title: Mechanisms of genistein protection on pancreas cell damage in high glucose condition.
abstract: OBJECTIVE
  An adequate β cell number is important to prevent the onset and development of type 2 diabetes. The aim of this study was to determine if phytoestrogen gesintein has protective effects against high glucose-induced cell apoptosis in human pancreas cells, and to try to determine the possible mechanism for this protection.
  
  
  METHODS
  Human pancreatic β cells were subjected to normal (5 mM) or high glucose (25 mM) with and without the presence of 100 nM genistein, and also in the presence and absence of the pure anti-estrogen ICI-182780 (100 nM). Bcl-2 siRNA transfection was performed to investigate if the effect of genistein was also Bcl-2 dependent. Cell proliferation and apoptosis were determined by Tritiated Thymidine Incorporation Assay and Cell Apoptosis Detection ELISA. Estrogen receptor and Bcl-2 mRNA expression was measured by Real-time Quantitative PCR.
  
  
  RESULTS
  High glucose concentration caused cell proliferation inhibition and apoptosis in cultured human pancreatic β cells, and these effects were significantly reversed by genistein (P<0.01). Estrogen receptor beta was expressed in the cultured cells, and genistein protection was blocked by ICI-182780 administration as well as Bcl-2 siRNA transfection.
  
  
  CONCLUSIONS
  Phytoestrogen gave protection against high glucose-induced pancreatic cell damage through estrogen receptor beta and Bcl-2 dependent pathways.
authors.affiliation: Department of Geriatric Endocrinology, The Chinese PLA General Hospital, China.
authors.forename: Wen-Wen
authors.initials: WW
authors.lastname: Zhong
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: Chun-Lin
authors.initials: CL
authors.lastname: Li
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D001483:Base Sequence; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D017931:DNA Primers / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D000077267:Fulvestrant; D019254:Genes, bcl-2; D019833:Genistein / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D048789:Phytoestrogens / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D011960:Receptors, Estrogen / Q000235:genetics
chemical_list: D017931:DNA Primers; D004965:Estrogen Antagonists; D048789:Phytoestrogens; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D011960:Receptors, Estrogen; D000077267:Fulvestrant; D004958:Estradiol; D019833:Genistein; D005947:Glucose