2018
DOI: 10.1016/j.ejphar.2017.09.052
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Vaccarin protects human microvascular endothelial cells from apoptosis via attenuation of HDAC1 and oxidative stress

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Cited by 23 publications
(15 citation statements)
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“…Several studies have used this Ang II dose-range to induce inflammatory and oxidative responses [ 36 , 37 , 38 , 39 , 40 ]. On the other hand, HMEC-1 cells were chosen as a model because they are employed in various studies to induce endothelial dysfunction, increasing the production of ROS and inflammatory factors [ 41 , 42 , 43 ].…”
Section: Discussionmentioning
confidence: 99%
“…Several studies have used this Ang II dose-range to induce inflammatory and oxidative responses [ 36 , 37 , 38 , 39 , 40 ]. On the other hand, HMEC-1 cells were chosen as a model because they are employed in various studies to induce endothelial dysfunction, increasing the production of ROS and inflammatory factors [ 41 , 42 , 43 ].…”
Section: Discussionmentioning
confidence: 99%
“…Cells were plated at a density of 3 × 10 3 per well in a 96-well microplate and incubated at 37 °C overnight. The cells were treated with various concentrations of test compounds (the final concentrations of the compounds were 0, 5, 10, 20, and 40 µM) for 48 h. Then, cell viability was determined by CCK-8 assay [19,20].…”
Section: Methodsmentioning
confidence: 99%
“…The total protein was extracted by RIPA lysis buffer (Cwbio, Nanjing, China) with protease and phosphatase inhibitor (Cwbio, Nanjing, China) as peer-described [9] and quantified with BCA protein assay kit (Beyotime Biotechnology, Shanghai, China). Equal amounts of protein were electrophoresed, blotted, and incubated with the required antibodies at 4 • C overnight.…”
Section: Western Blottingmentioning
confidence: 99%
“…In vitro experiments revealed that VAC promoted proliferation of human microvascular endothelial cells (HMEC-1) by activating the fibroblast growth factor-2 (FGF-2) mediated fibroblast growth factor receptor (FGFR-1) signaling pathway under normal conditions [7]. Recently, it has been found that VAC could promote NO production via inhibition of the ROS/AMPK/miRNA-34a/eNOS signaling cascade [8], and protect HG-induced endothelial cell apoptosis by inhibiting the accumulation of reactive oxygen species and the expression of histone deacetylase 1 (HDAC1) [9]. In addition, bacterial cellulose-vaccarin (BC-VAC) membranes not only enhanced the mechanical and physical properties of the cellulose membrane but also promoted acute mechanical wound healing [10].…”
Section: Introductionmentioning
confidence: 99%