Abstract
Background
The study aimed to examine whether methylene blue (MB) prevents different pulmonary
aspiration materials-induced lung injury in rats.
Methods
The experiments were designed in 60 Sprague–Dawley rats, ranging in weight from 250–300 g,
randomly allotted into one of six groups (n = 10): saline control, Biosorb Energy Plus (BIO), hydrochloric acid (HCl), saline + MB
treated, BIO + MB treated, and HCl + MB treated. Saline, BIO, and HCl were injected
into the lungs in a volume of 2 mL/kg. After surgical procedure, MB was administered
intraperitoneally for 7 days at a daily dose of 2 mg/kg per day. Seven days later,
rats were killed, and both lungs in all groups were examined biochemically and histopathologically.
Results
Our findings show that MB inhibits the inflammatory response reducing significantly
(P < 0.05) peribronchial inflammatory cell infiltration, alveolar septal infiltration,
alveolar edema, alveolar exudate, alveolar histiocytes, interstitial fibrosis, granuloma,
and necrosis formation in different pulmonary aspiration models. Pulmonary aspiration
significantly increased the tissue hydroxyproline content, malondialdehyde levels,
and decreased (P < 0.05) the antioxidant enzyme (superoxide dismutase and glutathione peroxidase) activities.
MB treatment significantly (P < 0.05) decreased the elevated tissue hydroxyproline content and malondialdehyde levels
and prevented the inhibition of superoxide dismutase and glutathione peroxidase (P < 0.05) enzymes in the tissues. Furthermore, there is a significant reduction in the
activity of inducible nitric oxide synthase (iNOS), terminal deoxynucleotidyl transferase
dUTP nick end labeling, and arise in the expression of surfactant protein D in lung
tissue of different pulmonary aspiration models with MB therapy.
Conclusions
MB treatment might be beneficial in lung injury and therefore shows potential for
clinical use.
Keywords
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Article info
Publication history
Published online: September 04, 2014
Accepted:
August 22,
2014
Received in revised form:
August 15,
2014
Received:
March 21,
2014
Identification
Copyright
© 2015 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
