title: Effects of folic acid on cardiac myocyte apoptosis in rats with streptozotocin-induced diabetes mellitus.
abstract: BACKGROUND
  The effect of folic acid on cardiac myocyte apoptosis secondary to diabetes is unknown.
  
  
  METHODS
  Diabetic rats were divided into diabetic control (DC, n = 11), low-dose (LDF, 0.4 mg/kg/day, n = 12) and high-dose (HDF, 1.2 mg/kg/day, n = 12) folic acid groups. Non-diabetic rats (n = 11) were used as the normal control (NC).
  
  
  RESULTS
  After 11 weeks of treatment, compared with the NC group, the DC group showed a reduced blood levels of reactive oxygen species (ROS, P < 0.01). The rate of cardiac myocyte apoptosis in the diabetic control group was also greater than in the non-diabetic control group (P < 0.01). In folic acid-treated rats, the blood levels of ROS was higher than in the diabetic control group (P < 0.05). There was a dose-dependent reduction in the rate of cardiac myocyte apoptosis in the folic acid groups (P < 0.01), and this was accompanied by an increased level of anti-apoptotic protein Bcl-2 and decreased level of pro-apoptotic protein Bax and Fas (P < 0.01).
  
  
  CONCLUSIONS
  Dietary folic acid supplementation diminishes the cardiac myocyte apoptosis in streptozotocin-induced diabetes. The apoptosis suppression is accompanied by an increase in the expression of Bcl-2 and a decrease in Bax and Fas.
authors.affiliation: Department of Cardiology, Guangzhou Red Cross Hospital, the Fourth Affiliated Hospital of Ji-Nan University, Guangzhou 510220, People's Republic of China. wutongguo@sohu.com
authors.forename: Tong-Guo
authors.initials: TG
authors.lastname: Wu
authors.forename: Wei-Hong
authors.initials: WH
authors.lastname: Li
authors.forename: Zi-Qing
authors.initials: ZQ
authors.lastname: Lin
authors.forename: Le-Xin
authors.initials: LX
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001786:Blood Glucose / Q000378:metabolism; D048909:Diabetes Complications / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D005492:Folic Acid / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009569:Nitric Oxide / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D001786:Blood Glucose; C491898:Fas protein, rat; D007328:Insulin; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D009569:Nitric Oxide; D008315:Malondialdehyde; D005492:Folic Acid; D013482:Superoxide Dismutase