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Protective effect of carnosic acid on pulmonary fibrosis

About Protective effect of carnosic acid on pulmonary fibrosis

Idiopathic pulmonary fibrosis is a chronic and progressive disease, characterized by an aberrant proliferation of fibroblasts and an accumulation of extracellular matrix proteins leading to respiratory insufficiency. In this research work, we chose carnosic acid, a bioactive substance extracted from rosemary, to evaluate its efficacy in vivo on an experimental model of pulmonary fibrosis induced by bleomycin (BLM) in Wistar rats and in vitro on human lung fibroblasts (HLF). The first in vitro part showed that CA induces apoptosis in HLF in a dose-dependent manner, accompanied by cell cycle arrest in the G0/G1 phase and activation of the expression of the signaling proteins Akt, p38-MAPK and p21. The second part confirmed the protective effect of this biomolecule in vivo on the fibrosis process and oxidative stress induced by BLM. In the light of these results, it would be interesting to test the efficacy of CA on certain diseases whose physiopathology is dominated by inflammation, oxidative stress and cell proliferation.

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  • Language:
  • English
  • ISBN:
  • 9786205730171
  • Binding:
  • Paperback
  • Pages:
  • 76
  • Published:
  • January 30, 2024
  • Dimensions:
  • 150x6x220 mm.
  • Weight:
  • 131 g.
Delivery: 1-2 weeks
Expected delivery: March 9, 2025

Description of Protective effect of carnosic acid on pulmonary fibrosis

Idiopathic pulmonary fibrosis is a chronic and progressive disease, characterized by an aberrant proliferation of fibroblasts and an accumulation of extracellular matrix proteins leading to respiratory insufficiency. In this research work, we chose carnosic acid, a bioactive substance extracted from rosemary, to evaluate its efficacy in vivo on an experimental model of pulmonary fibrosis induced by bleomycin (BLM) in Wistar rats and in vitro on human lung fibroblasts (HLF). The first in vitro part showed that CA induces apoptosis in HLF in a dose-dependent manner, accompanied by cell cycle arrest in the G0/G1 phase and activation of the expression of the signaling proteins Akt, p38-MAPK and p21. The second part confirmed the protective effect of this biomolecule in vivo on the fibrosis process and oxidative stress induced by BLM. In the light of these results, it would be interesting to test the efficacy of CA on certain diseases whose physiopathology is dominated by inflammation, oxidative stress and cell proliferation.

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