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Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling.

Overview

Authors: Yezi Xia1, Yinwei Zhang1, Ying Li1, Xiaojing Li1, Yaling Wu1, Qi Yao1
  1. Department of Geriatrics, The First Affiliated Hospital of Ningbo University, Zhejiang Province, Ningbo, 315000 P.R. China
Institutions: Ningbo University (China)
Journal: Hereditas, volume 163, issue 1, article 51
Dates: received 26 November 2025; accepted 19 February 2026; published online 9 March 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1186/s41065-026-00660-3 · PMID 41803928 · PMCID PMC13085287 · OpenAlex W7134254706
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), mouse (organism), Parkinson's (population), cellular / molecular (subfield)
Methods: Statistics, Machine learning, Connectivity
Keywords: Parkinson's disease, machine learning, NF-κB, cardamonin
MeSH: Chalcones*, Inflammation*, Neuroinflammatory Diseases*, NF-kappa B*, Parkinson Disease*, Signal Transduction*, Animals, Cell Line, Humans, Mice, Microglia, Molecular Docking Simulation, Neurons, Protein Interaction Maps (* major topic)
Topic: Parkinson's Disease Mechanisms and Treatments (Neurology, Medicine), according to OpenAlex
Citations: cited by 1 paper (Europe PMC); 52 references in the paper

Abstract

Background: Neuroinflammation can accelerate neurodegeneration in Parkinson’s disease (PD). This study aims to identify biomarkers related to PD inflammation and investigate the function of cardamonin (CD) on microglia and neurons.

Methods: The differentially expressed genes (DEGs) in PD were screened out. Inflammation-related genes (IRGs) were obtained from the GSEA and GeneCards databases. The protein-protein interaction network was constructed, and three machine learning algorithms, least absolute shrinkage and selection operator (LASSO) regression analysis, random forest (RF) and support vector machine (SVM) were used to screen the core IRGs in PD pathogenesis. Potential drugs for core genes were screened through the ITCM and HERB databases, and the binding activity between the core targets and the drugs was verified by molecular docking. BV2 cells were induced with MPP + to construct a PD model. CCK-8 assay, flow cytometry, enzyme-linked immunosorbent assays, qPCR and western blotting were conducted to explore the function of CD on the activation of microglia and injury of neurons..

Results: One thousand one hundred eighty-three DEGs and 518 IRGs were obtained, and 31 genes were in the intersection, among which v-rel reticuloendotheliosis viral oncogene homolog A (RELA, p65), a crucial component in NF-κB signaling, was upregulated in the PD samples and demonstrated good diagnostic efficacy. CD had good binding ability with RELA. CD significantly improved the viability, repressed apoptosis, reduced the production of pro-inflammatory factors (TNF-α, IL-6 and IL-1β) of BV2 cells, which were induced by MPP+. In addition, CD significantly inhibited the activation of the NF-κB signaling pathway and the nuclear translocation of RELA.

Conclusion: CD inhibits the inflammatory response of PD induced by microglia by targeting RELA and regulating the activation of NF-κB signaling.

Supplementary Information: The online version contains supplementary material available at 10.1186/s41065-026-00660-3.

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

Code

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Data

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Data availability

The data used to support the findings of this study are available from the corresponding author upon request.

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, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 4 keywords, 14 MeSH terms, 52 references.

Cite

This paper

Xia, Y., Zhang, Y., Li, Y., Li, X., Wu, Y., & Yao, Q. (2026). Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling. Hereditas, 163(1), 51. https://doi.org/10.1186/s41065-026-00660-3

BibTeX

@article{xia2026cardamonin,
author = {Xia, Yezi and Zhang, Yinwei and Li, Ying and Li, Xiaojing and Wu, Yaling and Yao, Qi},
title = {{Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling}},
journal = {Hereditas},
year = {2026},
month = mar,
volume = {163},
number = {1},
pages = {51},
publisher = {BMC},
issn = {0018-0661},
doi = {10.1186/s41065-026-00660-3},
url = {https://doi.org/10.1186/s41065-026-00660-3},
pmid = {41803928},
pmcid = {PMC13085287}
}

RIS

TY - JOUR
AU - Xia, Yezi
AU - Zhang, Yinwei
AU - Li, Ying
AU - Li, Xiaojing
AU - Wu, Yaling
AU - Yao, Qi
TI - Cardamonin ameliorates neuroinflammation in Parkinson's disease by regulating NF-κB signaling
T2 - Hereditas
J2 - Hereditas
PY - 2026
DA - 2026/03/09
VL - 163
IS - 1
SP - 51
SN - 0018-0661
PB - BMC
DO - 10.1186/s41065-026-00660-3
UR - https://doi.org/10.1186/s41065-026-00660-3
LA - en
ER -

CSL-JSON

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