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This mechanism involves reducing cyclic adenosine monophosphate (AMP) accumulation and preventing CREB-mediated transcription of gluconeogenic genes, leading to reduced glucose 6-phosphatase (G6pc) and phosphoenolpyruvate carboxykinase 1 (Pck1) expression (He et al., 2009

Under renal injury and OS conditions, excessive ROS generation and the release of pro-apoptotic factors such as apoptosis-inducing factor impairs mitochondrial membrane potential and promotes both caspase-dependent and caspase-independent apoptotic pathways

There are several signaling pathways, such as the phosphoinositide 3-kinases (PI3K)/protein kinase-B (Akt) pathway and the nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor kappa B (NF-B) pathway, which demonstrates a decrease in the inflammatory reaction and mediators upon activation of 7nAChRs [35, 36]

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