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Introduction <p>Type 2 diabetes mellitus (T2DM) is increasingly linked to neurodegenerative changes driven by oxidative stress, mitochondrial dysfunction, and dysregulated signaling pathways, particularly under chronic hyperglycemia.</p> Aim <p>This study aimed to assess the neuroprotective effects of novel curcumin–indole-3-propionic acid conjugate (CUR-IPA) against high glucose (HG)-induced damage in SH-SY5Y neuronal cells.</p> Methods <p>Cells were exposed to HG to simulate diabetic stress and co-treated with CUR-IPA (6.25–25 µM). Cell viability, oxidative stress markers, mitochondrial membrane potential (MMP), and apoptosis were evaluated. Flow cytometry was used to quantify the expression of apoptotic (p53, Bax, caspase-3, and Bcl-2), survival (p-Akt and mTOR), and neurotrophic (BDNF, p-TrkB, and CREB) proteins.</p> Results <p>HG induced oxidative stress, loss of MMP, apoptosis, and suppression of PI3K/Akt/mTOR and BDNF/TrkB/CREB pathways.</p> Conclusion <p>In conclusion, CUR-IPA demonstrates strong neuroprotective potential under HG stress by modulating redox status, mitochondrial function, and survival signaling. The findings suggest its promise as a multi-target therapy for diabetes-linked neurodegeneration, and warrant an in vivo study.</p> Clinical trial number <p>Not applicable.</p>

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Neuroprotective potential of esterified indole-3-propionic acid with curcumin against high glucose stress: targeting oxidative damage, Akt/mTOR, and BDNF/TrkB pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月3日

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  • Jayanthi Sidhambaram,
  • Chitra Loganathan,
  • Penislusshiyan Sakayanathan,
  • Palvannan Thayumanavan

摘要

Introduction

Type 2 diabetes mellitus (T2DM) is increasingly linked to neurodegenerative changes driven by oxidative stress, mitochondrial dysfunction, and dysregulated signaling pathways, particularly under chronic hyperglycemia.

Aim

This study aimed to assess the neuroprotective effects of novel curcumin–indole-3-propionic acid conjugate (CUR-IPA) against high glucose (HG)-induced damage in SH-SY5Y neuronal cells.

Methods

Cells were exposed to HG to simulate diabetic stress and co-treated with CUR-IPA (6.25–25 µM). Cell viability, oxidative stress markers, mitochondrial membrane potential (MMP), and apoptosis were evaluated. Flow cytometry was used to quantify the expression of apoptotic (p53, Bax, caspase-3, and Bcl-2), survival (p-Akt and mTOR), and neurotrophic (BDNF, p-TrkB, and CREB) proteins.

Results

HG induced oxidative stress, loss of MMP, apoptosis, and suppression of PI3K/Akt/mTOR and BDNF/TrkB/CREB pathways.

Conclusion

In conclusion, CUR-IPA demonstrates strong neuroprotective potential under HG stress by modulating redox status, mitochondrial function, and survival signaling. The findings suggest its promise as a multi-target therapy for diabetes-linked neurodegeneration, and warrant an in vivo study.

Clinical trial number

Not applicable.