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To do this, we used a previous program to study whole-body acetaminophen metabolism [10]

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FIGURE 10 Notably, activators of SIRT1, such as metformin, have demonstrated the ability to inhibit Th17 cell differentiation and downregulate IL-17A and RORγt levels by promoting STAT3 deacetylation ( In summary, our study primarily investigated the beneficial effects of GHK-Cu in UC, using a DSS-induced colitis mouse model and an in vitro co-culture system, suggesting that GHK-Cu may exert anti-inflammatory properties and its role in facilitating the repair of UC by regulating SIRT1/STAT3 signaling pathway