Evidence map›Paper›PMID 28533545›Full record

ArticleScientific reports2017

Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress.

Haiyan Chu, Ying Shi, Shuai Jiang, Qicheng Zhong, Yongqiang Zhao, Qingmei Liu, Yanyun Ma, Xiangguang Shi, Weifeng Ding, Xiaodong Zhou and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 39 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

14 authors at 5 institutions in 2 countries.

Haiyan ChuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Ying ShiDepartment of Rheumatology and Immunology, Yiling Affiliated Hospital of Hebei Medical University, Shijiazhuang, 050091, China.
Shuai JiangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Qicheng ZhongDepartment of Rheumatology and Immunology, Yiling Affiliated Hospital of Hebei Medical University, Shijiazhuang, 050091, China.
Yongqiang ZhaoDepartment of Rheumatology and Immunology, Yiling Affiliated Hospital of Hebei Medical University, Shijiazhuang, 050091, China.
Qingmei LiuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Yanyun MaState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Xiangguang ShiState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Weifeng DingState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Xiaodong ZhouUniversity of Texas Health Science Center at Houston, 6431 Fannin St., Houston, Texas, 77030, USA.
Jimin CuiDepartment of Rheumatology and Immunology, Yiling Affiliated Hospital of Hebei Medical University, Shijiazhuang, 050091, China.
Li JinState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China.
Gang GuoDepartment of Rheumatology and Immunology, Yiling Affiliated Hospital of Hebei Medical University, Shijiazhuang, 050091, China. chenxiangmahuang@163.com.
Jiucun WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, P. R. China. jcwang@fudan.edu.cn.
Fudan University · CNHebei Medical University · CNState Key Laboratory of Genetic EngineeringHebei Yiling Hospital · CNThe University of Texas Health Science Center at Houston · US

Funding

Studies of HLA Region Genomics in Systemic Sclerosis and Ankylosing SpondyilitisU01AI090909 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN, REVEILLE, JOHN DUFFIN · 2010 to 2014
$2.9M
NIAID NIH HHS U01 AI090909
6 · The paper itself

Abstract

Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonary fibrosis. We found that regardless of the prophylactic or therapeutic treatment, Shenks was able to attenuate BLM-induced-fibrosis in mice, down regulate extracellular matrix genes expression, and reduce collagen production. The aberrantly high Smad3 phosphorylation levels and SBE activity in TGF-β-induced fibroblasts were dramatically decreased as a result of Shenks treatment. At the same time, Shenks was able to increase the expression of antioxidant-related genes, including Gclc and Ec-sod, while reduce the transcription levels of oxidative-related genes, such as Rac1 and Nox4 demonstrated by both in vivo and in vitro studies. Further investigations found that Shenks could decrease the oxidative productions of protein (3-nitrotyrosine) and lipid (malondialdehyde) and increase GSH content both in bleomycin treated mouse lungs and TGF-β stimulated fibroblasts, as well as inhibit the production of ROS stimulated by TGF-β to fight against oxidative stress. Overall, Shenks inhibited fibrosis by blocking TGF-β pathway and modulating the oxidant/antioxidant balance.

Indexed as

Medicine, Chinese TraditionalAnimalsAntibiotics, AntineoplasticBiomarkersBleomycinCells, CulturedCollagenDisease Models, AnimalFemaleFibroblastsGene Expression RegulationMiceOxidation-ReductionOxidative StressPhosphorylationPromoter Regions, GeneticAntibiotics, AntineoplasticBiomarkersBleomycinCollagenReactive Oxygen SpeciesSmad3 ProteinTransforming Growth Factor beta

Identifiers

PMID28533545
PMCPMC5440393
OpenAlexW2615477088

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.