Evidence map›Paper›PMID 31379467›Full record

ArticleMediators of inflammation2019

Dihydrotanshinone I Alleviates Crystalline Silica-Induced Pulmonary Inflammation by Regulation of the Th Immune Response and Inhibition of STAT1/STAT3.

Yiting Zhang, Chao Li, Siyi Li, Yiping Lu, Sitong Du, Xinning Zeng, Xi Chen, Jie Chen

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 31% 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, 22 citations in OpenAlex.

  1. Article
  2. CD4Frontiers in immunology · 2025
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  13. The Journal of international medical research · 2020
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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 1 institution in 1 country.

Yiting ZhangDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0003-0672-4811
Chao LiDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0001-5723-1414
Siyi LiDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0003-4916-8253
Yiping LuDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.
Sitong DuDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0003-1033-1535
Xinning ZengDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0001-8471-8084
Xi ChenDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0002-2524-1068
Jie ChenDivision of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0002-5183-4852
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Occupational exposure to crystalline silica (CS) results in a persistent pulmonary inflammatory response that eventually leads to abnormal tissue repair, disability, and death. The inflammatory-immune responses occur in the early stages of CS exposure, and both innate and adaptive immunity are involved. CD4+ T cells play a pivotal role in the pathogenesis of CS-induced pulmonary disease, which has no proven curative therapy. Dihydrotanshinone I (DHI), a natural product isolated from Salvia miltiorrhiza Bunge (Danshen), has anti-inflammatory and immunomodulatory properties. However, whether DHI has a protective effect on CS-induced lung disease, how it influences the Th immune response, and the potential underlying molecular mechanism(s) have not been fully clarified. In this study, DHI treatment of CS-exposed mice reduced the expression of proinflammatory cytokines and the infiltration of immune cells. It significantly ameliorated CS-induced pulmonary inflammation by attenuating T helper (Th)1 and Th17 responses, which were tightly related to the inhibition of STAT1 and STAT3. DHI significantly altered Th2 cytokines but not the Th2 nuclear transcription factor. Furthermore, our study found that DHI treatment also affected regulatory T cell activity in CS-injured mice. Taken together, our findings indicated that DHI could modulate Th responses and alleviate CS-induced pulmonary inflammation, suggesting a novel application of DHI in CS-induced pulmonary disease.

Indexed as

AnimalsBronchoalveolar Lavage FluidFemaleFlow CytometryLymph NodesMiceMice, Inbred C57BLPneumoniaSilicon DioxideSTAT1 Transcription FactorSTAT3 Transcription FactorSilicon DioxideSTAT1 Transcription FactorSTAT3 Transcription Factor

Identifiers

PMID31379467
PMCPMC6652093
OpenAlexW2956775005

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.