Effect of 3-Aminobenzamide, an Inhibitor of Poly (ADP-Ribose)Polymerase in Experimental Cardiac Hypertrophy
The male Wistar rats were anaesthetized with thiopentone sodium (35 mg kg-1, i.p.,) and were subjected to Partial Abdominal Aortic Constriction (PAAC) for 4 wk. 3-aminobenzamide (10, 20 mg kg-1 i.p., b.i.d) treatment was started three days before surgery and it was continued for 4 weeks after surgery. The Left Ventricular (LV) hypertrophy and LV dysfunction were assessed by measuring ratio of LV weight to body weight (LVW/BW), LV wall thickness (LVWT), LV collagen content, protein content, RNA concentration, Left Ventricular Developed Pressure (LVDP), rate of pressure development (dp/dtmax) and rate of pressure decay (dp/dtmin). Further, Venous Pressure (VP) and Mean Arterial Blood Pressure (MABP) were recorded. The PAAC produced LV hypertrophy by increasing LVW/BW, LVWT, LV protein content and LV RNA concentration. Further, PAAC was noted to produce LV dysfunction by decreasing LVDP, dp/dtmax, dp/dtmin and increasing LV collagen content. Moreover, PAAC has significantly increased VP and MABP. 3-Aminobenzamide, a PARP inhibitor markedly attenuated PAAC-induced LV hypertrophy, LV dysfunction, increase in VP and MABP. These results suggest that 3-aminobenzamide prevented PAAC-induced cardiac hypertrophy and LV dysfunction which may be due to inhibition of PARP.
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