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(2012) demonstrate that glucocorticoids suppress cellular antioxidant defence capacity by impairing Nrf2-dependent antioxidant response [67]
These in vivo results align with the in vitro data, consolidating the understanding that GHK-Cu exerts its protective effects in ALI by inhibiting excessive inflammatory responses through its anti-inflammatory and antioxidant properties, mediated by the suppression of NF-B and p38 MAPK signaling pathways [1]
Collectively, the expression profiles of genes involved in lipid metabolism were differentially modulated by EtOH in KO mice (relative to WT mice)
However, excessive ROS accumulation can lead to oxidative damage, disrupting cellular components and ultimately triggering cell death [4]