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<p>Pulmonary fibrosis (PF), including post-COVID fibrotic sequelae, is a progressive and irreversible lung disorder characterized by excessive collagen deposition, inflammation, and structural remodeling, leading to respiratory failure. Current therapies such as pirfenidone and nintedanib only slow disease progression, highlighting the need for safer and more effective alternatives. This study investigated the therapeutic potential of intranasally administered Apelin-13, a bioactive peptide of the apelin/APJ signaling pathway, in a bleomycin-induced rat model of pulmonary fibrosis. Male albino rats were divided into control, fibrotic, and Apelin-13-treated groups. Fibrosis was induced using bleomycin (5&#xa0;mg/kg), followed by Apelin-13 treatment (100&#xa0;µg/kg) for 21 days. Biochemical, histological, and ultrastructural analyses were performed. Results demonstrated a significant increase in collagen deposition, elevated oxidative stress (MDA), along with reduced antioxidant enzyme activities (SOD, catalase, GPx) in fibrotic lungs. Apelin-13 treatment markedly attenuated these alterations by reducing collagen accumulation, restoring lung architecture and enhancing antioxidant defenses. In conclusion, intranasal Apelin-13 exerts protective effects against pulmonary fibrosis by mitigating oxidative stress, suggesting its potential as a noninvasive therapeutic strategy for fibrotic lung diseases.</p>

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Effect of intranasal Apelin-13 Peptide treatment on structural remodeling and biochemical alterations in fibrotic lung tissue in a rat model

  • 期刊论文

  • 发表日期：

    2026年7月3日

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  • Vaishali Singh,
  • Saurbh Kumar,
  • Ilya Ulasov,
  • Rajesh Kumar Kharwar

摘要

Pulmonary fibrosis (PF), including post-COVID fibrotic sequelae, is a progressive and irreversible lung disorder characterized by excessive collagen deposition, inflammation, and structural remodeling, leading to respiratory failure. Current therapies such as pirfenidone and nintedanib only slow disease progression, highlighting the need for safer and more effective alternatives. This study investigated the therapeutic potential of intranasally administered Apelin-13, a bioactive peptide of the apelin/APJ signaling pathway, in a bleomycin-induced rat model of pulmonary fibrosis. Male albino rats were divided into control, fibrotic, and Apelin-13-treated groups. Fibrosis was induced using bleomycin (5 mg/kg), followed by Apelin-13 treatment (100 µg/kg) for 21 days. Biochemical, histological, and ultrastructural analyses were performed. Results demonstrated a significant increase in collagen deposition, elevated oxidative stress (MDA), along with reduced antioxidant enzyme activities (SOD, catalase, GPx) in fibrotic lungs. Apelin-13 treatment markedly attenuated these alterations by reducing collagen accumulation, restoring lung architecture and enhancing antioxidant defenses. In conclusion, intranasal Apelin-13 exerts protective effects against pulmonary fibrosis by mitigating oxidative stress, suggesting its potential as a noninvasive therapeutic strategy for fibrotic lung diseases.