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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
The Anti-fibrotic and Anti-inflammatory Potential of Bone Marrow–Derived Mesenchymal Stem Cells and Nintedanib in Bleomycin-Induced Lung Fibrosis in Rats
Inflammation, Volume 43, No. 1, Year 2020
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Description
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by progressive lung damage. Tyrosine kinase inhibitors are approved to treat people with IPF while bone marrow–derived mesenchymal stem cell therapy was previously suggested to inhibit pulmonary fibrosis through the alveolar epithelial cell repair. The present study aimed to evaluate the anti-inflammatory and anti-fibrotic effect of the bone marrow–derived mesenchymal stem cell (BM-MSC) therapy in comparison with nintedanib, a tyrosine kinase inhibitor, on improving survival in bleomycin-induced lung fibrosis in rats. Moreover, the combined therapy of BM-MSCs and nintedanib will be evaluated. In the present study, IPF was induced through intra-tracheal instillation of bleomycin (5 mg/kg) in rats then treatments were administered 14 days thereafter. Nintedanib (100 mg/kg, I.P.) was administered daily for 28 days, while BM-MSCs were injected once intravenously in tail vein in the dose 1 × 106 cells/ml/rat. In the present study, both treatment regimens effectively inhibited lung fibrosis through several pathways, suppressing tumor growth factor-β (TGF-β)/SMAD3 expression which is considered the master signaling pathway. Nintedanib and BLM-MSCs exerted their anti-inflammatory effect through minimizing the expression of TNF-α and IL-6. In addition, the histopathological examination of the lung tissue showed a significant decrease in the alveolar wall thickening, in the inflammatory infiltrate, and in the collagen fiber deposition in response to either nintedanib or BM-MSC and their combination. In conclusion, the therapeutic pulmonary anti-fibrotic activity of nintedanib or BM-MSC is mediated through their anti-inflammatory properties and inhibition of SMAD-3/TGF-β expression. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Authors & Co-Authors
Gad, Enas S.
Egypt, Ismailia
Suez Canal University
Salama, Abeer A.A.
Egypt, Giza
National Research Centre
El-Shafie, M. F.
Egypt, Dar el Salam
Heliopolis University
Arafa, Hossam Mohamed
Egypt, 6th October
Ahram Canadian University
Abdelsalam, Rania M.
Egypt, Cairo
Faculty of Pharmacy
Khattab, M. M.
Egypt, Cairo
Faculty of Pharmacy
Statistics
Citations: 39
Authors: 6
Affiliations: 5
Identifiers
Doi:
10.1007/s10753-019-01101-2
ISSN:
03603997
Research Areas
Cancer