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10.12659/msm.906064 http://scihub22266oqcxt.onion/10.12659/msm.906064 C5930974!5930974 !29679467     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29679467 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Med+Sci+Monit 2018 ; 24 (ä): 2420-2428 Nephropedia Template TP {{tp|p=29679467 |t=2018. Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction |pdf=|usr=}}{{29679467 }} gab.com Text Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction JO: Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29679467 #FOAvip BACKGROUND Salidroside, the major active compound in Rhodiola, has been reported to provide beneficial effects on cardiovascular diseases, but its effects on diabetes-induced vascular endothelial dysfunction are less known. Here, we examined the protective effects of salidroside on endothelial function in diabetes and explored the potential underlying mechanism. MATERIAL AND METHODS First, we assessed the endothelium-dependent relaxation response to acetylcholine, with or without salidroside treatment, in aortas isolated from Sprague-Dawley rats. Then, cell viability, oxidative biomarkers, and protein expression were tested to determine the effect of salidroside treatment on human umbilical vein endothelial cells (HUVECs) in vitro. RESULTS Advanced glycation end product (AGE)-induced endothelial dysfunction was significantly improved by salidroside treatment (P<0.05), as shown by a reduced relaxation response to the vasodilator acetylcholine. Further, incubation with salidroside restored NO levels and reduced reactive oxygen species formation in AGE-stimulated HUVECs in a concentration-dependent manner (P<0.05). We also showed that nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) and nuclear factor kappa B (NF-?B) signaling was critical for the salidroside-mediated beneficial regulation. CONCLUSIONS Our results demonstrate that salidroside protects against AGE-induced endothelial dysfunction, and its effects may be in part attributed to the induction of HO-1 and attenuation of phosphorylated NF-?B p65. Twit Text FOAVip Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction ????Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29679467 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29679467 #FOAvip English Wikipedia <ref>{{Cite pmid|29679467 }}</ref> Salidroside Protects Against Advanced Glycation End Products-Induced Vascular Endothelial Dysfunction #MMPMID29679467 Zhang P ; Li Y ; Guo R ; Zang W Med Sci Monit 2018[Apr]; 24 (ä): 2420-2428 PMID29679467 show ga BACKGROUND Salidroside, the major active compound in Rhodiola, has been reported to provide beneficial effects on cardiovascular diseases, but its effects on diabetes-induced vascular endothelial dysfunction are less known. Here, we examined the protective effects of salidroside on endothelial function in diabetes and explored the potential underlying mechanism. MATERIAL AND METHODS First, we assessed the endothelium-dependent relaxation response to acetylcholine, with or without salidroside treatment, in aortas isolated from Sprague-Dawley rats. Then, cell viability, oxidative biomarkers, and protein expression were tested to determine the effect of salidroside treatment on human umbilical vein endothelial cells (HUVECs) in vitro. RESULTS Advanced glycation end product (AGE)-induced endothelial dysfunction was significantly improved by salidroside treatment (P<0.05), as shown by a reduced relaxation response to the vasodilator acetylcholine. Further, incubation with salidroside restored NO levels and reduced reactive oxygen species formation in AGE-stimulated HUVECs in a concentration-dependent manner (P<0.05). We also showed that nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) and nuclear factor kappa B (NF-?B) signaling was critical for the salidroside-mediated beneficial regulation. CONCLUSIONS Our results demonstrate that salidroside protects against AGE-induced endothelial dysfunction, and its effects may be in part attributed to the induction of HO-1 and attenuation of phosphorylated NF-?B p65. |Animals [MESH] |Aorta/*drug effects [MESH] |Apoptosis/drug effects [MESH] |Cell Survival/drug effects [MESH] |Diabetes Complications/drug therapy [MESH] |Disease Models, Animal [MESH] |Endothelial Cells/*drug effects [MESH] |Glucosides/*metabolism/pharmacology [MESH] |Glycation End Products, Advanced/adverse effects/drug effects [MESH] |Heme Oxygenase-1/metabolism [MESH] |Human Umbilical Vein Endothelial Cells/drug effects [MESH] |Humans [MESH] |Male [MESH] |NF-E2-Related Factor 2/metabolism [MESH] |NF-kappa B/metabolism [MESH] |Oxidative Stress/drug effects [MESH] |Phenols/*metabolism/pharmacology [MESH] |Phosphorylation/drug effects [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Reactive Oxygen Species/metabolism [MESH]Salidroside Protects Against Advanced Glycation End Products-Induced V(epmc).pdf DeepDyve Pubget Overpricing