Evidence map›Paper›PMID 39339707›Full record

ArticleNutrients2024

Hesperetin Attenuates T-2 Toxin-Induced Chondrocyte Injury by Inhibiting the p38 MAPK Signaling Pathway.

Chunqing Lu, Wenjing Yang, Fang Chu, Sheng Wang, Yi Ji, Zhipeng Liu, Hao Yu, Shaoxiao Qin, Dianjun Sun, Zhe Jiao and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

11 authors.

Chunqing LuInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Wenjing YangInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Fang ChuInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Sheng WangInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Yi JiHeilongjiang Provincial Key Laboratory of Trace Elements and Human Health & Key Laboratory of Etiology and Epidemiology, Education Bureau of Heilongjiang Province, Harbin Medical University, Harbin 150081, China.
Zhipeng LiuInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Hao YuInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Shaoxiao QinInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.
Dianjun SunInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.ORCID 0000-0003-1701-4305
Zhe JiaoHeilongjiang Provincial Key Laboratory of Trace Elements and Human Health & Key Laboratory of Etiology and Epidemiology, Education Bureau of Heilongjiang Province, Harbin Medical University, Harbin 150081, China.
Hongna SunInstitute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, National Health Commission Key Laboratory of Etiology and Epidemiology, Harbin Medical University, Harbin 150081, China.

Funding

Opening Foundation of NHC Key Laboratory of Etiology and Epidemiology（Harbin Medical University) NHCKLEE20230913
6 · The paper itself

Abstract

backgroundHesperetin, a flavonoid derived from citrus fruits, exhibits potent antioxidant and anti-inflammatory activities and has been implicated in cartilage protection. However, its effectiveness against T-2 toxin-induced knee cartilage damage remains unclear.

methodsIn this study, high-throughput sequencing analysis was employed to identify the key signaling pathways involved in T-2 toxin-induced articular cartilage damage in rats. Animal models were divided into the following groups: control, low-dose T-2 toxin, high-dose T-2 toxin, T-2 toxin + hesperetin, hesperetin, and vehicle. Pathological staining and immunohistochemistry were used to assess pathological changes, as well as the expression levels of the cartilage matrix-related proteins MMP13 and collagen II, along with the activation of the p38 MAPK signaling pathway. Additionally, primary rat chondrocytes were cultured to establish an in vitro model for investigating the underlying mechanism.

resultsHigh-throughput sequencing analysis revealed the involvement of the MAPK signaling pathway in T-2 toxin-induced articular cartilage damage in rats. Hesperetin intervention in T-2 toxin-exposed rats attenuated pathological cartilage damage. Immunohistochemistry results demonstrated a significant reduction in collagen II protein expression in the high-dose T-2 toxin group (

conclusionsT-2 toxin activates the p38 MAPK signaling pathway, causing knee cartilage damage in rats. Treatment with hesperetin inhibits the p38/MEF2C signaling axis, regulates collagen II and MMP13 protein expression, and reduces cartilage injury significantly.

Indexed as

Cartilage, ArticularChondrocytesHesperidinp38 Mitogen-Activated Protein KinasesT-2 ToxinAnimalsCells, CulturedCollagen Type IIDisease Models, AnimalMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 13RatsRats, Sprague-DawleySignal TransductionCollagen Type IIhesperetinHesperidinMatrix Metalloproteinase 13p38 Mitogen-Activated Protein KinasesT-2 ToxincartilagehesperetinKashin–Beck diseaseT-2 toxin

Identifiers

PMID39339707
PMCPMC11434908

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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 OpenQuestion graph.