The hormone atrial natriuretic peptide (ANP) decreased inflammation and fibrosis in a mouse model of idiopathic pulmonary fibrosis (IPF), according to a Japanese study.
The research, “Atrial natriuretic peptide protects against bleomycin-induced pulmonary fibrosis via vascular endothelial cells in mice,” was published in the journal Respiratory Research.
Certain cells secrete ANP naturally. Its anti-inflammatory and anti-fibrotic qualities protect several organs, including the heart, blood vessels, kidneys, and lungs. In fact, Japanese doctors use it to treat heart failure.
Researchers treated mice with ANP before subjecting them to IPF. They compared the results with those in controls who did not get the hormone.
The team analyzed the mice’s lungs for inflammatory cells and bronchoalveolar lavage seven days and 21 days after they were subjected to IPF.
They measured pro-inflammatory and pro-fibrotic cytokines in the lungs to conclude that ANP reduced both inflammation and pulmonary fibrosis. The cytokines that cells release help them interact and communicate with each other.
ANP not only reduced cytokines in mice, but also decreased collagen deposits associated with pulmonary fibrosis.
Although ANP reduced inflammation and fibrosis, it also inhibited a signaling pathway that helps prevent fibrosis: the TGF-beta/Smad2 pathway of the lungs’ vascular endothelial cells. Endothelial cells secrete pro-inflammatory cytokines and pro-fibrotic factors that trigger fibrosis. TGF-beta asks as a check on the fibrosis process.
“In conclusion, this study is the first to show that ANP exerts anti-fibrotic and anti-inflammatory effects in BLM [bleomycin]-induced pulmonary fibrosis via vascular endothelial cells,” the team wrote.
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