Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide

Background: Cilostazol is an antiplatelet agent, which is known also to have protective effects on endothelial cell. We studied effects of cilostazol on markers of inflammation and endothelial cell damage in patients with severe carotid disease, who underwent carotid endoarterectomy (CEA). Methods: We measured high sensitivity CRP (hsCRP), soluble vascular cellular adhesion molecule (VCAM)-1, soluble E-selectin, soluble intercellular adhesion molecule-1 and von Willebrand Factor antigen (vWF) in 45 patients who underwent CEA (38 males and 7 females, mean age was 69 years). Venous blood was taken from each patient before (Pre) and 3 days (Day3), 10 days (Day10), 4 weeks and 1 year (Post) after CEA. Each marker was compared between patients who were treated with aspirin alone (aspirin group, 18 cases) and those treated with cilostazol alone or cilostazol plus aspirin (cilostazol group, 17 cases). Results: The levels of hsCRP, VCAM-1, E-selectin and vWF at Day3 and the levels of hsCRP and VCAM-1 on Day10 were significantly higher than those at PreCEA. The alterations of those markers were not significantly different between the aspirin and cilotazol groups. The levels of hsCRP in the cilostazol group were significantly lower than those in aspirin group at both PreCEA and PostCEA. The levels of VCAM-1 at PreCEA in the cilostazol group were significantly lower than those in the aspirin group. Conclusions: The results suggested that cilostazol inhibits inflammation and endothelial cell damage in patients with severe carotid disease, although its protective effects did not reduce the endothelial cell damage induced by CEA when compared with aspirin.

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Protective effect of Xin Mai Jia ultrafiltration extract on human umbilical vein endothelial cell injury induced by hydrogen peroxide and the effect on the NO-cGMP signaling pathway

Experimental and Therapeutic Medicine ◽

10.3892/etm.2014.1700 ◽

2014 ◽

Vol 8 (1) ◽

pp. 38-48 ◽

Cited By ~ 4

Author(s):

YALING YIN ◽

JIA WAN ◽

PENG LI ◽

YANLONG JIA ◽

RUILI SUN ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Endothelial Cell ◽

Protective Effect ◽

Signaling Pathway ◽

Cell Injury ◽

Umbilical Vein ◽

Endothelial Cell Injury ◽

Human Umbilical Vein ◽

Cgmp Signaling

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Vitamin D ameliorated endothelial cell damage induced by diabetes via regulation of lncRNA MEG3 in human umbilical vein endothelial cells

Archives of Medical Science ◽

10.5114/aoms.2020.101248 ◽

2020 ◽

Author(s):

Hua Wei ◽

Qiongfang Zhang ◽

Jun Li ◽

Jing Yang ◽

Bin Huang ◽

...

Keyword(s):

Vitamin D ◽

Endothelial Cells ◽

Endothelial Cell ◽

Cell Damage ◽

Umbilical Vein ◽

Nuclear Volume ◽

Endothelial Cell Damage ◽

Tnf Α ◽

Gene And Protein Expression ◽

Umbilical Vein Endothelial Cells

IntroductionThe purpose of this study was to investigate long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) effects in vitamin D (Vit. D) treatment in endothelial cell damage induced by diabetes.Material and methodsWe used human umbilical vein endothelial cells (HUVECs) as a research objective in our study and used high glucose in a diabetic cell model. We evaluated cell apoptosis by flow cytometry, inflammatory factors (IL-6, IL-1β and TNF-α) concentrations by ELISA assay, relative gene and protein expression by RT-qPCR and WB assay, and NF-κB(p65) nuclear volume by cellular immunofluorescence.ResultsCompared with the NC (normal control) group, the cell apoptosis rate was significantly increased, inflammatory factor (IL-6, IL-1β and TNF-α) concentrations were significantly up-regulated, lncRNA MEG3 gene expression was significantly depressed, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor B p65 (NF-κB(p65)) gene and protein expression levels were significantly increased and NF-κB(p65) nuclear volume was significantly up-regulated (p < 0.001, respectively). With Vit. D supplementation, compared with the Model group, Vit. D improved endothelial cell damage induced by diabetes, while lncRNA MEG3 was significantly increased and the TLR4/MyD88/NF-κB(p65) pathway was significantly depressed dose-dependently (all p < 0.05). With sh-MEG3 transfection, the Vit. D treatment effects were significantly reduced.ConclusionsVit. D improved endothelial cell damage induced by diabetes via lncRNA MEG3 up-regulation in vitro study.

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