Evidence map›Paper›PMID 34053448›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.

Dexun Hao, Yanshuang Li, Jiang Shi, Junguang Jiang

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

  1. Review
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  5. Origin Identification ofMolecules (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
    Review
  13. Luteolin 7-Glucuronide inAntioxidants (Basel, Switzerland) · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

4 authors.

Dexun HaoDepartment of Geriatric Respiratory and Sleep, The First Affiliated Hospital of Zhengzhou University, No.1, Jianshe East Road, Erqi District, Zhengzhou, 450000, Henan Province, China.
Yanshuang LiDepartment of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jiang ShiDepartment of Geriatric Respiratory and Sleep, The First Affiliated Hospital of Zhengzhou University, No.1, Jianshe East Road, Erqi District, Zhengzhou, 450000, Henan Province, China.
Junguang JiangDepartment of Geriatric Respiratory and Sleep, The First Affiliated Hospital of Zhengzhou University, No.1, Jianshe East Road, Erqi District, Zhengzhou, 450000, Henan Province, China. jjgzzu@163.com.ORCID 0000-0002-9995-4028

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is characterized by airway obstruction and progressive lung inflammation. As the primary ingredient of a traditional Chinese medical herb, Baicalin has been previously shown to possess anti-inflammatory abilities. Thus, the current study aimed to elucidate the mechanism by which baicalin alleviates COPD.

methodsBaicalin was adopted to treat cigarette smoke in extract-exposed MLE-12 cells after which cell viability and apoptosis were determined. The production of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-8 were determined by enzyme-linked immunoassay. A COPD mouse model was constructed via exposure to cigarette smoke and lipopolysaccharide, baicalin treatment. Lung function and inflammatory cell infiltration were determined and the production of Muc5AC, TNF-α, IL-6, IL-8 in the bronchoalveolar lavage fluid (BALF) was assayed by ELISA. The effect of HSP72 and JNK on COPD following treatment with baicalin was assessed both in vivo and in vitro by conducting loss- and gain- function experiments.

resultsBaicalin improved lung function evidenced by reduction in inflammatory cell infiltration and Muc5AC, TNF-α, IL-6 and IL-8 levels observed in BALF in mice. Baicalin was further observed to elevate cell viability while inhibited apoptosis and TNF-α, IL-6 and IL-8 levels in MLE-12 cells. Baicalin treatment increased HSP72 expression, while its depletion reversed the effect of baicalin on COPD. HSP72 inhibited the activation of JNK, while JNK activation was found to inhibit the effect of baicalin on COPD.

conclusionsBaicalin upregulated the expression of HSP72, resulting in the inhibition of JNK signaling activation, which ultimately alleviates COPD.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBiomarkersBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalFlavonoidsGene Knockdown TechniquesHSP72 Heat-Shock ProteinsInflammation MediatorsLipopolysaccharidesMAP Kinase Signaling SystemMiceModels, BiologicalPulmonary Disease, Chronic ObstructiveRespiratory Function TestsAnti-Inflammatory Agents, Non-SteroidalbaicalinBiomarkersCytokinesFlavonoidsHSP72 Heat-Shock ProteinsInflammation MediatorsLipopolysaccharidesBaicalinChronic obstructive pulmonary diseasec-Jun N-terminal kinase signalingHeat shock protein 72Inflammation

Identifiers

PMID34053448
PMCPMC8165801

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Registered trials

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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.