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Mesenchymal Stem Cells Alleviate Hydrochloric Acid-induced Lung Injury Through Suppression of Inflammation, Oxidative Stress and Apoptosis in Comparison to Moxifloxacin and Sildenafil

Overview
Journal Heliyon
Specialty Social Sciences
Date 2019 Dec 25
PMID 31872097
Citations 7
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Abstract

Introduction: Acute lung injury (ALI) is a severe life-threatening disease causing uncontrolled pulmonary inflammation and oxidative damage. There are still no effective therapies for this disease. The aim of this study was to evaluate the protective role of mesenchymal stem cells, moxifloxacin, sildenafil or a combination of moxifloxacin and sildenafil against hydrochloric Acid (HCl) - induced ALI.

Methods: HCl or saline was injected intra-tracheally and after 2 h, moxifloxacin, sildenafil, moxifloxacin + sildenafil or mesenchymal stem cells were injected. After 7 days, rats were sacrificed for evaluation of the blood chemistry and inflammation via determination of the level of oxidative stress markers, apoptosis and the histopathological alterations by H&E.

Results: In HCl-injected rats, there were a significant increase in total white blood cells (WBCs), lymphocytes, malondialdehyde (MDA) and gene expression. Also, there were a significant decrease in superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and Hemeoxygenase-1 (HO-1) gene expression in lung tissue. On the other hand, treatment of lung injured rats with mesenchymal stem cell, moxifloxacin, sildenafil or a combination of moxifloxacin and sildenafil showed a significant decrease in WBCs and lymphocytes and ameliorated the histopathological changes. MDA level in lung tissue was only significantly lowered in rats treated with moxifloxacin alone or in combination with sildenafil or MSCs. GSH was just increased in rats treated with moxifloxacin, sildenafil or with MSCs. Antioxidant parameters and gene expression of and were significantly modulated in rats treated with MSCs.

Conclusion: MSCs ameliorated the toxic effects of HCl through their ability to decrease inflammation, oxidative stress, and apoptosis in acute lung injury.

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