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Pharmacologic inhibition of poly(adenosine diphosphate-ribose) polymerase may represent a novel therapeutic approach in chronic heart failure.

Abstract：

OBJECTIVES:We investigated the effects of a novel ultrapotent poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, PJ34, on cardiac and endothelial dysfunction in a rat model of chronic heart failure (CHF). BACKGROUND:Overactivation of the nuclear enzyme PARP importantly contributes to the development of cell dysfunction and tissue injury in various pathophysiologic conditions associated with oxidative stress, including myocardial reperfusion injury, heart transplantation, stroke, shock, and diabetes. METHODS:Chronic heart failure was induced in Wistar rats by chronic ligation of the left anterior descending coronary artery. Left ventricular (LV) function and ex vivo vascular contractility and relaxation were measured 10 weeks after the surgery. Nitrotyrosine (NT) formation and PARP activation were detected by immunohistochemistry. RESULTS:Chronic heart failure induced increased NT formation and PARP activation in the myocardium and intramural vasculature, depressed LV performance, and impaired vascular relaxation of aortic rings. PJ34 significantly decreased myocardial PARP activation but not NT formation, and improved both cardiac dysfunction and vascular relaxation. CONCLUSIONS:Poly(ADP-ribose) polymerase inhibition represents a novel approach for the experimental treatment of CHF.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Pacher P,Liaudet L,Mabley Jg,Komjáti K,Szabó C

doi

10.1016/s0735-1097(02)02062-4

subject

Has Abstract

pub_date

2002-09-04 00:00:00

pages

1006-16

issue

5

eissn

0735-1097

issn

1558-3597

pii

S0735109702020624

journal_volume

40

pub_type

杂志文章

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