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Dexmedetomidine Regulates Autophagy via the AMPK/mTOR Pathway to Improve SH-SY5Y-APP Cell Damage Induced by High

Pinzhong Chen1, Xiaohui Chen1, Honghong Zhang1

  • 1Department of Anesthesiology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, No.134 Dong Street, Fuzhou, 350001, Fujian, People's Republic of China.

Neuromolecular Medicine
|April 5, 2023
PubMed

Insights

Dexmedetomidine (DEX) protects against high glucose neurotoxicity by enhancing autophagy via the AMPK/mTOR pathway. This mechanism suggests DEX could treat postoperative cognitive dysfunction in diabetic patients.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Neurodegenerative diseases and postoperative cognitive dysfunction are linked to beta-amyloid peptide (Aβ) accumulation.
  • High glucose levels can impair autophagy, a process crucial for clearing intracellular Aβ.
  • Dexmedetomidine (DEX), an α2-adrenoreceptor agonist, shows neuroprotective potential, but its mechanism is unclear.

Purpose of the Study:

  • To investigate if DEX upregulates autophagy through the AMPK/mTOR pathway.
  • To determine if DEX mitigates high glucose-induced neurotoxicity in SH-SY5Y/APP695 cells.

Main Methods:

  • SH-SY5Y/APP695 cells were exposed to high glucose with or without DEX, rapamycin (RAPA), 3-methyladenine (3-MA), or compound C.
  • Cell viability, apoptosis, and autophagy were assessed using CCK-8, flow cytometry, and monodansylcadaverine staining.
  • Protein expression and phosphorylation of AMPK/mTOR pathway components were analyzed via western blotting.

Main Results:

  • DEX significantly reduced high glucose-induced neurotoxicity, improving cell viability and reducing apoptosis.
  • Autophagy modulation (RAPA, 3-MA) affected DEX's protective effects, indicating its involvement.
  • DEX-induced autophagy was mediated by the AMPK/mTOR pathway, as confirmed by compound C inhibition.

Conclusions:

  • DEX protects against high glucose neurotoxicity by enhancing autophagy via the AMPK/mTOR pathway in neuronal cells.
  • This study elucidates a novel mechanism for DEX's neuroprotection.
  • DEX may be a potential therapeutic agent for postoperative cognitive dysfunction in diabetic patients.
Keywords:
AMPKApoptosisAutophagyDexmedetomidineHigh glucose

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