Chitosan oligosaccharide ameliorates acute lung injury induced by blast injury through the DDAH1/ADMA pathway
Autor: | Cang-Ci Tong, Peifang Cong, Yubiao Zhang, Ming-Xiao Hou, Ying Liu, Hongxu Jin, Zhou Tong, Lin Shi, Xiuyun Shi, Yun-En Liu |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male Physiology Protein Expression lcsh:Medicine Apoptosis medicine.disease_cause Pathology and Laboratory Medicine p38 Mitogen-Activated Protein Kinases Mice Heart Rate Blast Injuries Immune Physiology Medicine and Health Sciences Enzyme-Linked Immunoassays lcsh:Science Immune Response chemistry.chemical_classification Innate Immune System Multidisciplinary Cell Death Chemistry Animal Models respiratory system Experimental Organism Systems Cell Processes Cytokines Tumor necrosis factor alpha Inflammation Mediators Research Article p38 mitogen-activated protein kinases Immunology Acute Lung Injury Cardiology Mouse Models Enzyme-Linked Immunosorbent Assay Lung injury Research and Analysis Methods Amidohydrolases 03 medical and health sciences Signs and Symptoms Model Organisms Diagnostic Medicine medicine Gene Expression and Vector Techniques Animals Protein kinase A Molecular Biology Techniques Immunoassays Molecular Biology Inflammation Reactive oxygen species Molecular Biology Assays and Analysis Techniques Chitosan lcsh:R Biology and Life Sciences Cell Biology Molecular Development Molecular biology respiratory tract diseases Oxidative Stress 030104 developmental biology Terminal deoxynucleotidyl transferase Immune System Immunologic Techniques lcsh:Q Oxidative stress Developmental Biology |
Zdroj: | PLoS ONE, Vol 13, Iss 2, p e0192135 (2018) PLoS ONE |
ISSN: | 1932-6203 |
Popis: | Objective To investigate the protective effect of chitosan oligosaccharide (COS) on acute lung injury (ALI) caused by blast injury, and explore possible molecular mechanisms. Methods A mouse model of blast injury-induced ALI was established using a self-made explosive device. Thirty mice were randomly assigned to control, ALI and ALI + COS groups. An eight-channel physiological monitor was used to determine the mouse physiological index. Enzyme linked immunosorbent assay was used to measure serum inflammatory factors. Hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling assay, immunofluorescence staining, real time-polymerase chain reaction and western blot assay were used to detect inflammatory reactions, oxidative stress and apoptosis. Results Mice were sacrificed 24 hours after successful model induction. Compared with the ALI group, the heart rate, respiration and PCO2 were significantly lower, but the PO2, TCO2 and HCO3- were significantly higher in the ALI + COS group. Compared to ALI alone, COS treatment of ALI caused a significant decrease in the wet/dry lung weight ratio, indicating a reduction in lung edema, inflammatory cell infiltration, levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-4, IL-6 and nuclear factor kappa B mRNA and protein expression were reduced and IL-10 mRNA and protein expression was increased (P < 0.05). COS significantly inhibited reactive oxygen species, MDA5 and IREα mRNA and protein expressions, cell apoptosis and Bax and Caspase-3 mRNA and protein expressions, and significantly increased superoxide dismutase-1 mRNA expression, and Bcl-2 and Caspase-8 mRNA and protein expression (all P |
Databáze: | OpenAIRE |
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