title: Study of molecular mechanism of Prostaglandin E1 in inhibiting coronary heart disease.
abstract: Prostaglandin E1 has been used clinically for improving heart diseases. In this study, we examined the effect of Prostaglandin E1 on blood lipid levels, heart protein and genes expression in coronary heart disease (CHD) rats. Female rats were fed either a control diet or hypercholesterolemic diet for 14 weeks. The feeding of a hypercholesterolemic diet (HCD) increased the serum TC, TG, and LDL-c levels, decreased the serum HDL-c, E2, P, FSH, LH and PRL levels in CHD rats. In addition, The feeding of a HCD diet markedly increased the content of serum TXA2, TXB2, and decreased the content of serum PGI2, and PGI2/TXA2, 6-Keto PGF1a. Furthermore, the feeding of a hypercholesterolemic diet markedly increased expression levels of myocardium Fas and Caspase-3 protein and mRNA levels, vascular endothelial growth factor and basic fibroblast growth factor mRNA, and decreased RyR2 mRNA in CHD rats. The feeding of Prostaglandin E1 for 14 weeks significantly reversed these abnormal biochemical indexes in rats. These findings suggest that Prostaglandin E1 play a obvious heart protective effect. The mechanisms may be related to restraining the excessive activation of Fas and Caspase-3 protein and modulating some gene expressions associated with CHD.
authors.affiliation: Department of Cardiology, Fengxian Branch of Shanghai 6th People's Hospital, Shanghai, 201400, China.
authors.forename: H J
authors.initials: HJ
authors.lastname: Liu
authors.forename: J W
authors.initials: JW
authors.lastname: Ma
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Qiao
authors.forename: B
authors.initials: B
authors.lastname: Xu
mesh_terms: D000527:Alprostadil / Q000627:therapeutic use*; D000818:Animals; D053148:Caspase 3 / Q000378:metabolism; D002791:Cholesterol, Dietary; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy* / Q000235:genetics*; D004958:Estradiol / Q000097:blood; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D009206:Myocardium / Q000201:enzymology; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019837:Ryanodine Receptor Calcium Release Channel / Q000235:genetics / Q000378:metabolism; D013931:Thromboxanes / Q000097:blood; D014280:Triglycerides / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: D002791:Cholesterol, Dietary; D008078:Cholesterol, LDL; C491898:Fas protein, rat; D012333:RNA, Messenger; D019837:Ryanodine Receptor Calcium Release Channel; D013931:Thromboxanes; D014280:Triglycerides; D042461:Vascular Endothelial Growth Factor A; D019014:fas Receptor; D016222:Fibroblast Growth Factor 2; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin; D007986:Luteinizing Hormone; D053148:Caspase 3; D000527:Alprostadil