Vitamin D Attenuates Cardiac Hypertrophy in Rats through mRNA Regulation of Interleukin-6 and Its Receptor

Abstract

Abstract Context: Interleukin-6 (IL-6), a pro-inflammatory cytokine, plays an important role in the pathogenesis of myocardial hypertrophy. By integrating its membrane receptor complex (gp80), IL-6 activates the signal guidance components (gp130) and activates the hypertrophic signaling pathways. There is some evidence that 1,25 dihydroxyvitamin D exerts antihypertrophic effects, but the cellular and molecular mechanisms are not fully understood. The aim of this study was to evaluate the effect of calcitriol on the level of IL-6 and its receptor components in hypertrophied rat heart. Subjects and Methods: Male rats were divided into control, hypertrophy, Vitamin D + hypertrophy, and propylene glycol + hypertrophy groups. The groups receiving Vitamin D and propylene glycol were treated 2 weeks before induction of hypertrophy and 2 weeks after hypertrophy. Myocardial hypertrophy was induced by abdominal aortic stenosis. Mean arterial blood pressure was measured by cannulation of the left carotid artery, and expression of genes was determined by reverse transcription-polymerase chain reaction. Results: Blood pressure and heart-to-body weight ratio increased in hypertrophic groups compared to the control group (P < 0.01), but Vitamin D administration decreased these parameters (P < 0.05). Abdominal aortic stenosis increased IL-6 expression levels (P < 0.001) and Vitamin-D decreased IL-6 mRNA levels (P < 0.01). The expression of gp80 in the hypertrophic group increased compared to the control group (P < 0.05), but Vitamin D did not affect the expression of receptor subunits genes. Conclusions: The data from this study suggest a possible mechanism for the antihypertrophic effects of Vitamin D through the regulation of inflammatory responses during hypertrophy. Thus, Vitamin D can reduce IL-6 expression levels, thereby reducing hypertrophy.