Artemether Activation of AMPK/GSK3β(ser9)/Nrf2 Signaling Confers Neuroprotection towards β-Amyloid-Induced Neurotoxicity in 3xTg Alzheimer’s Mouse Model

Figure 12

A schematic diagram of Artemether-induced AMPK/GSK3β(ser9)/Nrf2 activation towards reduction of amyloid-β-evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3β(ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and Aβ-induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.