Sulforaphane alleviates methamphetamine-induced oxidative damage and apoptosis via the Nrf2-mediated pathway in vitro and in vivo

Food and Agricultural Immunology

Weiling Li¹  Lin Chen¹  Xiang Tian¹  Mei Zhou¹  Congyue Xu¹  Qi Xiong¹  Qin Ru¹ 

[1] Wuhan Institute of Biomedical Sciences, School of Medicine, Jianghan University;

关键词: sulforaphane;    methamphetamine;    nrf2;    oxidative stress;    apoptosis;   

DOI  :  10.1080/09540105.2020.1784099

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown