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Platycodin D ameliorates ammonia-induced pulmonary fibrosis by repressing TGF-β1-mediated extracellular matrix
Wenqi Lian1, Shihao Ge1, Quanhai Pang1
1College of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, China.
Abstract:
Ammonia can induce pulmonary fibrosis in humans and animals. Platycodin D (PLD) possesses various bioactive activities including anti-fibrotic properties. In this study, we aimed to explore the activity and mechanism of PLD in pulmonary fibrosis induced by ammonia. The mouse model of ammonia-induced lung fibrosis was established, and the role of PLD was assessed by H&E and Masson's trichrome staining. The differentially expressed genes (DEGs) were identified by RNA-seq and subjected to GO and KEGG pathway analyses. BEAS-2B cells were treated with NH4 Cl alone or along with PLD. Results showed that PLD attenuated ammonia-induced pulmonary inflammation and fibrosis in vivo. The extracellular matrix (ECM)-receptor interaction pathway was predicted as a prominent pathway underlying the anti-fibrotic function of PLD. In ammonia-induced mouse models and NH4 Cl-treated BEAS-2B cells, PLD could repress the activation of the TGF-β1 pathway. By incubating lung fibroblast HFL1 cells with the conditioned medium of BEAS-2B cells treated with NH4Cl alone or along with PLD, PLD was confirmed to attenuate NH4 Cl-induced ECM deposition in HFL1 cells. Our findings demonstrate that PLD exerts a protective function in ammonia-induced pulmonary fibrosis by repressing TGF-β1-mediated ECM remodeling, suggesting the potential therapeutic value of PLD in this disease.
Insights
Platycodin D (PLD) effectively reduces ammonia-induced lung fibrosis by inhibiting the TGF-β1 pathway and extracellular matrix remodeling. This research highlights PLD
Area of Science:
- Pulmonary Medicine
- Pharmacology
- Cell Biology
Background:
- Ammonia exposure is a known cause of pulmonary fibrosis in humans and animals.
- Platycodin D (PLD) exhibits anti-fibrotic properties, suggesting potential therapeutic applications.
- Understanding PLD's mechanism in ammonia-induced lung fibrosis is crucial for developing new treatments.
Purpose of the Study:
- To investigate the protective effects and underlying mechanisms of Platycodin D (PLD) against ammonia-induced pulmonary fibrosis.
- To elucidate how PLD modulates key molecular pathways involved in fibrosis development.
Main Methods:
- Establishment of a mouse model for ammonia-induced lung fibrosis.
- Histopathological analysis using H&E and Masson's trichrome staining.
- RNA sequencing (RNA-seq) for differential gene expression analysis, followed by GO and KEGG pathway analysis.
- In vitro studies using BEAS-2B and HFL1 cell lines treated with ammonia chloride (NH4Cl) and PLD.
Main Results:
- PLD significantly attenuated inflammation and fibrosis in ammonia-exposed mice.
- RNA-seq analysis identified the extracellular matrix (ECM)-receptor interaction pathway as a key target.
- PLD was found to inhibit the activation of the TGF-β1 pathway in both in vivo and in vitro models.
- PLD reduced ammonia-induced ECM deposition in lung fibroblasts.
Conclusions:
- Platycodin D (PLD) demonstrates significant protective effects against ammonia-induced pulmonary fibrosis.
- PLD exerts its anti-fibrotic action by suppressing TGF-β1-mediated ECM remodeling.
- These findings suggest PLD holds considerable therapeutic potential for treating ammonia-induced lung diseases.
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