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FIGURE 8 The aforementioned abnormalities at the molecular level (downregulation of the Nrf2/HO-1 axis and GPX4) and subcellular structural level (neuronal somata and mitochondrial impairment) were consistent with the GSH metabolism perturbations identified by multi-omics analyses, collectively reflecting oxidative stress-associated damage in the hippocampus during SAE

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Mouse models have been predominantly used, but they have limitations in studying the early dissemination of tumors