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doi: 10.1016/j.freeradbiomed.2016.03.032

Although FOS is only one proxy for neuronal activity-dependent gene expression, these results suggest that acute cagrilintide treatment in rats activates Glu4.2 Calcr/Ramp3 neurons, whereas subchronic treatment additionally engages Glu8.2 NTS Calcr/Prlh neurons, with no evidence for Glu8.0 activation under any condition

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In gene expression profiling, GHK-Cu treatment of human fibroblasts upregulated superoxide dismutase (SOD1, SOD2, SOD3) and glutathione-related genes while suppressing NF-kB-driven inflammatory signaling [3]

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