Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress

Table 1

The role of NRF2 in the oxidative stress induced by METH.

Species	Research object	Mechanism	Consequence	Ref.
Rats	Striatum	Nrf2 enter the nucleus through DAD1 reception-dependent transport	Activated and played its regulatory role on endoplasmic reticulum stress-related molecular events	[32]
Rat	Primary astrocytes and midbrain neuron	Astrocytes effectively upregulated Nrf2 transcription, expression, and nuclear translocation	Response to oxidative stress	[69]
Mouse	Dopaminergic neurons	Astrocytes derived expression, nuclear translocation, and binding activity of Nrf2 to metallothionein-1 (MT-1) gene significantly increased	Quinone quenching and neuroprotective effect	[70]
Nrf2 +/+ and -/- gene mouse	Dopaminergic neurons	Nrf2 deficiency	Exacerbates METH induced dopamine neuron damage and glial proliferation; DNA oxidation and dopaminergic nerve endings toxicity more severe	[71]
Nrf2 +/+ and -/- gene mouse	Dopaminergic neurons	Upregulate the mRNA levels of antioxidants and cellular protective proteins regulated by Nrf2	Prevent neurodegenerative effects and functional defects caused by oxidative stress of METH	[72]
Sprague-Dawley rat	Striatum and prefrontal cortex	Nrf2-mediated classical pathways were enhanced in microglias after METH exposure	Differential expression of inflammatory mRNA	[73]
Fetal	Brain	Nrf2 deficiency	Enhance oxidative DNA damage, toxicity, and postnatal neurodevelopmental deficits induced by METH	[7]
Human	Dopamine SH-SY5Y cell lines	Through the NF-κB dependent pathway, down-regulates Nrf2 associated with the expression of several antioxidant/detoxification enzymes	Induces neuronal inflammation	[74]