Activation of somatostatin receptors attenuates pulmonary fibrosis

R Borie1, A Fabre, F Prost

  • 1INSERM, Unit 700, Paris, France.

Thorax
|October 24, 2007
PubMed
Abstract

Insights

Somatostatin analogue SOM230 reduced lung fibrosis in mice and human cells. This suggests a potential new treatment for pulmonary fibrotic disorders.

Area of Science:

  • Pulmonary medicine
  • Pharmacology
  • Fibrosis research

Background:

  • Somatostatin analogues show potential antifibrotic effects in lung tissue.
  • The expression of somatostatin receptors (sst1-sst5) in normal and fibrotic mouse lungs requires investigation.
  • The efficacy of SOM230 (pasireotide), a novel somatostatin analogue, in treating lung fibrosis needs evaluation.

Purpose of the Study:

  • To assess somatostatin receptor expression in mouse lungs.
  • To determine the antifibrotic effects of SOM230 in a bleomycin-induced lung fibrosis model.
  • To investigate the in vitro effects of SOM230 on human lung fibroblasts.

Main Methods:

  • Bleomycin was administered intratracheally to mice, followed by daily SOM230 or saline injections.
  • Lung tissues were analyzed at 3, 7, and 14 days post-bleomycin administration.
  • In vitro studies involved human lung fibroblasts treated with SOM230 under basal and TGF-beta stimulated conditions.

Main Results:

  • All somatostatin receptors were expressed in normal mouse lungs; sst2 mRNA increased post-bleomycin.
  • SOM230 improved survival, reduced lung collagen, and modulated growth factor mRNA levels in mice.
  • SOM230 decreased fibroblast proliferation and collagen production in vitro.

Conclusions:

  • SOM230 demonstrates significant antifibrotic activity in a mouse model of lung fibrosis.
  • The study highlights the potential of SOM230 as a therapeutic agent for pulmonary fibrotic diseases.
  • Further research into somatostatin analogues for treating lung fibrosis is warranted.