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Here, we showed that MG132 treatment effectively reversed Keap1-dependent Nrf2 degradation and the reduced expression of downstream antioxidant genes in HSV-1-infected cells and mice, indicating that the inhibition of Nrf2 degradation by MG132 contributes to the alleviation of HSV-1-induced ferroptosis and pathogenesis

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GliSODin was shown to protect against cellular oxidative stress damage in a dramatic human model

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