Journal: Redox Biology

Article Title: Procyanidin B2 mitigates endothelial endoplasmic reticulum stress through a PPARδ-Dependent mechanism

doi: 10.1016/j.redox.2020.101728

Figure Lengend Snippet: Inhibition of PPARδ abrogated the effects of PCB2 on NO and ROS production. ECs were pretreated with GSK0660 (1 μM) for 1 h and then treated with PCB2 (10 μM) for 12 h before exposure to HG (30 mM) for 24 h. (A) Confocal microscopic detection of superoxide with DHE. (B) The mean fluorescence intensity was evaluated. Scale bar: 25 μm (n = 3). (C) Production of ROS was measured with L-012 chemiluminescence (n = 5). (D) Summerized levels of intracellular NO production in ECs detected as DAF FM-DA signals before (F0) and after (F1) the addition of A23187 (n = 5). (E) Nitrite levels in EC supernatants was measured by using the Griess reagent (n = 4). All data were expressed as mean ± SEM. * P < 0.05, ** P < 0.01 vs. vehicle; # P < 0.05, ## P < 0.01 vs. HG; † P < 0.05, †† P < 0.01 vs. PCB2+HG.

Article Snippet: Antibodies against adenosine monophosphate-activated protein kinase (AMPK), phospho-AMPK (Thr 172 ), activating transcription factor 4 (ATF4), ATF6, GRP78, protein-disulfide isomerase (PDI), IRE1α and Griess reagent nitrite measurement kit were from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Inhibition, Fluorescence