title: Apocynin decreases AGEs-induced stimulation of NF-κB protein expression in vascular smooth muscle cells from GK rats.
abstract: BACKGROUND
  Elevated oxidative stress plays a key role in diabetes-associated vascular disease. Excessive production of reactive oxygen species via advanced glycation end products (AGEs) activates peroxisome proliferator-activated receptor gamma (PPARγ) and the transcription factor nuclear factor-kB (NF-κB) in aortic vascular smooth muscle cells (VSMCs). Apocynin, a drug with an antioxidant effect, has also been proposed as a therapeutic agent for atherosclerotic disease.
  
  
  OBJECTIVE
  This work investigates the effects of apocynin on the PPARγ and NF-κB protein expression evoked by AGEs in cultured VSMCs from Goto-Kakisaki (GK) rats, a non-obese insulin model of both insulin resistance and type 2 diabetes.
  
  
  METHODS
  VSMCs, isolated from aortas of GK and non-diabetic rats, were cultured. The expression of proteins was evaluated by Western blot. The blood glucose concentration was measured with a blood glucose test meter. The diabetes of GK rats was controlled by blood glucose and insulin determinations (non-fasting values). The serum insulin concentration was determined by radioimmunoassay.
  
  
  RESULTS
  In VSMCs from non-diabetic and GK rats, apocynin (1 and 10 µM) abolished the protein overexpression of NF-κB induced by glycated bovine serum albumin (AGEs-BSA) incubation. However, apocynin (1 and 10 µM) enhanced the expression of PPARγ protein in the presence of AGEs-BSA (100 μg/mL) in VSMCs from non-diabetic, but not from GK rats.
  
  
  CONCLUSIONS
  These findings suggest that apocynin decreases the incidence of alterations in VSMCs induced by AGEs through the reduction of NF-κB and may represent an attractive therapeutic approach to treat diabetes mellitus.
authors.affiliation: Núcleo de Nutrição, Centro Acadêmico de Vitória, Universidade Federal de Pernambuco , Recife, PE , Brasil .
authors.forename: Cristina Oliveira
authors.initials: CO
authors.lastname: Silva
authors.forename: Odair Alves
authors.initials: OA
authors.lastname: da Silva
authors.forename: Gloria Pinto
authors.initials: GP
authors.lastname: Duarte
authors.forename: Bernard
authors.initials: B
authors.lastname: Descomps
authors.forename: Saad
authors.initials: S
authors.lastname: Lahlou
mesh_terms: D000098:Acetophenones / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D015153:Blotting, Western; D018929:Cell Culture Techniques; D002478:Cells, Cultured; D004591:Electrophoresis, Polyacrylamide Gel; D017127:Glycation End Products, Advanced / Q000494:pharmacology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000096:biosynthesis*; D047495:PPAR gamma / Q000096:biosynthesis; D011919:Rats, Inbred Strains; D012710:Serum Albumin, Bovine / Q000494:pharmacology*
chemical_list: D000098:Acetophenones; D000975:Antioxidants; D017127:Glycation End Products, Advanced; D016328:NF-kappa B; D047495:PPAR gamma; C081628:advanced glycation end products-bovine serum albumin; D012710:Serum Albumin, Bovine; C056165:acetovanillone
keywords: Advanced glycation end-product; PPARγ protein expression; antioxidant; diabetes mellitus