title: Effects of emodin and irbesartan on ventricular fibrosis in Goldblatt hypertensive rats.
abstract: Left ventricular (LV) fibrosis is one of the most prominent pathophysiological results of hypertension. We initiated this study to investigate the effects and mechanisms of emodin and its combination with irbesartan on LV fibrosis in Goldblatt (2K1C) hypertensive rats. Goldblatt hypertension rats were prepared by two kidney one clip (2K1C) operations and then treated with either emodin, irbesartan or their combination. As a result, the systolic blood pressure (SBP) and the left ventricular mass index (LVMI) increased significantly (P < or = 0.05) in all 2K1C rats. After drugs treatment, irbesartan and the drug combination remarkably decreased SBP, LVMI, contents of angiotensinII (AngII), hydroxyproline and collagen, the mRNA and protein expression levels of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) (P < or = 0.05). As for the emodin, LVMI, contents of hydroxyproline and collagen, and MMP-2 and TIMP-2 expression were found to decrease significantly; however, the SBP and AngII contents stayed stable within certain extent. Therefore, emodin, irbesartan or two drugs together can potentially inhibit the ventricular fibrosis in Goldblatt hypertensive rats by reducing MMP-2 and TIMP-2 expression. Furthermore, the combination of these two drugs may provide a better anti-fibrosis effect than the single application.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Chen
authors.forename: Lingpin
authors.initials: L
authors.lastname: Pang
authors.forename: Shian
authors.initials: S
authors.lastname: Huang
authors.forename: Wei
authors.initials: W
authors.lastname: Lei
authors.forename: Dangsheng
authors.initials: D
authors.lastname: Huang
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D001713:Biphenyl Compounds / Q000494:pharmacology*; D015153:Blotting, Western; D009202:Cardiomyopathies / Q000188:drug therapy / Q000473:pathology; D003094:Collagen / Q000378:metabolism; D004452:Echocardiography; D004642:Emodin / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005355:Fibrosis; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology*; D006909:Hydroxyproline / Q000378:metabolism; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000473:pathology*; D017379:Hypertrophy, Left Ventricular / Q000517:prevention & control; D000077405:Irbesartan; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D013777:Tetrazoles / Q000494:pharmacology*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001713:Biphenyl Compounds; D004791:Enzyme Inhibitors; D012333:RNA, Messenger; D013777:Tetrazoles; D000804:Angiotensin II; D003094:Collagen; D020778:Matrix Metalloproteinase 2; D000077405:Irbesartan; D004642:Emodin; D006909:Hydroxyproline