Evidence map›Paper›PMID 40206944›Full record

ArticleFrontiers in nutrition2025

Luteolin attenuates LPS-induced damage in IPEC-J2 cells by enhancing mitophagy via AMPK signaling pathway activation.

Jianyun Yuan, Ke Zhang, Lingling Yang, Xinyi Cheng, Jinyan Chen, Xiaoquan Guo, Huabin Cao, Caiying Zhang, Chenghong Xing, Guoliang Hu and 1 more

Abstract read
In one paragraph

Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Assessing theAntioxidants (Basel, Switzerland) · 2026
    Article
  3. Article
  4. Frontiers in nutrition · 2025
    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.

Jianyun Yuan *Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Ke Zhang *Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Lingling YangJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Xinyi ChengJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Jinyan ChenJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Xiaoquan GuoJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Huabin CaoJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Caiying ZhangJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Chenghong XingJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Guoliang HuJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Yu ZhuangJiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Luteolin (LUT), a flavonoid compound widely present in natural plants, has been extensively studied for its diverse biological properties, involving anti-inflammatory,antioxidant, anti-apoptosis and other properties. Methods: The aim of this study was to investigate the effect of LUT on lipopolysaccharide (LPS)-induced Intestinal Porcine Epithelial Cell line-J2 (IPEC-J2 cells) damage and its underlying mechanism. Results: The experiment showed that LPS treatment induced injury in IPEC-J2 cells, leading to tight junction disruption, ROS accumulation, and cell apoptosis. Remarkably, LUT attenuated LPS-induced IPEC-J2 cells damage by the up-regulation of Zonula Occludens-1(ZO-1), Occludin, and Claudin protein 1 (Claudin-1) protein expression levels.Besides, LUT increased the activities of CAT, and SOD and prevented LPS-induced MDA and ROS production. LUT suppressed Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation in LPS-induced IPEC-J2 cells, reducing (Interleukin-1beta) IL-1β and Interleukin-6 (IL-6) expression. Moreover, LUT attenuated LPS-induced apoptosis in IPEC-J2 cells by up-regulating expression of B-cell lymphoma 2 (Bcl-2) and down-regulating expression of Cysteine-aspartic acid protease 3 (Caspase-3), Cysteine - aspartic acid protease 9 (Caspase-9) and Bcl-2-associated X protein (Bax). Furthermore, LUT upregulated the AMP-activated protein kinase (AMPK)/Unc-51 like autophagy activating kinase (ULK) signaling pathway and Parkin-RBR E3 ubiquitin protein ligase (Parkin)/PTEN induced putative kinase 1 (PINK1)-mediated mitophagy in a dose-dependent manner. When AMPK was knocked down by short-hairpin RNA (shRNA), the protective effects of LUT against LPS-induced IPEC-J2 cell damage were weakened, as evidenced by the accumulation of excessive ROS and impaired mitophagy. Conclusion: In summary, LUT exhibits the ability to protect against LPS-induced damage to intestinal tight junctions by enhancing mitophagy through AMPK activation.

Indexed as

AMPKIPEC-J2 cellslipopolysaccharideluteolinmitophagy

Identifiers

PMID40206944
PMCPMC11978636

What OpenQuestion holds

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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.