Evidence map›Paper›PMID 25973011›Full record

ArticleInternational journal of clinical and experimental pathology2015

Dihydroartemisinin supresses inflammation and fibrosis in bleomycine-induced pulmonary fibrosis in rats.

Dongxia Yang, Wendan Yuan, Changjun Lv, Naie Li, Tongshen Liu, Liang Wang, Yufei Sun, Xueshan Qiu, Qiang Fu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 45 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

9 authors at 3 institutions in 1 country.

Dongxia YangCollege of Basic Medicine, China Medical University China ; College of Basic Medicine, Binzhou Medical University China.
Wendan YuanCollege of Basic Medicine, Binzhou Medical University China.
Changjun LvCollege of Basic Medicine, Binzhou Medical University China.
Naie LiCollege of Basic Medicine, Binzhou Medical University China.
Tongshen LiuCollege of Basic Medicine, Binzhou Medical University China.
Liang WangCollege of Basic Medicine, Binzhou Medical University China.
Yufei SunCollege of Basic Medicine, Binzhou Medical University China.
Xueshan QiuCollege of Basic Medicine, China Medical University China.
Qiang FuCollege of Basic Medicine, Binzhou Medical University China.
Binzhou Medical University · CNBinzhou University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is a respiratory disease with a high mortality rate and its pathogenesis involves multiple mechanisms including epithelial cell injury, fibroblast proliferation, inflammation, and collagen coagulation. The treatment regimens still fail to recover this disease. We have previously found that dihydroartemisinin inhibits the development of pulmonary fibrosis in rats. This study aimed to determine the mechanisms of dihydroartemisinin in bleomycin-induced pulmonary fibrosis. The experimental rats were divided into six groups as normal saline control group (NS group), bleomycin group (BLM group), dihydroartemisinin-1, -2, or -3 group (DHA-1, DHA-2 and DHA-3 group) and dexamethasone group (DXM group). In BLM group, rats were treated with intratracheal instillation of bleomycin. NS group received the same volume of saline instead of bleomycin. In DHA-1, DHA-2 and DHA-3 group, in addition to intratracheal instillation of bleomycin, respectively, dihydroartemisinin (25 mg/kg, 50 mg/kg, 100 mg/kg daily) was administrated by intraperitoneal instillation. In DXM group, rats were treated with intraperitoneal instillation of dexamethasone as control. Immunocytochemical assay, reverse transcription PCR and western blot were used for detecting the expression of TGF-β1, TNF-α, α-SMA and NF-κB in lung tissues. What's more, morphological change and collagen deposition were analyzed by hematoxylin-eosin staining and Masson staining. Collagen synthesis was detected by hydroxyproline chromatometry. Results showed that dihydroartemisinin significantly decreased the amount of inflammatory cytokines and collagen synthesis, and inhibited fibroblast proliferation in bleomycin-induced pulmonary fibrosis (P < 0.001). This study provides experimental evidence that dihydroartemisinin could decrease cytokines, alveolar inflammation and attenuates lung injury and fibrosis.

Indexed as

ActinsAnimalsArtemisininsBleomycinFibrosisInflammationMaleNF-kappa BPulmonary FibrosisRatsRats, Sprague-DawleyTransforming Growth Factor beta1Tumor Necrosis Factor-alphaActa2 protein, ratActinsArtemisininsartenimolBleomycinNF-kappa BTransforming Growth Factor beta1Tumor Necrosis Factor-alphableomycincollagenDihydroartemisininpulmonary fibrosisrats

Identifiers

PMID25973011
PMCPMC4396330
OpenAlexW2417326320

What OpenQuestion holds

Textmetadata
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.