An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by the fibrotic thickening of the alveolar walls, resulting in compromised gas exchange, restricted ventilation, and respiratory failure. It has been indicated that elastase inhibitors reduced the severity of IPF by neutrali...

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Main Authors: Xi Lian, Bin Liu, Dan Li, Xinyao Wang, Chengbo Long, Xing Feng, Qiong Liao, Mingqiang Rong
Format: Article
Language:English
Published: MDPI AG 2025-04-01
Series:Toxins
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Online Access:https://www.mdpi.com/2072-6651/17/5/213
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author Xi Lian
Bin Liu
Dan Li
Xinyao Wang
Chengbo Long
Xing Feng
Qiong Liao
Mingqiang Rong
author_facet Xi Lian
Bin Liu
Dan Li
Xinyao Wang
Chengbo Long
Xing Feng
Qiong Liao
Mingqiang Rong
author_sort Xi Lian
collection DOAJ
description Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by the fibrotic thickening of the alveolar walls, resulting in compromised gas exchange, restricted ventilation, and respiratory failure. It has been indicated that elastase inhibitors reduced the severity of IPF by neutralizing excessive elastase levels in the lungs. ShSPI is an elastase inhibitor derived from centipede toxin. The present study evaluates the therapeutic effects of ShSPI in a bleomycin-induced idiopathic pulmonary fibrosis model. According to the results, ShSPI markedly reduced the weight loss, showing the improvement of health status in bleomycin-induced mice. Its robust antifibrotic effects were evidenced by the mitigation of alveolar structural damage, reduction in inflammatory cell infiltration, inhibition of collagen deposition, and suppression of fibrotic nodule formation. ShSPI effectively attenuated inflammatory responses by downregulating pro-inflammatory factors (IL-6, IL-1β, and MCP-1) and upregulating the anti-inflammatory factor interleukin-10 (IL-10). After delivered via inhalation, ShSPI exhibited favorable pharmacokinetic properties. It could be detected at 8 h at doses of 1 mg/kg and achieved maximum plasma concentrations (Cmax) of 188.00 ± 64.40 ng/mL in vivo. At high doses (160 mg/kg), ShSPI maintained a strong safety profile, with no detectable toxicity observed. This feature shows the therapeutic potential of ShSPI in the treatment of idiopathic pulmonary fibrosis and provides valuable evidence for its development as a novel peptide-based therapy.
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spelling doaj-art-187551f917204c09800bdd304b7e02002025-08-20T01:56:38ZengMDPI AGToxins2072-66512025-04-0117521310.3390/toxins17050213An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary FibrosisXi Lian0Bin Liu1Dan Li2Xinyao Wang3Chengbo Long4Xing Feng5Qiong Liao6Mingqiang Rong7College of Life Sciences, Hunan Normal University, Changsha 410004, ChinaCollege of Life Sciences, Hunan Normal University, Changsha 410004, ChinaCollege of Life Sciences, Hunan Normal University, Changsha 410004, ChinaCollege of Life Sciences, Hunan Normal University, Changsha 410004, ChinaChengdu PDBio Co., Ltd., Chengdu 610225, ChinaKey Laboratory of Study and Discovery of Small Targeted Molecules of School of Pharmaceutical Sciences, Hunan Normal University, Changsha 410013, ChinaCollege of Life Sciences, Hunan Normal University, Changsha 410004, ChinaCollege of Life Sciences, Hunan Normal University, Changsha 410004, ChinaIdiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by the fibrotic thickening of the alveolar walls, resulting in compromised gas exchange, restricted ventilation, and respiratory failure. It has been indicated that elastase inhibitors reduced the severity of IPF by neutralizing excessive elastase levels in the lungs. ShSPI is an elastase inhibitor derived from centipede toxin. The present study evaluates the therapeutic effects of ShSPI in a bleomycin-induced idiopathic pulmonary fibrosis model. According to the results, ShSPI markedly reduced the weight loss, showing the improvement of health status in bleomycin-induced mice. Its robust antifibrotic effects were evidenced by the mitigation of alveolar structural damage, reduction in inflammatory cell infiltration, inhibition of collagen deposition, and suppression of fibrotic nodule formation. ShSPI effectively attenuated inflammatory responses by downregulating pro-inflammatory factors (IL-6, IL-1β, and MCP-1) and upregulating the anti-inflammatory factor interleukin-10 (IL-10). After delivered via inhalation, ShSPI exhibited favorable pharmacokinetic properties. It could be detected at 8 h at doses of 1 mg/kg and achieved maximum plasma concentrations (Cmax) of 188.00 ± 64.40 ng/mL in vivo. At high doses (160 mg/kg), ShSPI maintained a strong safety profile, with no detectable toxicity observed. This feature shows the therapeutic potential of ShSPI in the treatment of idiopathic pulmonary fibrosis and provides valuable evidence for its development as a novel peptide-based therapy.https://www.mdpi.com/2072-6651/17/5/213idiopathic pulmonary fibrosis (IPF)elastasecentipedeneutrophilsinflammatory factorsShSPI
spellingShingle Xi Lian
Bin Liu
Dan Li
Xinyao Wang
Chengbo Long
Xing Feng
Qiong Liao
Mingqiang Rong
An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
Toxins
idiopathic pulmonary fibrosis (IPF)
elastase
centipede
neutrophils
inflammatory factors
ShSPI
title An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
title_full An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
title_fullStr An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
title_full_unstemmed An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
title_short An Elastase Inhibitor ShSPI from Centipede Attenuates Bleomycin-Induced Pulmonary Fibrosis
title_sort elastase inhibitor shspi from centipede attenuates bleomycin induced pulmonary fibrosis
topic idiopathic pulmonary fibrosis (IPF)
elastase
centipede
neutrophils
inflammatory factors
ShSPI
url https://www.mdpi.com/2072-6651/17/5/213
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