Evidence map›Paper›PMID 41253270›Full record

ArticleJournal of advanced research2026

Lactoferrin alleviates non-alcoholic steatohepatitis via remodeling gut microbiota to regulate serotonin-related pathways.

Li Ding, Jia-Ying Xu, Li-Li Zhang, Yan Liu, Kai-Tian Gu, Yan-Zi Liang, Khemayanto Hidayat, Zhongxiao Wan, Guo-Chong Chen, Li-Qiang Qin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. 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. Review
  2. Review
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

10 authors.

Li DingSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Jia-Ying XuState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Li-Li ZhangSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Yan LiuSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Kai-Tian GuSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Yan-Zi LiangSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Khemayanto HidayatSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Zhongxiao WanSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Guo-Chong ChenSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China; MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China.
Li-Qiang QinSchool of Public Health, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China; MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China. Electronic address: qinligiang@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLactoferrin (LF), a multifunctional glycoprotein, has been implicated in the regulation of glucose and lipid metabolism. OBJECTIVES AND

methodsThis study employed in vivo and in vitro models to investigate the direct effects of LF on non-alcoholic steatohepatitis (NASH) and to elucidate its underlying mechanisms.

resultsLF intervention alleviated hepatic lipid metabolic disorders and liver injury in high-fat, high-cholesterol cholate-containing diet (HFCCD)-fed mice by mitigating oxidative stress, suppressing the inflammatory cGAS/STING pathway, and reducing M1 proinflammatory macrophage polarization. These effects were validated in free fatty acid (FFA)-treated HepG2 cells and AML12 cells. Furthermore, LF ameliorated HFCCD-induced gut microbiota dysbiosis and increased short-chain fatty acid levels. The critical role of gut microbiota in mediating the hepatoprotective effects of LF was confirmed through antibiotic-induced microbiome depletion and fecal microbiota transplantation. Mechanistically, LF modulated gut-liver serotonin signaling and promoted fatty acid β-oxidation through the HTR2A-PPARα-CPT-1A pathway, an effect abolished by the HTR2A agonist DOI. In a co-culture system, LF treatment of the Caco-2/HT29 monolayer alleviated lipid accumulation and regulated the HTR2A-PPARα-CPT-1A pathway in FFA-treated HepG2 cells.

conclusionsThese findings indicate that LF attenuates NASH by remodeling gut microbiota to modulate microbiota-derived serotonin signaling and enhance fatty acid oxidation.

Indexed as

Gastrointestinal MicrobiomeLactoferrinNon-alcoholic Fatty Liver DiseaseSerotoninAnimalsDiet, High-FatDisease Models, AnimalHep G2 CellsHumansLipid MetabolismLiverMaleMiceMice, Inbred C57BLOxidative StressSignal TransductionLactoferrinSerotonincGAS/STINGGut microbiotaLactoferrinNon-alcoholic steatohepatitisserotonin receptor 2A

Identifiers

PMID41253270
PMCPMC13453864

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.