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

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.

KEYWORDS:

• Sulforaphane
• methamphetamine
• Nrf2
• oxidative stress
• apoptosis

Acknowledgements

The authors gratefully acknowledge the financial support by the China Scholarship Council (No.201908420112) and Hubei Province Department of Education (China) guidance project (B2017273). We also thank Professor Binlian Sun for critical reviews in this manuscript editing.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the China Scholarship Council [grant number 201908420112]; Hubei Provincial Department of Education guidance project [grant number B2017273].