Evidence map›Paper›PMID 34362286›Full record

ArticlePharmaceutical biology2021

A metabolomic approach to elucidate the inhibitory effects of baicalin in pulmonary fibrosis.

Hong Chang, Hong-Yu Meng, Wan-Fu Bai, Qing-Gang Meng

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.2field-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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Advances in metabolic reprogramming of pulmonary fibrosis.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  3. Metabolomics and bioinformatics study of baicalin in treating pulmonary fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  4. Review
  5. Integrating Metabolomics and Network Analyses to Explore Mechanisms ofInternational journal of molecular sciences · 2025
    Article
  6. Review
  7. Review
  8. Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
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 at 3 institutions in 1 country.

Hong ChangDepartment of Pharmacy, Baotou Medical College, Baotou, China.
Hong-Yu MengNephroendocrine Department, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Wan-Fu BaiDepartment of Pharmacy, Baotou Medical College, Baotou, China.
Qing-Gang MengDepartment of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Baotou Medical College · CNBeijing University of Chinese Medicine · CNDongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextBaicalin, a major flavonoid extracted from

objectiveTo use serum metabolomics combined with biochemical and histopathological analyses to clarify anti-PF mechanisms of baicalin on metabolic pathways and the levels of potential biomarkers. MATERIALS AND

methodsForty male Sprague-Dawley rats were randomly divided into the control, PF model, prednisolone acetate-treated (4.2 mg/kg/day) and baicalin-treated (25 and 100 mg/kg/day) groups. A rat model of PF was established using a tracheal injection of bleomycin, and the respective drugs were administered intragastrically for 4 weeks. Histomorphology of lung tissue was examined after H&E and Masson's trichrome staining. Biochemical indicators including SOD, MDA and HYP were measured. Serum-metabonomic analysis based on UPLC-Q-TOF/MS was used to clarify the changes in potential biomarkers among different groups of PF rats.

resultsBoth doses of baicalin effectively alleviated bleomycin-induced pathological changes, and increased the levels of SOD (from 69.48 to 99.50 and 112.30, respectively), reduced the levels of MDA (from 10.91 to 5.0 and 7.53, respectively) and HYP (from 0.63 to 0.41 and 0.49, respectively). Forty-eight potential biomarkers associated with PF were identified. Meanwhile, the metabolic profiles and fluctuating metabolite levels were normalized or partially reversed after baicalin treatment. Furthermore, baicalin was found to improve PF potentially by the regulation of four key biomarkers involving taurine and hypotaurine metabolism, glutathione metabolism, and glycerophospholipid metabolism.

conclusionsThese findings revealed the anti-fibrotic mechanisms of baicalin and it may be considered as an effective therapy for PF.

Indexed as

AnimalsBiomarkersFlavonoidsGlutathioneGlycerophospholipidsLungMaleMetabolomicsModels, AnimalPulmonary FibrosisRatsRats, Sprague-DawleyTaurinebaicalinBiomarkersFlavonoidsGlutathioneGlycerophospholipidshypotaurineTaurinemechanism researchserum metabolomicsTraditional Chinese medicineUPLC-QTOF/MS

Identifiers

PMID34362286
PMCPMC8354164
OpenAlexW3189053890

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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.