OSCR

<i>Epimedium</i> attenuates neuroinflammation and ameliorates Alzheimer's disease through a KAT2B-dependent mechanism.

Overview

Authors: Jie Gao1, Ming Lang Song1, Jie Liu1, ZhiBin Jiang1, Wen Li1, YunZhi Chen1
  1. Basic Chinese Medicine School (Qihuang College), Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou, China
Institutions: Guizhou University (China)
Journal: Frontiers in medicine, volume 13, article 1811410
Dates: received 14 February 2026; accepted 27 March 2026; published online 20 April 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fmed.2026.1811410 · PMID 42089062 · PMCID PMC13135922 · OpenAlex W7154954633
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: histology / microscopy (modality), Alzheimer's / dementia (population), cellular / molecular (subfield)
Methods: Statistics, Machine learning, Connectivity, Spectral & time-frequency
Keywords: Alzheimer's disease, Epimedium, KAT2B, neuroinflammation, NF-κB, Traditional Chinese Medicine Systems Pharmacology
Topic: Medicinal Plant Pharmacodynamics Research (Pharmacology, Pharmacology, Toxicology and Pharmaceutics), according to OpenAlex
Citations: not cited yet (Europe PMC); 48 references in the paper

Abstract

Background: Alzheimer's disease (AD) is the leading cause of dementia worldwide, yet effective therapies for this neurodegenerative disorder remain scarce. Epimedium, a herb with a history of thousands of years in traditional Chinese medicine, exhibits diverse biological activities and holds potential therapeutic effects against Alzheimer's disease. However, studies on its modern pharmacological mechanisms remain relatively limited.

Methods: TCMSP and PubChem were used to retrieve Epimedium constituents, and SwissTargetPrediction was used to predict potential targets. GeneCards, OMIM, and GEO databases were used to identify targets associated with AD. The AD model was established by intragastric administration of AlCl3 combined with intraperitoneal injection of D-galactose, with the normal saline group serving as controls. Cognitive function was assessed by the Morris water maze, and histopathological changes were observed by H&E staining. ELISA detected IL-1β and TNF-α levels, and qRT-PCR detected KAT2B, NF-κB, IL-1β, and TNF-α expression.

Results: We identified 172 key targets, with KAT2B and ACACB determined as core genes through transcriptomic screening. In vivo studies showed that Epimedium significantly ameliorated cognitive deficits and alleviated histopathological damage in hippocampal neurons. Furthermore, Epimedium suppressed neuroinflammation by reducing IL-1β and TNF-α levels and modulated the mRNA expression of key targets (KAT2B, NF-κB) in the hippocampus.

Conclusion: Epimedium improves pathological alterations in the hippocampal tissue and alleviates cognitive and behavioral impairments in rats by modulating neuroinflammation through KAT2B, thereby providing a scientific basis for its potential application and development as a therapeutic agent.

Reproduced under the paper's license (CC BY), from the paper cited above.

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Data

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Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 6 authors, 6 keywords, 1 funder, 47 references.

Cite

This paper

Gao, J., Song, M. L., Liu, J., Jiang, Z., Li, W., & Chen, Y. (2026). <i>Epimedium</i> attenuates neuroinflammation and ameliorates Alzheimer's disease through a KAT2B-dependent mechanism. Frontiers in medicine, 13, 1811410. https://doi.org/10.3389/fmed.2026.1811410

BibTeX

@article{gao2026lt,
author = {Gao, Jie and Song, Ming Lang and Liu, Jie and Jiang, ZhiBin and Li, Wen and Chen, YunZhi},
title = {{\<i\>Epimedium\</i\> attenuates neuroinflammation and ameliorates Alzheimer's disease through a KAT2B-dependent mechanism}},
journal = {Frontiers in medicine},
year = {2026},
month = apr,
volume = {13},
pages = {1811410},
publisher = {Frontiers Media SA},
issn = {2296-858X},
doi = {10.3389/fmed.2026.1811410},
url = {https://doi.org/10.3389/fmed.2026.1811410},
pmid = {42089062},
pmcid = {PMC13135922}
}

RIS

TY - JOUR
AU - Gao, Jie
AU - Song, Ming Lang
AU - Liu, Jie
AU - Jiang, ZhiBin
AU - Li, Wen
AU - Chen, YunZhi
TI - <i>Epimedium</i> attenuates neuroinflammation and ameliorates Alzheimer's disease through a KAT2B-dependent mechanism
T2 - Frontiers in medicine
J2 - Front Med (Lausanne)
PY - 2026
DA - 2026/04/20
VL - 13
SP - 1811410
SN - 2296-858X
PB - Frontiers Media SA
DO - 10.3389/fmed.2026.1811410
UR - https://doi.org/10.3389/fmed.2026.1811410
LA - en
ER -

CSL-JSON

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