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NF-B/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK

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This is further supported by the finding that SOD activity is increased during active disease and returns to normal in remission (157).Additionally, the presence of oxidative damage and the inhibition of catalase, an antioxidant enzyme, in CD patients immune cells further underscores oxidative stresss role in the disease (158)

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