ArticleBMC pulmonary medicine2025
Rhoifolin improves bleomycin-induced fibrosis in vivo and cell damage in vitro both related to NRF2/HO-1 pathway.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Alogliptin/Amentoflavone Combination Mitigates Bleomycin-Induced Lung Fibrosis: The Role of Oxidative Stress, TXNIP-Mediated Pyroptosis, and Autophagy/Apoptosis Balance.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundPulmonary fibrosis (PF) is a chronic interstitial lung illness characterized by its high worldwide prevalence, unknown etiology, and dismal prognosis. Lonicerae Japonicae Flos, a commonly used traditional Chinese medicine for treating PF, is rich in Rhoifolin (ROF). Although numerous studies have demonstrated the anti-inflammatory properties of ROF, its potential anti-fibrotic effects remain uncertain.
methodsIn this study, we established a PF model in Sprague-Dawley (SD) rats utilizing Bleomycin (BLM). We then assessed the impact of ROF on lung histology and appearance, measured the content level of Superoxide dismutase (SOD) in rat serum, and analyzed changes in α-SMA, TGF-β relative mRNA expression using PCR, measured SMAD Family Member 7 (Smad7), and Heme Oxygenase-1 (HO-1) protein expression in rat lung tissue by Western Blot. Additionally, we induced a cell injury model in A549 cells with BLM. Then after ROF administration, we detected the cell viability by MTT assay, measured N-cadherin, α-SMA, and Vimentin mRNA levels via real-time PCR, and analyzed the expression changes of N-cadherin, Nuclear factor erythroid 2-related factor 2(Nrf2), HO-1, Smad7 proteins by Western Blot.
resultsThe results indicated that ROF mitigated lung tissue damage and reduced the degree of PF in the lung tissue of rats with PF. Furthermore, In vivo, ROF reduced the expression of N-cadherin protein while increasing the expression of Smad7, and HO-1 proteins and decreasing the relative mRNA expression of α-SMA and TGF-β, and increased the expresson of SOD in rat serum In vitro, cell injury was induced in A549 cells using BLM. After ROF administration, the relative mRNA expression of α-SMA, N-cadherin, and Vimentin decreased significantly, and the protein expression of N-cadherin decreased, while the protein expression of Nrf2, HO-1, and Smad7 increased significantly.
conclusionThis study demonstrates that ROF can mitigate the symptoms of PF to a certain degree, and its mechanism of action is intimately linked to the Nrf2/HO-1 signaling pathway. Therefore, this study indicates that ROF may serve as a potential therapeutic agent for treating PF. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.