Evidence map›Paper›PMID 42865340›Full record

ArticleOxidative medicine and cellular longevity2026

Protective Role of Holothuria leucospilota Extract Against Amyloid-β Toxicity via Autophagy and Antioxidant Mechanisms in Caenorhabditis elegans Model.

Chanathip Kamonnat, Salinthip Thongdechsri, Pichnaree Kraokaew, Nakorn Niamnont, Prasert Sobhon, Krai Meemon

Abstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Chanathip KamonnatDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand, mahidol.ac.th.ORCID https://orcid.org/0009-0005-4905-8240
Salinthip ThongdechsriDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand, mahidol.ac.th.ORCID https://orcid.org/0009-0009-7844-2443
Pichnaree KraokaewDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand, mahidol.ac.th.ORCID https://orcid.org/0000-0001-9392-1738
Nakorn NiamnontDepartment of Chemistry, Faculty of Science, King Mongkut's University of Technology Thonburi, Bang Mod, Bangkok, 10140, Thailand, kmutt.ac.th.ORCID https://orcid.org/0000-0002-9786-6024
Prasert SobhonDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand, mahidol.ac.th.
Krai MeemonDepartment of Anatomy, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand, mahidol.ac.th.ORCID https://orcid.org/0000-0001-5700-2646

Funding

Central Instrument Facility (CIF) AN-KME-3-66-02Mahidol University N42A660511National Research Council of Thailand
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a major global health challenge characterized by cognitive decline and neuronal degeneration driven by amyloid-β (Aβ) aggregation and oxidative stress. Given the limited efficacy and adverse effects of current pharmacological therapies, food-derived bioactive compounds have gained increasing attention as potential preventive strategies against neurodegenerative disorders. In this study, we investigated the neuroprotective effects of Holothuria leucospilota extracts using a transgenic Caenorhabditis elegans model of AD. Our results demonstrated that H. leucospilota hexane extract (HLHE) at 500 µg/mL significantly delayed Aβ-induced paralysis and improved chemotaxis behavior. Consistently, HLHE treatment reduced Aβ deposition and decreased both high- and low-molecular weights of Aβ oligomers, as determined by automated Western blot analysis. Additionally, HLHE also reduced reactive oxygen species (ROS) levels. Transcriptomic and RT-qPCR analyses revealed that HLHE enhanced autophagic activity through the upregulation of bec-1 (autophagy initiation) and lysosomal genes (cpr-1, cpr-2, and cpr-5). Furthermore, HLHE activated antioxidant defense pathways via the insulin/IGF-1 signaling (IIS) axis, specifically upregulating genes associated with SKN-1 pathway (pmk-1, skn-1, gst-4, and gst-10) and HSF-1 pathway (hsf-1, hsp-16.1, hsp-12.6, and mtl-1). HLHE also promoted nuclear localization of SKN-1 and increased expression of its downstream target gst-4. Chemical analysis revealed that HLHE contained arachidonic acid (21.12%) and other bioactive lipid compounds as major constituents, suggesting a synergistic role in promoting autophagy and antioxidant responses. Collectively, this study suggests that HLHE confers neuroprotection against Aβ-induced toxicity by activating autophagy and oxidative stress defense mechanisms, supporting its potential development as a food-derived preventive or therapeutic agent for AD.

Indexed as

Amyloid beta-PeptidesAntioxidantsAutophagyCaenorhabditis elegansHolothuriaPlant ExtractsAlzheimer DiseaseAnimalsAnimals, Genetically ModifiedCaenorhabditis elegans ProteinsDisease Models, AnimalOxidative StressReactive Oxygen SpeciesAmyloid beta-PeptidesAntioxidantsCaenorhabditis elegans ProteinsPlant ExtractsReactive Oxygen SpeciesAlzheimer’s diseaseamyloid-βautophagyCaenorhabditis elegansHolothuria leucospilota

Identifiers

PMID42865340
PMCPMC13659408

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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 OpenQuestion graph.