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Bletilla striata polysaccharide attenuated the progression of pulmonary fibrosis by inhibiting TGF-ß1/Smad signaling pathway.
Wang, Siqi; Yu, Jiabao; Liu, Yang; Yu, Jinjin; Ma, Yajing; Zhou, Lili; Liu, Xinyao; Liu, Lingyi; Li, Weifeng; Niu, Xiaofeng.
Afiliación
  • Wang S; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Yu J; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Liu Y; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Yu J; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Ma Y; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Zhou L; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Liu X; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Liu L; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China.
  • Li W; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China. Electronic address: liwf@mail.xjtu.edu.cn.
  • Niu X; School of Pharmacy, Xi'an Jiaotong University, Xi'an, PR China. Electronic address: niuxf@mail.xjtu.edu.cn.
J Ethnopharmacol ; 323: 117680, 2024 Apr 06.
Article en En | MEDLINE | ID: mdl-38171465
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE Bletilla striata, a traditional medicinal plant, has been utilized as a folk medicine for many years because of its superior biological activity in China. However, Bletilla striata polysaccharide (BSP) has received less attention, and its specific mechanism for ameliorating pulmonary fibrosis is completely unclear. AIMS OF THE STUDY In this study, we aim to assess BSP on the treatment of PF and explore potential mechanisms. MATERIALS AND

METHODS:

BSP was successfully extracted and purified from Bletilla striata. The mechanisms were assessed in bleomycin-induced pulmonary fibrosis model and lung fibroblasts activated by transforming growth factor-ß1 (TGF-ß1). Histological analysis, immunofluorescence, Western blot and flow cytometry were used to explore the alterations after BSP intervention.

RESULTS:

The results in vivo showed an anti-PF effect of BSP treatment, which reduced pathogenic damages. Furthermore, TGF-ß1-induced abnormal migration and upregulated expression of collagen I (COL1A1), vimentin and α-smooth muscle actin (α-SMA) were suppressed by BSP in L929 cells. Moreover, the abnormal proliferation was retarded by inhibiting the cell cycle of G1 to S phase. Immunofluorescence assay showed that BSP activated autophagy and played an antifibrotic role by inhibiting the expression of p62 and phospho-mammalian target of rapamycin (p-mTOR). Last but not least, the suppression of TGF-ß1/Smad signaling pathway was critical for BSP to perform therapeutic effects in vitro and in vivo.

CONCLUSION:

The possible mechanisms were involved in improving ECM deposition, regulating cell migration and proliferation, and promoting cellular autophagy. Briefly, all of the above revealed that BSP might be a novel therapy for treating pulmonary fibrosis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fibrosis Pulmonar Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: J Ethnopharmacol Año: 2024 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fibrosis Pulmonar Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: J Ethnopharmacol Año: 2024 Tipo del documento: Article