Evidence map›Paper›PMID 32293377›Full record

ArticleBMC pulmonary medicine2020

The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study.

Jianqing Su, Jian Li, Yufan Lu, Ning Li, Peijun Li, Zhengrong Wang, Weibing Wu, Xiaodan Liu

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Jianqing SuDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Jian LiDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Yufan LuDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Ning LiDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Peijun LiDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Zhengrong WangDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China.
Weibing WuDepartment of Sports Medicine, Shanghai University of Sport, Shanghai, 200438, China. wwb75@126.com.ORCID http://orcid.org/0000-0003-0609-7889
Xiaodan LiuSchool of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Shanghai University of Sport · CNShanghai University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81902307
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) skeletal muscle dysfunction is a prevalent malady that significantly affects patients' prognosis and quality of life. Although the study of this disease has attracted considerable attention, a definite animal model is yet to be established. This study investigates whether smoke exposure could lead to the development of a COPD skeletal muscle dysfunction model in rats.

methodsSprague Dawley rats were randomly divided into model (MG, n = 8) and control groups (CG, n = 6). The MG was exposed to cigarette smoke for 16 weeks while the CG was not. The body weight and forelimb grip strength of rats were monitored monthly. The pulmonary function and the strength of tibialis anterior muscle were assessed in vitro and compared after establishing the model. The histological changes in lung and gastrocnemius muscles were observed. The expressions of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α were detected by ELISA, while the expressions of Atrogin-1 and MuRF1 in the gastrocnemius muscle were determined by Western blotting.

resultsSmoke exposure slowly increases the body weight and forelimb grip strength of MG rats, compared to CG rats. However, it significantly decreases the pulmonary ventilation function and the skeletal muscle contractility of the MG in vitro. Histologically, the lung tissues of MG show typical pathological manifestations of emphysema, while the skeletal muscles present muscular atrophy. The expressions of IL-6, IL-8, and TNF-α in MG rats are significantly higher than those measured in CG rats. Increased levels of Atrogin-1 and MuRF1 were also detected in the gastrocnemius muscle tissue of MG.

conclusionProgressive smoking exposure decreases the contractile function of skeletal muscles, leading to muscular atrophy. It also increases the expressions of inflammatory and muscle protein degradation factors in COPD rats. This indicates that smoke exposure could be used to establish a COPD skeletal muscle dysfunction model in rats.

Indexed as

AnimalsCigarette SmokingDisease Models, AnimalInterleukin-6Interleukin-8LungMaleMuscle ContractionMuscle ProteinsMuscle, SkeletalMuscular AtrophyPilot ProjectsPulmonary Disease, Chronic ObstructivePulmonary EmphysemaRatsRats, Sprague-DawleyInterleukin-6Interleukin-8Muscle ProteinsTumor Necrosis Factor-alphaChronic obstructive pulmonary diseaseModeling methods,a pilot studySkeletal muscle dysfunction

Identifiers

PMID32293377
PMCPMC7092612
OpenAlexW3013888409

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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.