کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5831972 1559754 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Astilbin alleviates LPS-induced ARDS by suppressing MAPK signaling pathway and protecting pulmonary endothelial glycocalyx
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Astilbin alleviates LPS-induced ARDS by suppressing MAPK signaling pathway and protecting pulmonary endothelial glycocalyx
چکیده انگلیسی
Acute respiratory distress syndrome (ARDS) is a devastating disorder that is characterized by increased vascular endothelial permeability and inflammation. Unfortunately, no effective treatment beyond supportive care is available for ARDS. Astilbin, a flavonoid compound isolated from Rhizoma Smilacis Glabrae, has been used for anti-hepatic, anti-arthritic, and anti-renal injury treatments. This study examined the effects of Astilbin on pulmonary inflammatory activation and endothelial cell barrier dysfunction caused by Gram-negative bacterial endotoxin lipopolysaccharide (LPS). Endothelial cells from human umbilical veins or male Kunming mice were pretreated with Astilbin 24 h before LPS stimulation. Results showed that Astilbin significantly attenuated the pulmonary histopathological changes and neutrophil infiltration 6 h after the LPS challenge. Astilbin suppressed the activities of myeloperoxidase and malondialdehyde, as well as the expression of tumor necrosis factor-α and interleukin-6 in vivo and in vitro. As indices of pulmonary edema, lung wet-to-dry weight ratios, were markedly decreased by Astilbin pretreatment. Western blot analysis also showed that Astilbin inhibited LPS-induced activation of mitogen-activated protein kinase (MAPK) pathways in lung tissues. Furthermore, Astilbin significantly inhibited the activity of heparanase and reduced the production of heparan sulfate in the blood serum as determined by ELISA. These findings indicated that Astilbin can alleviate LPS-induced ARDS, which potentially contributed to the suppression of MAPK pathway activation and the degradation of endothelial glycocalyx.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 36, July 2016, Pages 51-58
نویسندگان
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