12 cells and the prefrontal cortex of SD rats. Meanwhile SFN effectively prevented METH-induced cell oxidative damage, apoptosis and mitochondrial membrane potential; however, the knockdown of Nrf2 expression partly reversed the protective effect of SFN in reducing METH-induced oxidative damage and apoptosis in PC12 cells. These results indicate that SFN might be a promising functional food-derived compound for preventing METH-induced neurotoxicity via the Nrf2-mediated pathway.

中文翻译：

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萝卜硫素通过 Nrf2 介导的体外和体内途径减轻甲基苯丙胺诱导的氧化损伤和细胞凋亡

摘要 本研究旨在研究抗氧化剂萝卜硫素 (SFN) 是否通过激活 Nrf2 介导的通路来减轻甲基苯丙胺 (METH) 诱导的神经毒性。在有/没有 SFN 的 METH 治疗后，在 PC12 细胞或 SD 大鼠的前额叶皮层中评估氧化损伤、细胞凋亡和线粒体膜电位。此外，PC12 细胞中 Nrf2 表达的敲低被用于进一步研究潜在机制。结果表明，METH 暴露可导致 SD 大鼠 PC12 细胞和前额叶皮层中 Nrf2、HO-1 和 GCS 表达降低，从而导致氧化损伤和细胞凋亡增加。同时SFN有效阻止METH诱导的细胞氧化损伤、细胞凋亡和线粒体膜电位；然而，Nrf2 表达的敲低部分逆转了 SFN 在减少 METH 诱导的 PC12 细胞氧化损伤和细胞凋亡方面的保护作用。这些结果表明，SFN 可能是一种有前途的功能性食品衍生化合物，用于通过 Nrf2 介导的途径预防 METH 诱导的神经毒性。