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Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR

Tingting Yan1, Feng Ding1, Yiting Zhang1

  • 1Department of Bioengineering, Harbin Institute of Technology, Weihai 264209, China.

Marine Drugs
|February 23, 2024
PubMed

Insights

Astaxanthin protects neuronal cells from oxidative stress by preserving mitochondrial function and reducing mitophagy. This antioxidant may be a potential therapeutic for neurodegenerative diseases by activating the Akt/mTOR pathway.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Oxidative stress and mitochondrial dysfunction are implicated in neurological disorders.
  • Mitophagy, the clearance of damaged mitochondria, is crucial for cellular health.
  • Astaxanthin, a potent antioxidant, shows neuroprotective potential, but its mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the neuroprotective mechanisms of astaxanthin against hydrogen peroxide (H₂O₂)-induced oxidative stress in SH-SY5Y cells.
  • To elucidate the role of the Akt/mTOR signaling pathway and mitophagy in astaxanthin's protective effects.

Main Methods:

  • SH-SY5Y cells were treated with H₂O₂ to induce oxidative stress.
  • Cells were pretreated with astaxanthin.
  • Levels of activated Akt and mTOR, and mitophagy were assessed.
  • The effect of Akt inhibition on astaxanthin's protective action was evaluated.

Main Results:

  • Astaxanthin inhibited H₂O₂-induced apoptosis, ameliorated mitochondrial damage, and enhanced cell survival.
  • H₂O₂ reduced Akt and mTOR activation and induced mitophagy; astaxanthin reversed these effects.
  • Inhibition of Akt attenuated the protective effects of astaxanthin, highlighting its critical role.

Conclusions:

  • Astaxanthin protects against H₂O₂-induced neuronal apoptosis by preserving mitochondrial function and reducing mitophagy.
  • The Akt/mTOR signaling pathway is essential for astaxanthin's neuroprotective effects.
  • Astaxanthin shows potential for preventing neurotoxicity in neurodegenerative diseases.
Keywords:
Akt/mTORH2O2apoptosisastaxanthinmitophagy

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