Chemistry can be defined as the study of matter and the changes it undergoes. You¡¯ll sometimes hear it called the central science because it is the connection between physics and all the other sciences, starting with biology. 2032-35-1, Name is 2-Bromo-1,1-diethoxyethane, molecular formula is , belongs to bromides-buliding-blocks compound. In a document, author is Yang, Peng, Category: bromides-buliding-blocks.
Overexpression of miR-129-5p Mitigates Sepsis-Induced Acute Lung Injury by Targeting High Mobility Group Box 1
Background: MicroRNAs are dysregulated in sepsis. Acute lung injury is a progressive syndrome during sepsis. However, the role of miR-129-5p in the development of acute lung injury induced by sepsis remains unclear. Methods: The acute lung injury of sepsis model was established by cecal ligation puncture (CLP)-treated mice and lipopolysaccharide (LPS)-treated murine alveolar epithelial cell line (MLE)-12 cells. The lung injury in vivo was investigated by hematoxylin and eosin staining, terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling staining, enzyme-linked immunosorbent assay, lung wet-to-dry weight ratio, and myeloperoxidase activity. The lung injury in vitro was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assay. The expression levels of miR-129-5p and high mobility group box 1 (HMGB1) were measured by quantitative real-time polymerase chain reaction and Western blot. The association between miR-129-5p and HMGB1 was validated by luciferase assay and RNA immunoprecipitation. Results: The expression of miR-129-5p was decreased in CLP model and LPS-treated MLE-12 cells. Overexpression of miR-129-5p attenuated inflammatory response, apoptosis, lung wet/dry weight ratio, and myeloperoxidase activity induced by CLP surgery in vivo. Moreover, addition of miR-129-5p increased cell viability and suppressed cell apoptosis and inflammatory response in vitro. HMGB1 as a target of miR-129-5p alleviated miR-129-5p emediated injury suppression in LPS-treated MLE-12 cells. Conclusions: miR-129-5p protects against sepsis-induced acute lung injury by decreasing HMGB1 expression, providing new target for sepsis treatment. (C) 2020 Elsevier Inc. All rights reserved.
Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 2032-35-1, in my other articles. Category: bromides-buliding-blocks.