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HCl-induced acute lung injury: a study of the curative role of mesenchymal stem/stromal cells and cobalt protoporphyrin

Background This study was designed to investigate bone marrow mesenchymal stem/stromal cells (BM-MSCs) and cobalt protoporphyrin (CoPP) curable effects on HCl-induced acute lung injury (ALI) and its underlying mechanisms hoping this might aid to offer a therapeutic opportunity for ALI. Results Forty...

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Published in:Journal of Genetic Engineering and Biotechnology 2021-03, Vol.19 (1), p.41-11, Article 41
Main Authors: EL-Shahat, Reham A, EL-Demerdash, Reda S, El Sherbini, El Said, Saad, Entsar A
Format: Article
Language:English
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Summary:Background This study was designed to investigate bone marrow mesenchymal stem/stromal cells (BM-MSCs) and cobalt protoporphyrin (CoPP) curable effects on HCl-induced acute lung injury (ALI) and its underlying mechanisms hoping this might aid to offer a therapeutic opportunity for ALI. Results Forty male Sprague Dawley rats were randomly allocated into four groups; normal (normal rats), ALI (rats injected with 2 ml hydrochloric acid (HCl)/kg via trachea), ALI + BM-MSCs (ALI rats intravenously injected twice with 1 x 10.sup.6 BM-MSCs/rat/week), and ALI + CoPP (ALI rats intraperitoneally injected twice with CoPP (0.5 mg/100 g/week)). White blood cells (WBCs), red blood cells (RBCs), hemoglobin (Hb), serum tumor necrosis factor-alpha (TNF-[alpha]), lung histopathology, apoptosis markers (caspase-3 and Bcl2), and oxidative stress markers (malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT)) were measured. ALI caused increases in WBCs, TNF-[alpha], caspase-3, and MDA, and morphological damage score of lungs with decreases in RBCs, Hb, Bcl2, SOD, and CAT (p < 0.05). BM-MSCs or CoPP treatment reversed these ALI-induced changes (p < 0.05) towards normal. Conclusions BM-MSCs and CoPP could attenuate ALI by modulation of inflammation, oxidative stress, and apoptosis. Curative roles of BM-MSCs were more effective than those of CoPP. This highlights BM-MSCs as a potent therapy for HCl-associated ALI.
ISSN:1687-157X
2090-5920
DOI:10.1186/s43141-021-00139-w