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Fig. 9 | Cell & Bioscience

Fig. 9

From: Remote ischemic preconditioning protects against spinal cord ischemia–reperfusion injury in mice by activating NMDAR/AMPK/PGC-1α/SIRT3 signaling

Fig. 9

Molecular mechanisms of the three different treatments of RIPC, I/R and HKL administration. RIPC: Sub-lethal remote ischemic preconditioning activates NMDAR2B receptors on the neuronal surface by slightly up-regulating glutamate concentrations outside the spinal anterior horn motor neurons, leading to a transient mild increase in intracellular Ca2+ concentration, activation of the AMPK-PGC-1α signaling pathway via CaMKKβ, increase in mitochondrial SIRT3 expression, and improved neuronal ischemic tolerance. I/R: Lethal ischemia causes an extreme increase in glutamate concentration and excessive activation of NMDAR, resulting in sustained high levels of Ca2+ in neurons, inhibiting AMPK activation, down-regulation of mitochondrial SIRT3 expression, and generation of large amounts of ROS leading to neuronal apoptosis. HKL: HKL improves spinal cord antioxidant capacity after I/R by inhibiting NMDAR hyperactivation and increasing SIRT3 activity. HKL combined with RIPC better promotes neurological recovery in mice after SCIRI

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