Abstract

Introduction Pulmonary fibrosis (PF) is characterized by an accelerated decline in pulmonary function and has limited treatment options. Alamandine (ALA) is a recently described protective peptide of the renin-angiotensin system (RAS) with essential tasks in several conditions. Our group previously demonstrated that ALA is reduced by 365% in the plasma of patients with idiopathic PF, and thus, it is plausible to believe that stimulation of this peptide could represent an important therapeutic target. In this sense, this study investigates the effects of ALA in an experimental model of PF. Materials and Methods Bleomycin (BLM) was administrated in Wistar rats, and these fibrotic animals were treated with ALA for 14 days. Body weight, histology, respiratory, and hemodynamic parameters were analyzed to study the effects of ALA. Results ALA treatment attenuated the development of fibrosis (P < 0.0001), reduced respiratory system elastance (P < 0.0001), and preserved weight gain (P < 0.0001) in fibrotic animals without affecting the autonomic control of blood pressure and heart rate. Conclusion The data from this study demonstrate the potential of ALA to alleviate pulmonary fibrosis and improve respiratory system mechanics in vivo. The promising results encourage more detailed investigations of the potential of ALA as a future and efficient antifibrotic.

Highlights

  • Pulmonary fibrosis (PF) is characterized by an accelerated decline in pulmonary function and has limited treatment options

  • By day 14, PF rats gained significantly less body weight compared to the CO and ALA groups (P < 0:0001)

  • We have demonstrated for the first time the protective effect of ALA in attenuating PF and preserving respiratory mechanics

Read more

Summary

Introduction

Pulmonary fibrosis (PF) is characterized by an accelerated decline in pulmonary function and has limited treatment options. Our group previously demonstrated that ALA is reduced by 365% in the plasma of patients with idiopathic PF, and it is plausible to believe that stimulation of this peptide could represent an important therapeutic target. In this sense, this study investigates the effects of ALA in an experimental model of PF. Our previous study showed that patients with idiopathic PF present 365% less ALA in plasma [11], which probably indicates that the exogenous administration of this peptide may attenuate the development of PF and, reduce the decline in lung function

Objectives
Methods
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call