Evidence map›Paper›PMID 41745802›Full record

ArticleToxics2026

Combining Network Pharmacology and Experimental Verification to Investigate the Protective Effect of Melatonin on Fluoride-Induced Brain Injury.

Runjiang Ma, Chun Wang, Wenqi Qin, Yajie Li, Meng Zhang, Yongkang Liang, Lu Wang, Suya Wang, Gaoxuan Xie, Qiang Niu

Abstract read
In one paragraph

Article in Toxics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Runjiang MaSchool of Public Health, Shihezi University, Shihezi 832000, China.
Chun WangSchool of Public Health, Shihezi University, Shihezi 832000, China.
Wenqi QinSchool of Public Health, Shihezi University, Shihezi 832000, China.
Yajie LiSchool of Public Health, Shihezi University, Shihezi 832000, China.
Meng ZhangSchool of Public Health, Shihezi University, Shihezi 832000, China.
Yongkang LiangSchool of Public Health, Shihezi University, Shihezi 832000, China.
Lu WangSchool of Public Health, Shihezi University, Shihezi 832000, China.
Suya WangSchool of Public Health, Shihezi University, Shihezi 832000, China.
Gaoxuan XieSchool of Public Health, Shihezi University, Shihezi 832000, China.
Qiang NiuSchool of Public Health, Shihezi University, Shihezi 832000, China.ORCID 0009-0002-3465-9789

Funding

Niu Qiang the Science and Technology Program of XPCC (Grant Nos. 2025DB010 and 2024ZD025), the grants from the National Natural Science Foundation of China (Grant No. 82360671), the Shihezi University International Science and Technology Cooperation Promotion Progr
6 · The paper itself

Abstract

Excessive fluoride exposure induces developmental neurotoxicity, but effective preventive strategies are currently scarce. Melatonin (Mel), a lipophilic hormone secreted by the pineal gland, exerts antioxidant, anti-inflammatory, and neuroprotective properties. This study aimed to explore Mel's protective effect and mechanism against fluoride-induced developmental brain injury. We employed a network pharmacology approach to screen the common targets of Mel and fluoride-induced brain injury and performed enrichment analysis. A total of 189 common targets were identified, and these targets were mainly enriched in the HIF-1 signaling pathway and oxidative stress-related pathways. In vivo, Sprague Dawley rats were subjected to perinatal sodium fluoride (NaF) exposure with/without Mel; in vitro, HT22 cells were subjected to NaF and/or Mel. The results showed that Mel improved cognitive impairments and alleviated structural damage to hippocampal neurons and mitochondria. Furthermore, Mel upregulated SIRT3 and downregulated HIF-1α, thereby restoring mitochondrial oxidative phosphorylation and ATP content. This study demonstrates that Mel alleviates fluoride-induced developmental neurotoxicity by improving mitochondrial function through regulating the SIRT3/HIF-1α signaling pathway. This not only offers a novel perspective for elucidating the underlying molecular mechanisms of fluoride-induced developmental neurotoxicity but also provides a theoretical foundation for Mel as a potential protective candidate against fluoride exposure.

Indexed as

energy metabolismmelatoninnetwork pharmacologyneurotoxicitySIRT3/HIF-1αsodium fluoride

Identifiers

PMID41745802
PMCPMC12944959

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.