Evidence map›Paper›PMID 36850013›Full record

ArticleBMC pharmacology & toxicology2023

Protective effects of pentoxifylline against chlorine-induced acute lung injury in rats.

Meng-Meng Liu, Jiang-Zheng Liu, Chen-Qian Zhao, Peng Guo, Zhao Wang, Hao Wu, Weihua Yu, Rui Liu, Chun-Xu Hai, Xiao-di Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2023. 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
1.4field-weighted citation impact, top 20% of its field
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, 7 citations in OpenAlex.

  1. A human airway-on-a-chip microphysiological system for modeling chlorine gas toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  2. Article
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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

10 authors at 2 institutions in 1 country.

Meng-Meng Liu *Department of Health Service, Logistics College of Chinese People's Armed Police Force, Tianjin, 300309, China. liumeng1209@126.com.ORCID 0000-0002-7790-0504
Jiang-Zheng Liu *Department of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0002-6328-6320
Chen-Qian ZhaoDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0002-8443-9429
Peng GuoDepartment of Health Service, Logistics College of Chinese People's Armed Police Force, Tianjin, 300309, China.ORCID 0000-0002-9708-0953
Zhao WangDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0001-5135-0367
Hao WuDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0003-4563-3365
Weihua YuDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0002-4048-3049
Rui LiuDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0002-4477-4353
Chun-Xu HaiDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China.ORCID 0000-0001-7179-2496
Xiao-di ZhangDepartment of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China. zhangxiaodi@fmmu.edu.cn.ORCID 0000-0003-0326-8611
Air Force Medical University · CNLogistics University of People's Armed Police Force · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChlorine is a chemical threat agent that can be harmful to humans. Inhalation of high levels of chlorine can lead to acute lung injury (ALI). Currently, there is no satisfactory treatment, and effective antidote is urgently needed. Pentoxifylline (PTX), a methylxanthine derivative and nonspecific phosphodiesterase inhibitor, is widely used for the treatment of vascular disorders. The present study was aimed to investigate the inhibitory effects of PTX on chlorine-induced ALI in rats.

methodsAdult male Sprague-Dawley rats were exposed to 400 ppm Cl

resultsThe histopathological examination demonstrated that chlorine could destroy the lung structure with hemorrhage, alveolar collapse, and inflammatory infiltration. ROS accumulation was significantly higher in the lungs of rats suffering from inhaling chlorine (P<0.05). PTX markedly reduced concentrations of MAD and GSSG, while increased GSH (P<0.05). The protein expression levels of SOD1 and CAT also decreased (P<0.05). Furthermore, the activity of LDH in rats treated with PTX was significantly decreased compared to those of non-treated group (P<0.05). Additionally, the results also showed that PTX exerted an inhibition effect on protein expressions of HIF-1α, VEGF and occludin, and increased the level of E-cadherin (P<0.05). While the up-regulation of Beclin 1, LC 3II/I, Bcl-xl, and Parkin both in the lung tissues and mitochondria, were found in PTX treated rats (P<0.05). The other protein levels were decreased when treated with PTX (P<0.05).

conclusionPTX could ameliorate chlorine-induced lung injury via inhibition effects on oxidative stress, hypoxia and autophagy, thus suggesting that PTX could serve as a potential therapeutic approach for ALI.

Indexed as

Acute Lung InjuryPentoxifyllineAdultAnimalsBeclin-1ChlorineGlutathioneGlutathione DisulfideHumansHypoxiaMaleOccludinRatsRats, Sprague-DawleyReactive Oxygen SpeciesSuperoxide Dismutase-1Beclin-1ChlorineGlutathioneGlutathione DisulfideOccludinPentoxifyllineReactive Oxygen SpeciesSuperoxide Dismutase-1Ubiquitin-Protein LigasesVascular Endothelial Growth Factor AAutophagyChlorineHypoxiaOxidative stressPentoxifylline

Identifiers

PMID36850013
PMCPMC9969370
OpenAlexW4322499763

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.