title: Protective effect of resveratrol against caspase 3 activation in primary mouse fibroblasts.
abstract: OBJECTIVE
  To study the effect of resveratrol on survival and caspase 3 activation in non-transformed cells after serum deprivation.
  
  
  METHODS
  Apoptosis was induced by serum deprivation in primary mouse embryonic fibroblasts. Caspase 3 activation and lactate dehydrogenase release were assayed as cell viability measure by using their fluorogenic substrates. The involvement of PI3K, ERK, JNK, p38, and SIRT1 signaling pathways was also examined.
  
  
  RESULTS
  Serum deprivation of primary fibroblasts induced significant activation of caspase 3 within 3 hours and reduced cell viability after 24 hours. Resveratrol dose-dependently prevented caspase activation and improved cell viability with 50% inhibitory concentration (IC50)=66.3±13.81 μM. It also reduced the already up-regulated caspase 3 activity when it was added to the cell culture medium after 3 hour serum deprivation, suggesting its rescue effect. Among the major signaling pathways, p38 kinase was critical for the protective effect of resveratrol which was abolished completely in the presence of p38 inhibitor.
  
  
  CONCLUSIONS
  Resveratrol showed protective effect against cell death in a rather high dose. Involvement of p38 kinase in this effect suggests the role of mild stress in its cytoprotective action. Furthermore due to its rescue effect, resveratrol may be used not only for prevention, but also treatment of age-related degenerative diseases, but in the higher dose than consumed in conventional diet.
authors.forename: Zsófia
authors.initials: Z
authors.lastname: Ulakcsai
authors.forename: Fruzsina
authors.initials: F
authors.lastname: Bagaméry
authors.forename: István
authors.initials: I
authors.lastname: Vincze
authors.forename: Éva
authors.initials: É
authors.lastname: Szökő
authors.affiliation: Tamas Tábi, Nagyvarad ter 4, Budapest, H-1089, Hungary, tabi.tamas@pharma.semmelweis-univ.hu.
authors.forename: Tamás
authors.initials: T
authors.lastname: Tábi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004622:Embryo, Mammalian / Q000166:cytology; D005347:Fibroblasts / Q000187:drug effects* / Q000201:enzymology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000502:physiology; D051379:Mice; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000077185:Resveratrol; D015398:Signal Transduction; D056564:Sirtuin 1 / Q000378:metabolism; D013267:Stilbenes / Q000494:pharmacology*; D015854:Up-Regulation
chemical_list: D000975:Antioxidants; D013267:Stilbenes; D007770:L-Lactate Dehydrogenase; D019869:Phosphatidylinositol 3-Kinases; D053148:Caspase 3; C470545:Sirt1 protein, mouse; D056564:Sirtuin 1; D000077185:Resveratrol