Polydatin alleviates bleomycin-induced pulmonary fibrosis and alters the gut microbiota in a mouse model
Jia Yang1, Xiawei Shi2, Rundi Gao1
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Abstract:
To investigate the effect and mechanism of polydatin on bleomycin (BLM)-induced pulmonary fibrosis in a mouse model. The lung fibrosis model was induced by BLM. The contents of TNF-α, LPS, IL-6 and IL-1β in lung tissue, intestine and serum were detected by ELISA. Gut microbiota diversity was detected by 16S rDNA sequencing; R language was used to analyse species composition, α-diversity, β-diversity, species differences and marker species. Mice were fed drinking water mixed with four antibiotics (ampicillin, neomycin, metronidazole, vancomycin; antibiotics, ABx) to build a mouse model of ABx-induced bacterial depletion; and faecal microbiota from different groups were transplanted into BLM-treated or untreated ABx mice. The histopathological changes and collagen I and α-SMA expression were determined. Polydatin effectively reduced the degree of fibrosis in a BLM-induced pulmonary fibrosis mouse model; BLM and/or polydatin affected the abundance of the dominant gut microbiota in mice. Moreover, faecal microbiota transplantation (FMT) from polydatin-treated BLM mice effectively alleviated lung fibrosis in BLM-treated ABx mice compared with FMT from BLM mice. Polydatin can reduce fibrosis and inflammation in a BLM-induced mouse pulmonary fibrosis model. The alteration of gut microbiota by polydatin may be involved in the therapeutic effect.
Insights
Polydatin effectively reduces lung fibrosis and inflammation in a mouse model. Altering gut microbiota composition with polydatin may contribute to its therapeutic effects in pulmonary fibrosis.
Area of Science:
- Pharmacology
- Pulmonary Medicine
- Microbiology
Background:
- Pulmonary fibrosis is a progressive lung disease with limited treatment options.
- Bleomycin (BLM)-induced pulmonary fibrosis in mice is a common model to study this condition.
- The role of gut microbiota in pulmonary fibrosis is an emerging area of research.
Purpose of the Study:
- To investigate the therapeutic effects of polydatin on bleomycin-induced pulmonary fibrosis.
- To elucidate the underlying mechanisms, including the impact on gut microbiota and inflammation.
Main Methods:
- A mouse model of pulmonary fibrosis was established using bleomycin.
- Polydatin treatment was administered, and its effects on lung histology, collagen deposition, and inflammatory markers (TNF-α, IL-6, IL-1β) were assessed.
- Gut microbiota diversity was analyzed using 16S rDNA sequencing.
- Antibiotic-induced bacterial depletion and fecal microbiota transplantation (FMT) were employed to study the role of gut microbiota.
Main Results:
- Polydatin significantly reduced lung fibrosis and inflammation in bleomycin-treated mice.
- Bleomycin and polydatin altered the composition and diversity of gut microbiota.
- Fecal microbiota transplantation from polydatin-treated mice alleviated lung fibrosis in recipient mice, suggesting a microbiota-mediated effect.
Conclusions:
- Polydatin demonstrates therapeutic potential for pulmonary fibrosis by reducing lung damage and inflammation.
- The modulation of gut microbiota by polydatin appears to be a key mechanism contributing to its antifibrotic effects.
