Bisacurone Ameliorated Pressure Overload-Induced Cardiac Hypertrophy in Experimental Rats Through Inhibition of Oxidative Stress and Bax/Caspase-3 Pathway

Xiaohong Zeng, Houwen Gong, Li Zhang, Yaping Lan, Shuangyan Yang and Fengcheng Xu

Background and Objective: The sustained Left Ventricular Hypertrophy (LVH) causes cardiac function failure, resulting in Congestive Heart Failure (CHF) and mortality. Bisacurone, a bioactive terpenoid, has been reported for its antioxidant and anti-inflammatory potential. To determine the cardioprotective efficacy of bisacurone against pressure overload-induced cardiac hypertrophy in a rat model of Aortic Stenosis (AS). Materials and Methods: Constriction of abdominal aortic of Sprague-Dawley rats caused induction of pressure overload-induced cardiac hypertrophy. Then rats were treated with either vehicle (AS) group or lisinopril (15 mg kg^–1) or bisacurone (25, 50 and 100 μg kg^–1, p.o.) for 4 weeks. Results: AS control group showed a significant (p<0.05) in alteration hemodynamic and left ventricular function tests compared to sham control rats, however bisacurone (50 and 100 μg kg^–1) treatment markedly (p<0.05) inhibited these alterations. Bisacurone effectively (p<0.05) augmented pressure overload-induced diminished levels of cardiac SOD, GSH, Na-K-ATPase, Ca-ATPase and mRNA expressions of Bcl2. The up-regulated MDA, NO and mRNA expressions of ANP, BNP, cTn-I, Bax and Caspase-3were efficiently (p<0.05) were down-regulated by bisacurone. AS-induced histological alteration in cardiac tissue was reduced by bisacurone treatment. Conclusion: Bisacurone treatment inhibited pressure overload-induced progressive cardiac hypertrophy by inhibiting elevated oxidative stress (SOD, GSH, MDA and NO) and apoptosis (Bax, Bcl-2 and Caspase-3). Thus, bisacurone can be considered as an important therapeutic moiety in the management of congestive heart failure.

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