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When AICAR is present, it turns on a key enzyme called AMPK (AMP-activated protein steroids in USA kinase). This enzyme helps control how the cell uses energy, particularly from sugar and fat. AICAR is a peptide that has recently surfaced on to the research scene due to its prowess in stimulating AMPK activity in animal studies regarding skeletal muscles.

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Fresh pancreatic and liver tissues and blood samples were collected for biochemical analysis. The levels of serum amylase and lipase were measured by assay kit (C , A , Nanjing Jiancheng Bioengineering Institute, Nanjing, China) to evaluate the degree of pancreatitis. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured with commercial kit (C , C , Nanjing Jiancheng Bioengineering Institute, Nanjing, China) to evaluate the degree of liver injury and function. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in pancreas and liver homogenate were determined with commercial kit (A , A , Nanjing Jiancheng Bioengineering Institute, Nanjing, China).

Likewise, the pathological changes in liver sections of the Nrf2 KO SAP mice were more severe than those in the WT SAP groups by H&E staining (Figure 7B). Additionally, treatment of WT SAP mice with AICAR markedly reduced these negative pathological changes (Figure 7B); however, these protective effects mediated by AICAR were weakened in Nrf2 KO mice (Figure 7B). The liver injury scores, consistent with the pathological appearance in each group, further confirmed our findings (Figure 7C). Moreover, the serum levels of ALT and AST in both WT and Nrf2 KO mice were augmented after L-arginine administration. Notably, the levels of these two markers indicated that liver injury in Nrf2 KO mice was higher than that in WT mice (Figure 7E).

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The increase in AMPK activity, as a result, potentially leads to fat oxidation and energy production. Our results provide the first direct evidence of the beneficial effects of pharmacological activation of AMPK by AICAR against the progression of PALI, including reduced redox stress and decreased NLRP3 inflammasome activation. Moreover, Nrf2 deficiency dramatically weakened these beneficial effects of AICAR in L-arginine-induced PALI mice.

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• To further determine the roles of AICAR in PALI, we next investigated whether replenishment of AICAR can rescue the damaged antioxidant system in sodium taurocholate-induced SAP rats.
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• AICAr-induced glucose uptake in skeletal muscle was abolished in the knockout of the α 2 32,33,35 and α 3 isoforms of AMPK 34.

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Additionally, NAD+ aids in DNA repair, helping to prevent the accumulation of mutations that could contribute to neurodegenerative conditions like Alzheimer’s 8. It is a significant biochemical compound recognized for its role as an activator of AMP-activated protein kinase (AMPK). This activation is crucial as AMPK serves as a key regulator of energy homeostasis within cells 1. When introduced into the body, it enters cells and influences a key enzyme known as AMPK (AMP-activated protein kinase). This enzyme is integral to the lipid metabolism and energy balance within the body.