Background and Aims: Long-term surge of heart loads causes cell hypertrophy. Left ventricular hypertrophy is an adaptive response of the heart to pathological stimuli such as hypertension. B-cell lymphoma 2 (Bcl-2) family members play an essential role in this process regulation. This study aimed to evaluate the effect of thymol on the transcription level of Bcl-2 family factors in the rat model of left ventricular hypertrophy.
Materials and Methods: Male Wistar rats were divided into four groups: 1- Control 2-Untreated hypertrophy (H), 3 and 4 groups which received 25 and 50 mg/kg/day of thymol (H + Tym25 and H + Tym50 groups, respectively). Hypertrophy was induced by abdominal aortic banding, and the real time polymerase chain reaction technique was used for gene expression.
Results: Data showed that in the H group, the mRNA level of the BAD was increased significantly (p ˂ 0.001). However, the transcription level of BAX was increased in the H and H+Tym25 compared with the control group. In the H + Tym50 group, BAX mRNA level decreased significantly compared to the H group (p ˂ 0.05).
Conclusions: Our findings demonstrated that the expression rates of the antiapoptotic factor, Bcl-2, was significantly increased in the H group (p < 0.01) and thymol-treated hypertrophy groups (p < 0.001). Interestingly, the upregulation of Bcl-2 mRNA was statistically significant in the H+Tym50 group compared with H and H + Tym25 groups (p < 0.01). The results showed that thymol could protect heart hypertrophied by increasing the expression of anti-apoptotic factors.