ABSTRACT
Background and Aims: Cardiac hypertrophy is a compensatory augmentation response of the heart due to pressure overload that can lead to heart failure. Carvacrol is considered as the major compound of many plants, that possesses strong antioxidant properties. The present study aimed to evaluate effect of carvacrol on catalase activity and mRNA expression following left ventricular hypertrophy in rats
Materials and Methods: In the current study, male Wistar rats were divided into four groups [n=7]. Intact animals served as the control group [C], some rats were subjected to supra renal aortic banding without any treatment [H] in order to induce left ventricular hypertrophy, and some rats were pretreated with different doses of carvacrol [25, 50 and 75 mg/kg/day in H+C25, H+C50 and H+C75 groups respectively]. Serum and cardiac catalase [CAT] activity was determined by the biochemical methods. CAT mRNA expression was assessed using real-time polymeras chain reaction
Results: In H+C50 and H+C75 groups, the CAT activity was significantly higher in the left ventricular tissues [47.5 +/- 20 and 42 +/- 13.6, vs. H 22.4 +/- 17 U/mg protein respectively]. Serum CAT activity was increased in H+C50 and H+C75 groups [p<0.001], and CAT mRNA expression was increased in H+C50 group [p<0.05], as well
Conclusions: The findings of this study suggest that Carvacrol may protect the heart against left ventricular hypertrophy via augmentation of CAT mRNA expression and activity
ABSTRACT
Background and Aims: there has been scant information concerning antihypertrophic effects of vitamin D specifically on its cellular and molecular mechanisms. Sirtuin 1 [SIRT1] is regarded as a key deacetylase enzyme in cardiomyocytes which applies potential cardioprotective effects by functional regulation of different proteins. This study aimed to evaluate the effects of 1, 25-dihydroxyvitamin D on the hypertrophic markers and cardiac level of SIRT1 mRNA in rats following the aortic banding
Material and Methods: in this study, male Wistar rats [170-220g] were used, which were divided into 4 groups: rats subjected to hypertrophy without treatment [H], rats pretreated with 1, 25 dihydroxyvitamin D3 [H+VD], rats received propyleneglycol as a vitamin solvent [H+P], and intact animals which were elected as the control group. Arterial blood pressure was directly measured by the carotid cannulation. Transcription level of target genes was measured by real time polymerase chain reaction technique
Results: in H+VD group, systolic blood pressure as well as heart weight-to-body weight ratio decreased significantly compared to the group H [P<0.01]. Moreover, regarding hypertrophy marker genes in H+VD group, both atrial natriuretic peptide mRNA [H+VD: 64.8+/-14% vs. H: 127+/-26%; P<0.05] and brain natriuretic peptide mRNA [H+VD: 25.6+/-6% vs. H: 84.2+/-12%; P<0.01] levels decreased significantly. SIRT1 mRNA level was increased by 56.8+/-14% in group H and by 42.6+/-12% in group H+VD which were significant in comparison to the control group [P<0.01 and P<0.05, respectively]. No significant difference was noted between H+VD and H groups
Conclusions: the results of the present study revealed that administration of 1, 25- dihydroxyvitamin D decreases myocardial hypertrophy markers in rats following the abdominal aortic banding. The pressure overload-induced hypertrophy accompanies with SIRT1 mRNA upregulation, though antihypertrophic effects of vitamin did not nparticipate in SIRT1 transcription level