Introduction: Cardiomyocytes apoptosis contributes to the development of left ventricular hypertrophy. The Bcl-2 family members are important regulators of mitochondrial pathway of apoptosis. Monoterpenoid phenol –carvacrol– possesses strong antioxidant properties. The present study aimed to evaluate the effect of carvacrol on transcription level of pro-apoptotic (Bad and Bax) and anti-apoptotic (Bcl-2 and BCL-xL) members of Bcl-2 family in hypertrophied hearts. Methods: Male Wistar rats (170-200 g) were divided into the following groups: (I) intact animals served as the control (Ctl), (II) un-treated rats subjected to aortic banding to induce left ventricular hypertrophy (H group), (III, IV, V and VI): carvacrol (C)-pretreated rats (5, 10, 25 and 50 mg/kg/day) subjected to aortic banding (H+C5, H+C10, H+C25 and H+C50 groups, respectively). Blood pressure was recorded through the carotid artery cannulation. Fibrosis was assessed by Masson’s trichrome staining. Gene expression was evaluated by real time-PCR technique. Results: In the H+C10, H+C25 and H+C50 groups mean arterial pressure (P<0.05, P<0.001 and P<0.001, respectively) and heart weight to body weight ratio (P<0.05, P<0.01 and P<0.001, respectively) were decreased significantly in comparison with H group. In the H group the Bad mRNA level was increased significantly compared to Ctl (P<0.001); while in the H+C10, H+C25 and H+C50 groups Bad mRNA level was decreased significantly (P<0.0 5, P<0.001 and P<0.001 vs. H). In H+C25 and H+C50 groups Bcl-2 and Bcl-xL mRNA were also up-regulated when compared with Ctl. Conclusion: Taken together, our results suggest that carvacrol may protect the hypertrophied heart against apoptosis by affecting transcription of Bcl-2 family members.