Peptide PD29 treats bleomycin-induced pulmonary fibrosis by inhibiting the TGF-β/smad signaling pathway

Autor: Chen-Cheng Li, Pengcheng Yu, Ruihe Yu, Jialiang Hu, Hanmei Xu, Qingbo Sun, Bingjing Lin, Meng Liu, Guiyue Wu, Chuang Ge, Zhaohao Zhu, Huan Bian, Guang-Pan Liu, Shaochang Jia
Rok vydání: 2019
Předmět:
0301 basic medicine
Pulmonary and Respiratory Medicine
Pulmonary Fibrosis
Primary Cell Culture
Clinical Biochemistry
Anti-Inflammatory Agents
Drug Evaluation
Preclinical
Smad Proteins
Peptide
macromolecular substances
Bleomycin
Antioxidants
Rats
Sprague-Dawley
Extracellular matrix
Mice
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Transforming Growth Factor beta
Fibrosis
Pulmonary fibrosis
medicine
Animals
Humans
skin and connective tissue diseases
Fibroblast
Lung
Molecular Biology
chemistry.chemical_classification
Chemistry
Tissue Inhibitor of Metalloproteinases
medicine.disease
Matrix Metalloproteinases
030104 developmental biology
medicine.anatomical_structure
030228 respiratory system
A549 Cells
Lung disease
Cancer research
sense organs
Tgf β smad signaling
Signal Transduction
Zdroj: Experimental Lung Research. 45:123-134
ISSN: 1521-0499
0190-2148
Popis: Pulmonary fibrosis (PF) is an end-stage change in lung disease characterized by fibroblast proliferation, massive extracellular matrix (ECM) aggregation with inflammatory damage, and severe structural deterioration. PD29 is a 29-amino acid peptide which has the potential to alleviate PF pathogenesis via three mechanisms: anti-angiogenesis, inhibition of matrix metalloproteinase activities, and inhibition of integrins. In this study, fibrotic lung injuries were induced in SD rats by a single intratracheal instillation of 5 mg/kg bleomycin (BLM). Then, these rats were administered 7.5, 5, or 2.5 mg/kg PD29 daily for 30 days. BLM induced-syndromes including structure distortion, excessive deposition of ECM, excessive inflammatory infiltration, and pro-inflammatory cytokine release were used to evaluate the protective effect of PD-29. Oxidative stress damage in lung tissues was attenuated by PD29 in a dose-dependent manner. The expression of TGF-β1 and the phosphorylation of Smad-2/-3-its downstream targets-were enhanced by BLM and weakened by PD29.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje