Artesunate restraining MAPK passage by smad7 to resist pulmonary fibrosis

Eur Rev Med Pharmacol Sci. 2014;18(21):3199-204.

Abstract

Objectives: This study aims to discuss the function and molecular mechanism of artesunate in resisting pulmonary fibrosis.

Methods: Artesunate was used to stimulate the HFL-I cell line, which restrains the expression of Smad7 protein. Under different conditions, all treatment factors were checked, including Smad7, p-P38, ERK, and p-JNK protein expressions. Flow cytometry was used to detect the cell cycle. For the silent expression of the p-Smad7 protein, Western blot analysis revealed that Smad7, p-P38, and p-JNK proteins decreased compared with those of the non-treatment group.

Results: No significant changes were observed in Smad7, p-P38, and p-JNK proteins after the cells with silent p-Smad7 protein expression were stimulated by artesunate (p > 0.5). No significant changes were observed in the expression of Smad7, p-P38, and p-JNK proteins after using TGF-β1 recombination factor to cells whose p-Smad7 protein expression is silent (p > 0.5).

Conclusions: Artesunate blocks the MAPK cell conduction pathway through Smad7 to restrain idiopathic pulmonary fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimalarials / pharmacology*
  • Artemisinins / pharmacology*
  • Artesunate
  • Cell Line
  • Humans
  • Pulmonary Fibrosis / drug therapy*
  • Pulmonary Fibrosis / enzymology*
  • Signal Transduction
  • Smad7 Protein / metabolism*
  • Transforming Growth Factor beta1 / metabolism

Substances

  • Antimalarials
  • Artemisinins
  • SMAD7 protein, human
  • Smad7 Protein
  • Transforming Growth Factor beta1
  • Artesunate