|
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] |
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