title: Effect of docosahexaenoic acid on hypoxia/reoxygenation injury in human coronary arterial smooth muscle cells.
abstract: OBJECTIVE
  Hypoxia and reoxygenation (H/R) occur in a wide variety of important clinical conditions such as myocardial infarction. H/R injury is a complex phenomenon involving not only intracellular damage processes but also an injurious inflammatory response. Docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, has long been proved to be protective against several types of cardiovascular disease. However, its beneficial effect during H/R is inconclusive. In this study, we employed an in vitro model to examine whether DHA is protective against H/R-induced cell damage in human coronary artery smooth muscle cells (HCASMCs).
  
  
  METHODS
  HCASMCs in the absence or presence of DHA (1, 3, 10, and 30 μM) were subjected to control or H/R treatment using a modular incubator chamber to create hypoxic condition. Cell viability was evaluated by MTT assay. Spectrophotometric and spectrofluorometric assays were used to measure the generation of nitric oxide (NO) and reactive oxygen species (ROS), respectively. Inflammatory cytokines were determined by enzyme-linked immunosorbent assay. Intracellular calcium mobilization was estimated microfluorimetrically using calcium indicator dye, fura 2-acetomethyl ester.
  
  
  RESULTS
  Hypoxia/reoxygenation caused significant injury in cultured HCASMCs. DHA at low concentrations (1, 3, and 10 μM) did not afford protection, whereas at 30 μM, it caused deleterious effects, presumably by enhancing the production of NO, ROS, IL-1β, and IL-6 and altering the intracellular calcium dynamics.
  
  
  CONCLUSIONS
  Our results do not support the protective function of DHA in H/R-injured coronary arterial smooth muscle cells.
authors: Department of Plastic Surgery, E-Da Hospital, Kaohsiung, Taiwan, ROC.
authors: Guan-Ming
authors: GM
authors: Feng
authors: Jia-Huei
authors: JH
authors: Chen
authors: Cheng-I
authors: CI
authors: Lin
authors: Jung-Mou
authors: JM
authors: Yang
mesh_terms: D002118:Calcium / Q000378:metabolism; D015687:Cell Hypoxia; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000166:cytology* / Q000473:pathology; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D006321:Heart / Q000503:physiopathology; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000187:drug effects*; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D004281:Docosahexaenoic Acids; D009569:Nitric Oxide; D002118:Calcium