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24 hours) treatment increases the expression of p62 and Nrf2 in chemoresistant HN3R and HN3-rslR cells, inactivates Keap1, and increases expression of the phospho-PERK-ATF4-SESN2 pathway [2]

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It is vital to re‐establish blood flow, but this act also contributes to neuronal injury by activating an immunological response and leading to endotoxicity, neuroinflammation, and oxidative and nitrosative stress, thereby worsening the outcome of ischemia (Chamorro et al., 2016

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