Evidence map›Paper›PMID 39563345›Full record

ArticleRespiratory research2024

Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking.

Juanjuan Xiong, Li Xie, YiRan Huang, JiaHui Zhu, ZhiYan Hong, HaoYun Qian, Jingjing Liu

Abstract read
In one paragraph

Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

  1. Pooled it
  2. Melatonin in lung cancer: integrating molecular mechanisms, tumor microenvironment regulation, apoptotic signaling, and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Ambient PMBMC public health · 2026
    Article
  4. Article
  5. Article
  6. 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

7 authors.

Juanjuan XiongCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China. xjuan@jit.edu.cn.
Li XieCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.
YiRan HuangCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.
JiaHui ZhuCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.
ZhiYan HongCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.
HaoYun QianCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.
Jingjing LiuCollege of Animal Science and Food Engineering, Jinling Institute of Technology, Qixia, Nanjing, 210046, China.

Funding

High-level talent research project at Jinling Institute of Technology jit-6-202122High-level talent research project at Jinling Institute of Technology jit-6-202123Jinling Institute of Technology's 'Maker' Virtual Class Construction Project 2023006
6 · The paper itself

Abstract

backgroundPassive smoke has a significant impact on lung function and constitutes a critical public health issue, as smoking generates free radicals that damage the lungs and other tissues. Currently, limited research exists on whether the antioxidant melatonin can mitigate lung damage caused by smoking. This study aims to investigate the mechanisms through which melatonin alleviates acute lung disease induced by passive smoking.

methodsRats were divided into five groups (n = 6): a control group and three groups exposed to low, medium, and high concentrations of smoke, and a melatonin treatment group.

resultsData indicated that in the high concentration passive smoking group, the alveolar structure of the lung tissue was destroyed, and the total antioxidant capacity in lung tissue diminished as the concentration of smoke increased. The expressions of TNF-α, IL-6, and IL-1β exhibited similar results. The anti-apoptotic factors Bcl-2 and Bcl-xL mRNA level significantly decreased in the high concentration smoking group, while no significant changes were observed in the medium and low concentration groups. Conversely, the high concentration passive smoking increased the pro-apoptotic factors Bax and Caspase-3 mRNA levels. Additionally, endogenous melatonin levels in lung tissue gradually decreased following exposure to smoke, whereas the exogenous melatonin alleviated the changes in inflammatory factors and apoptosis-related factors in lung tissue. Furthermore, at high smoking concentrations, the mRNA levels of lung cancer-related genes vascular endothelial growth factor (VEGF), cytochromeP450 1A1 (CYP1A1), and cytochrome P450 1B1 (CYP1B1) were significantly increased, while exogenous melatonin reduced the expression of these genes in lung tissue.

conclusionsThese findings suggest that melatonin can diminish lung tissue damage, apoptosis, and inflammatory responses induced by passive smoking, as well as decrease the expression of lung cancer-related genes. Further experimental investigations involving exogenous melatonin treatments will be needed.

Indexed as

AntioxidantsLungMelatoninRats, Sprague-DawleyTobacco Smoke PollutionAnimalsApoptosisMaleRatsAntioxidantsMelatoninTobacco Smoke PollutionLungMelatoninOxidative stressPassive smoking

Identifiers

PMID39563345
PMCPMC11577718

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.