Evidence mapPaperPMID 42237308Full record

ArticleBMC pharmacology & toxicology2026

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

Jayanthi Sidhambaram, Chitra Loganathan, Penislusshiyan Sakayanathan, Palvannan Thayumanavan

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Article in BMC pharmacology & toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Jayanthi SidhambaramDepartment of Biochemistry, Periyar University, Salem, Tamil Nadu, 636011, India.
Chitra LoganathanBioinnov Solutions LLP, Research and Development Center, Salem, Tamil Nadu, 636002, India.
Penislusshiyan SakayanathanDepartment of Biomaterials, Saveetha Dental College and Hospitals, SIMATS, Saveetha University, Chennai, India.
Palvannan ThayumanavanDepartment of Biochemistry, Periyar University, Salem, Tamil Nadu, 636011, India. pal2912@periyaruniversity.ac.in.

Funding

Periyar University PU/AD-3URF Order/13629/23F81492/2023
6 · The paper itself

Abstract

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

aimThis 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.

methodsCells 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.

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

conclusionIn 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.

Indexed as

CurcuminGlucoseIndolesNeuroprotective AgentsApoptosisBrain-Derived Neurotrophic FactorCell Line, TumorCell SurvivalHumansMembrane GlycoproteinsMembrane Potential, MitochondrialOxidative StressProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptor, trkBSignal TransductionBDNF protein, humanBrain-Derived Neurotrophic FactorCurcuminGlucoseIndolesMembrane GlycoproteinsMTOR protein, humanNeuroprotective AgentsProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptor, trkBTOR Serine-Threonine Kinasestropomyosin-related kinase-B, humanBDNFCUR-IPAHigh GlucosemTORNeurodegenerationOxidative stress

Identifiers

PMID42237308
PMCPMC13450262

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.