Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling

Department of Physical Therapy and Graduate, Institute of Rehabilitation Science, China Medical University, Taichung, Taiwan, Republic of China.
Journal of vascular surgery: official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter (Impact Factor: 2.98). 01/2012; 55(4):1104-15. DOI: 10.1016/j.jvs.2011.10.011
Source: PubMed

ABSTRACT Fig 1. Effects of aspirin on resistin-induced reactive oxygen species (ROS) generation in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were pretreated for 2 hours with various concentrations of aspirin (10-500 μg/mL), followed by treatment with 100 ng/mL resistin for 48 hours. At the end of treatment, HUVECs were incubated with the superoxide-sensitive fluorescent probe dihydroethidium (DHE; 10 μM) for 1 hour. A, Fluorescence images show the ROS level in control cells (left) and in HUVECs stimulated with resistin (middle) in the presence of 500 μg/mL aspirin (right). B, Fluorescence intensity of HUVECs was measured with a fluorescence microplate reader. Fluorescence distribution of DHE oxidation was expressed as a percentage of increased intensity. The activities of superoxide dismutase (SOD) (C) and catalase (D) in HUVECs stimulated with resistin in the absence or presence of indicated concentrations of aspirin were determined. Data are expressed as the mean ± SEM of three independent analyses. #P < .05 vs untreated control; *P < .05 compared with resistin treatment.

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Available from: Wen-Jane Lee, Nov 18, 2014
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