International Journal of Medical Laboratory

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 didnot participate in SIRT1 transcription level.