ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Oridonin Inhibits Myofibroblast Differentiation and Bleomycin-induced Pulmonary Fibrosis by Regulating Transforming Growth Factor β (TGFβ)/Smad Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Oridonin Attenuates Cisplatin-Induced Ovarian Injury by Modulating Oxidative Stress, Inflammation, and TGF-β1/Smad3-Mediated Fibrosis in Rats.Medicina (Kaunas, Lithuania) · 2026Article
- Oridonin alleviates inflammation and endoplasmic reticulum stress in pediatric pneumonia via regulating the SIRT1-mediated Wnt/β-catenin signaling pathway.Histology and histopathology · 2024Article
- Vinpocetine alleviated alveolar epithelial cells injury in experimental pulmonary fibrosis by targeting PPAR-γ/NLRP3/NF-κB and TGF-β1/Smad2/3 pathways.Scientific reports · 2024Article
- Searching for Novel Candidate Small Molecules for Ameliorating Idiopathic Pulmonary Fibrosis: a Narrative Review.Biomolecules & therapeutics · 2023Review
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- From Basic Research to Clinical Practice: Considerations for Treatment Drugs for Silicosis.International journal of molecular sciences · 2023Review
- Recent Advances (2015-2020) in Drug Discovery for Attenuation of Pulmonary Fibrosis and COPD.Molecules (Basel, Switzerland) · 2023Review
- Mechanisms of NLRP3 inflammasome-mediated hepatic stellate cell activation: Therapeutic potential for liver fibrosis.Genes & diseases · 2023Review
- The Mechanism and Regulation of the NLRP3 Inflammasome during Fibrosis.Biomolecules · 2022Review
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases.Frontiers in aging neuroscience · 2022Review
- Oridonin: A Review of Its Pharmacology, Pharmacokinetics and Toxicity.Frontiers in pharmacology · 2021Review
- Emerging Role of IL-10 in Hypertrophic Scars.Frontiers in medicine · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Idiopathic pulmonary fibrosis (IPF) is a progressive disease with unknow. etiology and a high mortality rate. Oridonin is a diterpenoid isolated from the Rabdosia rubesecens with diverse biological functions. However, whether oridonin possess potential protective activity on IPF is still unclear. MATERIAL AND METHODS The aim of the present study was to explore the therapeutic effects of oridonin on IPF. First, TGF-β1-induced MRC-5 cells were employed for the evaluation of inhibitory activity in vitro. Then, a bleomycin (BLM)-induced mice pulmonary fibrosis model was used to verify the activity of oridonin in vivo. Several pathological changes, including alveolar space collapse, emphysema, and infiltration of inflammatory cells, were observed in the BLM‑treated mice. RESULTS Oridonin could significantly inhibit the mRNA and protein expression levels of α-SMA and COL1A1 in TGF-β1-induced MRC-5 cells. Oridonin could attenuate pathological changes, including alveolar space collapse, emphysema, and infiltration of inflammatory cells induced by BLM. In addition, oridonin could significantly inhibit BLM-induced upregulation of α-SMA and COL1A1 and the phosphorylation of Smad2/3 in lung tissues of mice. CONCLUSIONS Oridonin could be used as a potential therapeutic agent in treatment for patients with IPF. The mechanisms of anti-fibrosis effect of oridonin might be inhibition of the TGF-β/Smad pathway.
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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.