ReferenceID 5061
Curdione ameliorates bleomycin-induced pulmonary fibrosis by repressing TGF-β-induced fibroblast to myofibroblast differentiation
Respir Res
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible disease characterized by excessive fibroblast to myofibroblast differentiation with limited therapeutic options. Curdione, a sesquiterpene
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Record Fields
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- Reference Id
- 5061
- Evidence Id
- 21651
- Core Evidence Id
- 21651
- Source Reference Id
- 3400
- Herb2 Reference Id
- HBREF004197
- Subject Paper Key
- HBIN021993_32075634
- Pubmed Id
- 32075634
- Doi
- 10.1186/s12931-020-1300-y
- Paper Title
- Curdione ameliorates bleomycin-induced pulmonary fibrosis by repressing TGF-β-induced fibroblast to myofibroblast differentiation
- Paper Abstract
- BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible disease characterized by excessive fibroblast to myofibroblast differentiation with limited therapeutic options. Curdione, a sesquiterpene compound extracted from the essential oil of Curcuma aromatica Salisb, has anti-inflammatory and anti-tumor effects. However, the role of curdione in IPF is still unclear. METHODS: The effects of curdione were evaluated in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. C57BL/6 mice were treated with BLM on day 0 by intratracheal injection and intraperitoneal administered curdione or vehicle. In vitro study, expression of fibrotic protein was examined and the transforming growth factor (TGF)-beta-related signaling was evaluated in human pulmonary fibroblasts (HPFs) treated with curdione following TGF-beta1 stimulation. RESULTS: Histological and immunofluorescent examination showed that curdione alleviated BLM-induced lung injury and fibrosis. Specifically, curdione significantly attenuated fibroblast to myofibroblast differentiation in the lung in BLM induced mice. Furthermore, curdione also decreased TGF-beta1 induced fibroblast to myofibroblast differentiation in vitro, as evidenced by low expression of alpha-SMA, collagen 1 and fibronectin in a dose dependent manner. Mechanistically, curdione suppressed the phosphorylation of Smad3 following TGF-beta1 treatment, thereby inhibiting fibroblast differentiation. CONCLUSIONS: Overall, curdione exerted therapeutic effects against pulmonary fibrosis via attenuating fibroblast to myofibroblast differentiation. As curdione had been shown to be safe and well-tolerated in BLM-induced mouse model, curdione might be useful for developing novel therapeutics for IPF.
- Journal
- Respir Res
- Publish Year
- 2020
- Experiment Subject
- mouse; human
- Experiment Type
- Animal Experiment
- Phenotype Related
- Idiopathic Pulmonary Fibrosis; Lung Injury; Fibrosis; Pulmonary Fibrosis
- Paper Title Cn
- Paper Title En
- Curdione ameliorates bleomycin-induced pulmonary fibrosis by repressing TGF-β-induced fibroblast to myofibroblast differentiation
- Bilingual Status
- semi_complete