Abstract

BackgroundWhite smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute lung injury and acute respiratory distress syndrome for which no effective pharmaceutical treatment has been developed. This study aimed to determine the protective effects of human amnion-derived mesenchymal stem cells (hAMSCs) against WSI-induced lung injury in rats.MethodshAMSCs were injected into rats via the tail vein 4 h after WSI. At 1, 3, 7, 14, and 28 days after cell injection, hAMSCs labeled with PKH26 in lung, heart, liver, and kidney tissues were observed by fluorescence microscopy. The lung injury score was determined by hematoxylin and eosin staining. Lung fibrosis was assessed by Masson’s trichrome staining. The computed tomography (CT) score was assessed by CT scanning. The wet/dry weight ratio was calculated. The levels of interleukin (IL)-1β, IL-6, and IL-10 were determined by enzyme-linked immunosorbent assays. The expression of surfactant protein (SP)-A, SP-C, and SP-D was measured by Western blotting.ResultsThe injected hAMSCs were primarily distributed in the lung tissues in WSI-induced rats. Compared with the model and phosphate-buffered saline (PBS) group, hAMSC treatment led to reduced lung injury, lung fibrosis, CT score, and inflammation levels in WSI-induced mice. hAMSC treatment also resulted in increased cell retention in the lung, partial pressure of oxygen (PaO2), and PaO2/fraction of inspired oxygen (FiO2) levels, and pulmonary SP-A, SP-C, and SP-D expression compared with that in the model and PBS group.ConclusionshAMSCs are a potential cell-based therapy for WSI-induced lung injury.

Highlights

  • White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute lung injury and acute respiratory distress syndrome for which no effective pharmaceutical treatment has been developed

  • Distribution of Human amnionderived mesenchymal stem cell (hAMSC) in WSI-induced rats hAMSCs labeled with PKH26 in the lung, heart, liver, and kidney tissues were observed using fluorescence microscopy (Fig. 3). hAMSCs were clearly observed in the lung tissues but were gradually reduced at 1, 3, 7, 14, and 28 days after treatment with hAMSCs

  • The results suggest that hAMSCs mainly migrated to the lung tissue in WSI-induced rats

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Summary

Introduction

White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute lung injury and acute respiratory distress syndrome for which no effective pharmaceutical treatment has been developed. Compared to the smoke generated by the combustion of tobacco or wood dust, white smoke contains carbon tetrachloride, carbon monoxide, and carbon dioxide, but is mixed with other highly corrosive, irritating, and toxic substances that include tetrachloroethylene, zinc chloride, hexachloroethane, and oxides (zinc oxide, aluminum oxide, iron oxide, etc.), which increase the damage caused by white smoke inhalation (WSI) [1,2,3]. Many studies have reported that lung injury can be caused by a single or several components in white smoke, and confirmed that zinc chloride and hexachloroethane are important substances as inducers of lung injury [6,7,8]. It is necessary to develop effective therapeutic methods to treat lung injury induced by white smoke

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