Evidence map›Paper›PMID 37138582›Full record

ArticleDrug design, development and therapy2023

Integrating Network Pharmacology and Experimental Validation to Explore the Pharmacological Mechanism of Astragaloside IV in Treating Bleomycin-Induced Pulmonary Fibrosis.

Su Yuan, Biao Zuo, Si-Cong Zhou, Meng Wang, Kai-Yue Tan, Zhi-Wei Chen, Wen-Fu Cao

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  11. Frontiers in pharmacology · 2025
    Article
  12. Article
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  14. The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023
    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

7 authors at 2 institutions in 1 country.

Su YuanDepartment of Combination of Chinese and Western Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Biao ZuoChongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Cure of Metabolic Diseases, Chongqing, People's Republic of China.
Si-Cong ZhouDepartment of Combination of Chinese and Western Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Meng WangChongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Cure of Metabolic Diseases, Chongqing, People's Republic of China.
Kai-Yue TanChongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Cure of Metabolic Diseases, Chongqing, People's Republic of China.
Zhi-Wei ChenChongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Cure of Metabolic Diseases, Chongqing, People's Republic of China.
Wen-Fu CaoDepartment of Combination of Chinese and Western Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
First People's Hospital of Chongqing · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Our study aims to reveal the pharmacological mechanism of Astragaloside IV in the treatment of pulmonary fibrosis(PF) through network pharmacology and experimental validation. Methods: We first determined the in vivo anti-pulmonary fibrosis effect of Astragaloside IV by HE, MASSON staining, and lung coefficients, then used network pharmacology to predict the signaling pathways and molecularly docked key pathway proteins, and finally validated the results by in vivo and in vitro experiments. Results: In in vivo experiments, we found that Astragaloside IV improved body weight (P < 0.05), increased lung coefficients (P < 0.05), and reduced lung inflammation and collagen deposition in mice with pulmonary fibrosis. The network pharmacology results showed that Astragaloside IV had 104 cross-targets with idiopathic pulmonary fibrosis, and the results of KEGG enrichment analysis indicated that cellular senescence could be an important pathway for Astragaloside IV in the treatment of pulmonary fibrosis. Astragaloside IV also bound well to senescence-associated proteins, according to molecular docking results. The results of both in vivo and in vitro experiments showed that Astragaloside IV significantly inhibited senescence protein markers such as P53, P21, and P16 and delayed cellular senescence (P < 0.05). In in vivo experiments, we also found that Astragaloside IV reduced the production of SASPs (P < 0.05), and in in vitro experiments, Astragaloside IV also reduced the production of ROS. In addition, by detecting epithelial-mesenchymal transition(EMT)-related marker protein expression, we also found that Astragaloside IV significantly inhibited the development of EMT in both in vivo and in vitro experiments (P < 0.05). Conclusion: Our research found that Astragaloside IV could alleviate bleomycin-induced PF by preventing cellular senescence and EMT.

Indexed as

BleomycinIdiopathic Pulmonary FibrosisAnimalsEpithelial-Mesenchymal TransitionMiceMolecular Docking SimulationNetwork PharmacologySaponinsTriterpenesastragaloside ABleomycinSaponinsTriterpenesastragaloside IVcellular senescenceepithelial-mesenchymal transitionnetwork pharmacologypulmonary fibrosis

Identifiers

PMID37138582
PMCPMC10150770
OpenAlexW4367059255

What OpenQuestion holds

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LicenceCC BY-NC
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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.