Evidence map›Paper›PMID 41775324›Full record

ArticleJournal of advanced research2026

Lacticaseibacillus paracasei 36 attenuates D-GalN/LPS-induced acute liver injury in mice via suppressing the TLR4/NF-κB/MAPK pathway and NLRP3 inflammasome activation through modulating the intestinal microbiota.

Fei Wang, Lianchi Wu, Xiang Li, Yunzhen Yao, Aikun Fu, Hua Yang, Yingping Xiao, Weifen Li

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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. The Role ofInternational journal of molecular sciences · 2026
    Review
  3. Nutrients · 2026
    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

8 authors.

Fei WangKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China; State Key Laboratory for Quality and Safety of Agro-Products, Institute of Agro-Product Safety and Nutrition, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China.
Lianchi WuKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Xiang LiKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Yunzhen YaoKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Aikun FuKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Hua YangState Key Laboratory for Quality and Safety of Agro-Products, Institute of Agro-Product Safety and Nutrition, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China. Electronic address: yanghua@zaas.ac.cn.
Yingping XiaoState Key Laboratory for Quality and Safety of Agro-Products, Institute of Agro-Product Safety and Nutrition, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China. Electronic address: xiaoyp@zaas.ac.cn.
Weifen LiKey Laboratory of Animal Molecular Nutrition of Education of Ministry, Zhejiang Key Laboratory of Nutrition and Breeding for High-Quality Animal Products, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China. Electronic address: wfli@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAcute liver injury (ALI) is a severe clinical syndrome with high mortality, often triggered by toxins, viruses, or immune-mediated injury. The gut-liver axis serves as a key mediator in the progression of hepatic disorders, and probiotics are considered viable treatment options owing to their impact on modulating intestinal microbiota, reducing inflammation, and alleviating oxidative stress.

objectivesThis study was designed to elucidate the hepatoprotective mechanisms of L. paracasei 36 against D-GalN/LPS-induced ALI in mice, with a specific focus on its roles in inflammation, oxidative stress, apoptosis, and intestinal microbiota regulation.

methodsThe mice were pretreated with L. paracasei 36 for three weeks prior to the D-GalN/LPS challenge. Serum biomarkers, oxidative damage indicators, inflammatory cytokines, and apoptosis-related genes were measured. Intestinal microbiota composition was analyzed via 16S rRNA sequencing, and hepatic transcriptomics and metabolomics were performed to identify key pathways and metabolites.

resultsL. paracasei 36 pretreatment significantly reduced serum AST, ALT, and TBil levels, alleviated histopathological damage, and decreased oxidative stress and inflammatory cytokine production. It inhibited hepatocyte apoptosis by modulating Bcl-2/Bax expression and suppressed NLRP3 inflammasome activation. L. paracasei 36 restored intestinal microbiota balance, increasing beneficial genera (Ligilactobacillus, Akkermansia) and reducing harmful ones (Alistipes, Parasutterella). Multi-omics analysis revealed suppression of NF-κB/MAPK pathways along with an increase in hepatoprotective metabolites like berberine and flavin nucleotides.

conclusionL. paracasei 36 exerts potent hepatoprotective effects against D-GalN/LPS-induced ALI by mitigating inflammation, oxidative damage, and apoptosis, and by restoring intestinal microbiota homeostasis. Collectively, these results suggest that L. paracasei 36 represents a potential therapeutic strategy for ALI.

Indexed as

Chemical and Drug Induced Liver InjuryGastrointestinal MicrobiomeInflammasomesLacticaseibacillus paracaseiNLR Family, Pyrin Domain-Containing 3 ProteinProbioticsAnimalsApoptosisDisease Models, AnimalGalactosamineLipopolysaccharidesLiverMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLGalactosamineInflammasomesLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTlr4 protein, mouseToll-Like Receptor 4Acute liver injuryIntestinal microbiotaLacticaseibacillus paracasei 36NF-κB/MAPK signaling pathwayNLRP3 inflammasome

Identifiers

PMID41775324
PMCPMC13227168

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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 OpenQuestion graph.