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In vitro experiments confirmed that A 25-35 treatment significantly inhibited the activation of the NRF2/SLC7A11/GPX4 signaling pathway in HT22 cells, upregulated the expression of Fe 2+ , TFR1, ACSL4, MDA, and GSSG, and decreased the expression of FTH1, SOD, and GSH, as well as the GSH/GSSG ratio, resulting in dysregulated neuronal iron metabolism, impaired amino acid antioxidant systems, mitochondrial dysfunction, and ferroptosis, which ultimately promoted neuronal injury
It has also been confirmed that AD pathologic markers, oligomeric A and A plaque load, could be reduced by LG and microglial activation is decreased and memory behaviors are improved in APP swe /PS1_E9 (APP/PS1) mouse model after using LG (74)
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Glucose-6-phosphate is oxidized to 6-phosphogluconolactone by glucose-6-phosphate dehydrogenase (G6PD) with the transfer of two electrons to NADP+ to form NADPH