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This study was designed to systematically evaluate the therapeutic potential of GHK-Cu in a dextran sulfate sodium (DSS)-induced murine model of UC, with particular emphasis on elucidating its regulatory effects on the NAD-dependent deacetylase sirtuin-1 (SIRT1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway

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Biochemically, GABA levels were increased, leading to a slight reduction in glutamate levels and an improvement in the E/I balance

Indeed, Sp was able to restore cytosolic and mitochondrial redox balance in neuronal cell line SHSY-5Y subjected to 1-methyl-4-phenylpyridinium (MPP + ) treatment which is known to cause mitochondria dysfunction and oxidative stress through complex I inhibition 1 (Fig