Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model

摘要

Background. Dexamethasone is a type of steroid medication which enhances the rate of pericyte differentiation and mineralization in vitro with concomitant suppression of calcification inhibitory molecule matrix Gla-protein (MGP). Vitamin K is an essential cofactor in the carboxylation of glutamate residues in a small group of proteins, including MGP. This study tries to assess the efficacy of vitamin K1 on dexamethasone-induced media elastocalcinosis in aorta artery and heart muscle in a rat model. Materials and Methods. 110 male rats with a normal weight range of 270 ± 20 were enrolled in this study. They received a calcification-inducing diet containing both vitamin K1 and dexamethasone during 6 or 12 weeks and were randomly assigned into two groups; a basic group (n=30), and an experimental group (n=80). The experimental group was divided into two groups receiving treatment during 6 and 12 weeks. Administration of dexamethasone was 0.5 mg/kg, intraperitoneal (IP). Vitamin K intakes were different including 5, 10, and 20 μg/kg, which were considered as low, moderate, and high intake, respectively. Results. Plasma concentrations of calcium were not affected by the different regimes and ranged between 2.27 and 2.31 millimolar (mM) (mean ± SD: 2.29 ± 0.02). According to the findings of pathologic biopsy of aorta artery and heart muscle, treatment of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. Conclusion. Administration of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. On the other hand, structure and histology of vessels did not change following intake of vitamin K1, therefore, different dosages of vitamin K could not affect the aorta artery status.