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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Lee, Ju Hwan Pae, Hyun-Ock Son, Yong Park, Seong Hoon Cheong, Yong-Kwan Chung, Hun-Taeg Jeong, Sun-Oh |
| Description | Author Affiliation: Jeong SO ( Department of Microbiology and Immunology, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.); Son Y ( Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.); Lee JH ( Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.); Cheong YK ( Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.); Park SH ( Institute for Metabolic Disease, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.); Chung HT ( Department of Biological Science, University of Ulsan, Ulsan 680749, Republic of Korea.); Pae HO ( Department of Microbiology and Immunology, Wonkwang University School of Medicine, Iksan 570749, Republic of Korea.) |
| Abstract | Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS). Heme oxygenase-1 (HO-1) is important in the preservation of NO bioavailability. Piceatannol (Pic), with similar chemical structure to resveratrol, is suggested to possess similar protective effects as resveratrol. In the present study, human umbilical vein endothelial cells (HUVECs), stimulated with PA, were used to examine the endothelial protective effects of Pic. Pic increased the expression of HO-1 via nuclear factor erythroid-2-related factor-2 activation in the HUVECs, and decreased the PA-induced secretions of interleukin-6 and tumor necrosis factor- , and the formation of reactive oxygen species ROS via inhibition of NF-κB activation. Notably, following inhibition of HO-1 activity by tin protoporphryin-IX, Pic did not prevent cytokine secretion, ROS formation, and NF-κB activation in the PA-stimulated HUVECs. PA attenuated insulin-mediated insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, leading to decreased glucose uptake, and phosphorylation of eNOS, leading to a reduction in the production of NO. Pic effectively mitigated the inhibitory effects of PA on the insulin-mediated phosphorylation of IRS-1 and eNOS, which was not observed following inhibition of HO1 activity. The results of the present study suggested that Pic may have the potential to prevent PA-induced impairment of insulin signaling and eNOS function, by inducing the expression of the anti-inflammatory and antioxidant, HO-1. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2015.3553 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 12 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2015-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Anti-inflammatory Agents, Non-steroidal Pharmacology Antioxidants Heme Oxygenase-1 Genetics Human Umbilical Vein Endothelial Cells Drug Effects Insulin Metabolism Nitric Oxide Stilbenes Gene Expression Regulation Cytology Insulin Receptor Substrate Proteins Interleukin-6 Metalloporphyrins Nf-e2-related Factor 2 Nf-kappa B Nitric Oxide Synthase Type Iii Oxidants Antagonists & Inhibitors Oxidative Stress Palmitic Acid Protoporphyrins Reactive Oxygen Species Signal Transduction Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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