Anti-septic effects of phenolic glycosides from Rhododendron brachycarpum in vitro and in vivo
| Autor: | Sae-Kwang Ku, Hayoung Yoo, MinKyun Na, Wei Zhou, Min-Su Han, Jong-Sup Bae |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Leukocyte migration
Lipopolysaccharide Medicine (miscellaneous) Inflammation chemical and pharmacologic phenomena Pharmacology HMGB1 Sepsis chemistry.chemical_compound In vivo medicine TX341-641 chemistry.chemical_classification Nutrition and Dietetics biology Nutrition. Foods and food supply Glycoside Phenolic glycoside medicine.disease In vitro chemistry Biochemistry biology.protein medicine.symptom Food Science |
| Zdroj: | Journal of Functional Foods, Vol 16, Iss, Pp 448-459 (2015) |
| ISSN: | 1756-4646 |
| Popis: | Inhibition of high mobility group box 1 (HMGB1) and restoration of endothelial integrity is emerging as an attractive therapeutic strategy in the management of sepsis. Here, we examined the effects of three phenolic glycosides ( 1 – 3 ) found in Rhododendron brachycarpum , which has been used as food and medicinal resources for anti-rheumatic agent, diuretic, and anti-inflammatory in Asia, on inflammatory responses by monitoring the effects on lipopolysaccharide (LPS)- or cecal ligation and puncture (CLP)-mediated release of HMGB1, and on the modulation of HMGB1-mediated inflammatory responses. The anti-inflammatory activities of phenolic glycosides 1 – 3 were determined by measuring permeability, monocyte adhesion and migration, and the activation of pro-inflammatory proteins in HMGB1-activated HUVECs and mice. All three phenolic glycosides inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells. Phenolic glycosides 1 – 3 also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice. In addition, treatment with compounds 1 – 3 reduced CLP-induced release of HMGB1 and sepsis-related mortality and pulmonary injury. Our results indicate that phenolic glycosides 1 – 3 could be candidate therapeutic agents for various severe vascular inflammatory diseases via the inhibition of the HMGB1 signaling pathway. |
| Databáze: | OpenAIRE |
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