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A Cross-sectional In Vitro Study on the Synergistic Neuroprotective Effects of Phytochemicals Ferulic Acid and Ginkgolide B against Amyloid Beta-induced Oxidative Stress and Modulation of Multifunctional Enzyme APE1/Ref-1 in Human Neuroblastoma SH-SY5Y Cells

  • 0Department of Zoology, School of Basic Sciences, Central University of Punjab, Bathinda, Punjab, India.
Cell Biochemistry and Biophysics +

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June 16, 2025

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June 16, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Ferulic acid and Ginkgolide B protect neurons from oxidative stress by restoring Apurinic/Apyrimidinic endonuclease 1 (APE1) function. These phytochemicals show promise for Alzheimer's disease treatment.

Area Of Science

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background

  • Apurinic/Apyrimidinic endonuclease 1 (APE1/Ref-1) is crucial for DNA repair and redox signaling.
  • Oxidative stress, induced by amyloid-beta (Aβ) peptides, contributes to neurodegeneration in Alzheimer's disease (AD).
  • APE1's function is impaired by Aβ-induced oxidative stress, affecting neuronal homeostasis.

Purpose Of The Study

  • To investigate the protective effects of ferulic acid (FA) and Ginkgolide B (GB) against Aβ-induced oxidative stress.
  • To assess the impact of FA and GB on APE1 expression and activity in neuronal cells.
  • To evaluate the therapeutic potential of FA and GB in an AD context.

Main Methods

  • Human neuroblastoma SH-SY5Y cells were treated with Aβ25-35 peptide to induce oxidative stress.
  • Cells were pre-treated with ferulic acid (FA) and Ginkgolide B (GB), individually and in combination.
  • APE1 levels, DNA base damage, and transcription factor activation (Nrf-2, CREB) were analyzed in subcellular compartments.

Main Results

  • Aβ25-35 exposure reduced APE1 levels and activity, leading to DNA damage and impaired Nrf-2/CREB activation.
  • FA and GB pre-treatment restored APE1 expression and functionality across cellular compartments.
  • Phytochemicals improved Base Excision Repair (BER) efficiency, reduced oxidative DNA damage, and reactivated Nrf-2/CREB signaling.

Conclusions

  • Ferulic acid and Ginkgolide B effectively mitigate Aβ-induced neuronal oxidative stress and damage.
  • These phytochemicals restore APE1-dependent DNA repair and redox pathways.
  • FA and GB demonstrate significant therapeutic potential for Alzheimer's disease.

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