FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4307888974> ?p ?o ?g. }

• W4307888974 abstract "The endothelium, a crucial homeostatic organ, regulates vascular permeability and tone. Under physiological conditions, endothelial stimulation induces vasodilator endothelial nitric oxide (eNO) release and prevents adhesion molecule accessibility and leukocyte adhesion and migration into vessel walls. Endothelium dysfunction is a principal event in cardiovascular disorders, including atherosclerosis. Minimal attention is given to an important endothelial cell structure, the endothelial glycocalyx (GCX), a negatively charged heterogeneous polysaccharide that serves as a protective covering for endothelial cells and enables endothelial cells to transduce mechanical stimuli into various biological and chemical activities. Endothelial GCX shedding thus plays a role in endothelial dysfunction, for example by increasing vascular permeability and decreasing vessel tone. Consequently, there is increasing interest in developing therapies that focus on GCX repair to limit downstream endothelium dysfunction and prevent further downstream cardiovascular events. Here, we present diosmin (3′,5,7-trihydroxy-4′-methoxyflavone-7-rhamnoglucoside), a flavone glycoside of diosmetin, which downregulates adhesive molecule expression, decreases inflammation and capillary permeability, and upregulates eNO expression. Due to these pleiotropic effects of diosmin on the vasculature, a possible unidentified mechanism of action is through GCX restoration. We hypothesize that diosmin positively affects GCX integrity along with GCX-related endothelial functions. Our hypothesis was tested in a partial ligation left carotid artery (LCA) mouse model, where the right carotid artery was the control for each mouse. Diosmin (50 mg/kg) was administered daily for 7 days, 72 h after ligation. Within the ligated mice LCAs, diosmin treatment elevated the activated eNO synthase level, inhibited inflammatory cell uptake, decreased vessel wall thickness, increased vessel diameter, and increased GCX coverage of the vessel wall. ELISA showed a decrease in hyaluronan concentration in plasma samples of diosmin-treated mice, signifying reduced GCX shedding. In summary, diosmin supported endothelial GCX integrity, to which we attribute diosmin's preservation of endothelial function as indicated by attenuated expression of inflammatory factors and restored vascular tone." @default.
• W4307888974 created "2022-11-06" @default.
• W4307888974 creator A5024674417 @default.
• W4307888974 creator A5025225018 @default.
• W4307888974 creator A5054903556 @default.
• W4307888974 creator A5081759237 @default.
• W4307888974 creator A5082103323 @default.
• W4307888974 creator A5091006956 @default.
• W4307888974 date "2022-10-31" @default.
• W4307888974 modified "2023-09-24" @default.
• W4307888974 title "Diosmin and its glycocalyx restorative and <scp>anti‐inflammatory</scp> effects on injured blood vessels" @default.
• W4307888974 cites W1595658449 @default.
• W4307888974 cites W1969319463 @default.
• W4307888974 cites W1979486625 @default.
• W4307888974 cites W1986853688 @default.
• W4307888974 cites W1996524802 @default.
• W4307888974 cites W1999217768 @default.
• W4307888974 cites W2002267563 @default.
• W4307888974 cites W2006683524 @default.
• W4307888974 cites W2008868622 @default.
• W4307888974 cites W2024184035 @default.
• W4307888974 cites W2025125263 @default.
• W4307888974 cites W2025900960 @default.
• W4307888974 cites W2028991299 @default.
• W4307888974 cites W2030105817 @default.
• W4307888974 cites W2047136147 @default.
• W4307888974 cites W2056938528 @default.
• W4307888974 cites W2057002961 @default.
• W4307888974 cites W2058172582 @default.
• W4307888974 cites W2058626506 @default.
• W4307888974 cites W2058890881 @default.
• W4307888974 cites W2065618553 @default.
• W4307888974 cites W2068370169 @default.
• W4307888974 cites W2068820307 @default.
• W4307888974 cites W2071163714 @default.
• W4307888974 cites W2083442559 @default.
• W4307888974 cites W2083688412 @default.
• W4307888974 cites W2088505684 @default.
• W4307888974 cites W2089130484 @default.
• W4307888974 cites W2089292440 @default.
• W4307888974 cites W2091638984 @default.
• W4307888974 cites W2096517726 @default.
• W4307888974 cites W2097000915 @default.
• W4307888974 cites W2101096780 @default.
• W4307888974 cites W2101773230 @default.
• W4307888974 cites W2104052152 @default.
• W4307888974 cites W2111247242 @default.
• W4307888974 cites W2112540241 @default.
• W4307888974 cites W2115000187 @default.
• W4307888974 cites W2126429178 @default.
• W4307888974 cites W2126630940 @default.
• W4307888974 cites W2129759704 @default.
• W4307888974 cites W2137287545 @default.
• W4307888974 cites W2145415920 @default.
• W4307888974 cites W2146190354 @default.
• W4307888974 cites W2147604745 @default.
• W4307888974 cites W2165130888 @default.
• W4307888974 cites W2167279371 @default.
• W4307888974 cites W2170109807 @default.
• W4307888974 cites W2230203535 @default.
• W4307888974 cites W2480349329 @default.
• W4307888974 cites W2490785976 @default.
• W4307888974 cites W2509095239 @default.
• W4307888974 cites W2590134608 @default.
• W4307888974 cites W2619587738 @default.
• W4307888974 cites W2739722802 @default.
• W4307888974 cites W2747816469 @default.
• W4307888974 cites W2763249451 @default.
• W4307888974 cites W2767573195 @default.
• W4307888974 cites W2889288786 @default.
• W4307888974 cites W2889931938 @default.
• W4307888974 cites W2895187644 @default.
• W4307888974 cites W2901557743 @default.
• W4307888974 cites W2904535451 @default.
• W4307888974 cites W2915526534 @default.
• W4307888974 cites W2915852744 @default.
• W4307888974 cites W2919684368 @default.
• W4307888974 cites W2962565119 @default.
• W4307888974 cites W2963630514 @default.
• W4307888974 cites W2993557344 @default.
• W4307888974 cites W2996078002 @default.
• W4307888974 cites W2997805831 @default.
• W4307888974 cites W3002926097 @default.
• W4307888974 cites W3005273655 @default.
• W4307888974 cites W3010166539 @default.
• W4307888974 cites W3011763970 @default.
• W4307888974 cites W3043470457 @default.
• W4307888974 cites W3087181490 @default.
• W4307888974 cites W3088919755 @default.
• W4307888974 cites W3132973190 @default.
• W4307888974 cites W3152191068 @default.
• W4307888974 cites W3215439881 @default.
• W4307888974 cites W4300461882 @default.
• W4307888974 doi "https://doi.org/10.1096/fj.202200053rr" @default.
• W4307888974 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36315163" @default.
• W4307888974 hasPublicationYear "2022" @default.
• W4307888974 type Work @default.
• W4307888974 citedByCount "0" @default.
• W4307888974 crossrefType "journal-article" @default.
• W4307888974 hasAuthorship W4307888974A5024674417 @default.

• next