en اثر تیمول بر میزان رونوشت خانواده BCL2 در قلب هیپرتروف موش ها عمومى General پژوهشي Research <div style="text-align: justify;"><strong>Background and Aims:</strong> 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 (<em>Bcl-2</em>) family members play an essential role in this process regulation. This study aimed to evaluate the effect of thymol on the transcription level of <em>Bcl-2</em> family factors in the rat model of left ventricular hypertrophy.<br> <strong>Materials and Methods</strong>: 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.<br> <strong>Results: </strong>Data showed that in the H group, the mRNA level of the <em>BAD</em> was increased significantly (p&nbsp;˂&nbsp;0.001). However, the transcription level of <em>BAX</em> was increased in the H and H+Tym25 compared with the control group. In the H + Tym50 group, <em>BAX</em> mRNA level decreased significantly compared to the H group (p ˂ 0.05).<br> <strong>Conclusions:</strong> Our findings demonstrated that the expression rates of the antiapoptotic factor, <em>Bcl-2</em>, was significantly increased in the H group (p < 0.01) and thymol-treated hypertrophy groups (p&nbsp;<&nbsp;0.001). Interestingly, the upregulation of <em>Bcl-2</em> mRNA was statistically significant in the H+Tym50 group compared with H and H + Tym25 groups (p&nbsp;<&nbsp;0.01). The results showed that thymol could protect heart hypertrophied by increasing the expression of anti-apoptotic factors.</div> BAX , Bcl-2, Bcl-xl, Hypertrophy, Thymol 206 214 http://ijml.ssu.ac.ir/browse.php?a_code=A-10-202-5&slc_lang=en&sid=1 Fatemeh Safari fa.cardio@gmail.com No Department of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Reza Atarodi rezaatarodi@yahoo.com 0000-0000-0000-0000 No Department of Pharmacology-Toxicology, Faculty of Pharmacy, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Hamid Reza Jamshidi حمیدرضا جمشیدی hrz.jamshidi@gmail.com 0000-0002-2739-2847 Yes Department of Pharmacology-Toxicology, Faculty of Pharmacy, Shahid Sadoughi University of Medical Sciences, Yazd, Iran, Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Shahid Sadoughi University of Medical Sciences, Yazd, Iran