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This was confirmed in one MS mouse model, which showed that DMF-mediated protection against acute inflammatory autoimmune encephalomyelitis was observed in both NRF2-proficient and NRF2-deficient animals (Schulze-Topphoff et al., 2016) and likewise, SFN has been demonstrated to have hundreds of molecular targets next to KEAP1 (Li et al., 2020)
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Previous reports have shown increased hepatic Tnf- concentrations and NF-B DNA binding after APAP treatment, which correlated with increased cyclin-D1 (a key regulator of cell cycle entry) protein expression and liver regeneration, in mice.17, 38, 39 In contrast, decreased serum Tnf- concentration, lower NF-B DNA binding, and decreased expression of cyclin-D1 were reported after interventions that impaired liver regeneration after APAP-induced liver injury.17, 40 This association was further substantiated by a study of incremental doses of APAP, which revealed direct binding of p65-subunit of NF-B to cyclin-D1 promoter after a moderately toxic and regenerating dose of APAP
