Evidence map›Paper›PMID 40819082›Full record

ArticleHereditas2025

β-Nicotinamide mononucleotide alleviates Alcohol-Induced liver injury in a mouse model through activation of NAD

Xinxin Yang, Endian Zheng, Yuxian Lin, Haoyue Sun, Ji Zhang, Yingcong Yu

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PubMed Full text at PMC Publisher
In one paragraph

Article in Hereditas, 2025. 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

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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
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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

6 authors.

Xinxin YangDepartment of Infectious Diseases, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, The Third Affiliated Hospital of Shanghai University, Wenzhou People's Hospital, Wenzhou, 325000, Zhejiang, China.
Endian ZhengDepartment of Gastroenterology, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, The Third Affiliated Hospital of Shanghai University, Wenzhou People's Hospital, Wenzhou, 325000, Zhejiang, China.
Yuxian LinDepartment of Pharmacy, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, The Third Affiliated Hospital of Shanghai University, Wenzhou People's Hospital, Wenzhou, 325000, Zhejiang, China.
Haoyue SunDepartment of Gastroenterology, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, The Third Affiliated Hospital of Shanghai University, Wenzhou People's Hospital, Wenzhou, 325000, Zhejiang, China.
Ji ZhangSchool of Medicine, Shanghai University, Shanghai, 200000, Shanghai, China.
Yingcong YuDepartment of Gastroenterology, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, The Third Affiliated Hospital of Shanghai University, Wenzhou People's Hospital, Wenzhou, 325000, Zhejiang, China. yuyingcong_yyc@126.com.

Funding

the "Pioneer" and "Leading Goose" R&D Program of Zhejiang No. 2022C03145
6 · The paper itself

Abstract

backgroundAlcoholism is a significant contributor to the development of alcoholic liver disease, for which no universally accepted and effective treatment currently exists. A precursor of NAD

methodsThe objective of this study was to assess the protective effects of NMN and elucidate its potential mechanisms using a mouse model subjected to chronic and binge ethanol feeding. Eight-week-old C57BL/6J mice were randomly assigned to one of four groups (n = 10 per group): control (CTRL), ethanol (EtOH), ethanol with low-dose NMN (EtOH + NMN(L)), and ethanol with high-dose NMN (EtOH + NMN(H)). Following the completion of the experimental protocol, the mice were euthanized at designated time points, and blood, liver, and ileum tissues were collected for analysis of relevant biomarkers.

resultsCompared to the CTRL group, the EtOH group demonstrated increased liver specific gravity and elevated blood ALT levels. Administration of NMN improved histopathological changes in the liver and ileum of the mice. NMN significantly counteracted the ethanol-induced elevation in liver MDA levels and restored the diminished glutathione (GSH) and superoxide dismutase (SOD) activity levels caused by ethanol exposure. Additionally, NMN inhibited the ethanol-induced expression of cytochrome P450 2E1 (CYP2E1). It also reduced the release of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β, which were triggered by ethanol exposure, improved energy homeostasis in the ileum, and reversed the downregulation of mRNA and protein expression of key tight junction proteins in the ileum, specifically ZO-1, Claudin-1, and Occludin, thereby restoring their functional integrity. Furthermore, NMN activated the NAD

conclusionNMN supplementation provides protection against alcoholic liver injury in a mouse model, potentially through the upregulation of the cellular NAD

Indexed as

Liver Diseases, AlcoholicNADNicotinamide MononucleotideSignal TransductionSirtuin 1AnimalsCytochrome P-450 CYP2E1Disease Models, AnimalEthanolLiverMaleMiceMice, Inbred C57BLOxidative StressCytochrome P-450 CYP2E1EthanolNADNicotinamide MononucleotideSirt1 protein, mouseSirtuin 1Alcoholic hepatic injuryInflammationIntestinal permeabilityOxidative stressSilent information regulator 1Β-nicotinamide mononucleotide

Identifiers

PMID40819082
PMCPMC12357478

What Socratic holds

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LicenceCC BY
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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 Socratic graph.