Carvacrol Ameliorates Pathological Cardiac Hypertrophy in Both In-vivo and In-vitro Models

Hypertension-induced left ventricular hypertrophy is the most important risk factor for heart failure. This study aimed at investigating the effects of monoterpenoid phenol, carvacrol, on myocardial hypertrophy using both in-vivo and in-vitro models. Male Wistar rats were divided into the control (Ctl), un-treated hypertrophy (H), and carvacrol-treated hypertrophy groups (25, 50 and 75 mg/kg/day, Car+H). In the hypertrophy groups animals underwent abdominal aorta banding. Blood pressure (BP) was recorded via carotid artery cannulation. TUNEL assay and Masson's trichrome staining were used to assess apoptosis and fibrosis, respectively. The 2-2-diphenyl 1-picril-hydrasil )DPPH( radical scavenging activity and malondialdehyde (MDA) level were estimated by biochemical tests. In in-vitro study H9c2 cardiomyoblasts were treated with angiotensin II (Ang II) to promote hypertrophy. Cell size was measured using crystal violet staining. Gene expression was evaluated by real-time RT-PCR technique. In the carvacrol-treated rats BP, heart rate, and heart weight to the body weight ratio were significantly decreased. In-vitro study showed that H9c2 cell size was significantly reduced compared to Ang II-treated cells. Both in-vivo and in-vitro studies demonstrated that carvacrol decreased atrial natriuretic peptide )ANP( mRNA level significantly (vs. H groups). The number of apoptotic cells increased in H group, while it was decreased in the Car50+H and Car75+H. In Car+H groups, in comparison with H group, the serum concentration of MDA was decreased and DPPH was increased significantly. Our findings demonstrated that carvacrol decreases hypertrophy markers in in-vivo and in-vitro models of hypertrophy.