Idiopathic pulmonary fibrosis (IPF) is a chronic
lung disease with unknown etiology and pathogenesis. With high mortality risks, most of the IPF cases emerged after a damage of alveolar epithelium, where this situation stimulates the over expression of matrix components. Inflammatory process observed as a reaction to emerged damage.
Prolidase as an
iminodipeptidase significantly increased during the development of
fibrosis. The aim of this study is to measure
prolidase activity as a marker of treatment and diagnosis in an experimental lung
fibrosis animal model. Thirty male Wistar rats randomly divided into three experimental groups, with ten rats in each group. Group 1, control group; group 2,
bleomycin (BLM)-induced lung
fibrosis group, and group 3, BLM-induced lung
fibrosis treated with
palosuran (
urotensin-II receptor antagonist). For histopathology, the middle lobes of right lungs were embedded in
paraffin, followed by fixation in 10 % buffered
formalin, and evaluation of IPF was performed using the Ashcroft scoring method.
Prolidase activity was determined by a photometric method based on the measurement of
proline levels produced by
prolidase. The
fibrosis scores and the
prolidase activity were significantly enhanced by BLM stimulation. The BLM +
palosuran treatment decreased
prolidase activity in group 3. There was a positive correlation between
prolidase activity and
fibrosis scores.
Palosuran seems to be effective in the treatment of lung
fibrosis, and
prolidase activity can be used for the diagnosis and/or for management of the treatment. However, further clinical and experimental studies with animals and/or patients are needed to verify these conclusions.