Grases Félix, Sanchis Pilar, Perelló Joan, Isern Bernat, Prieto Rafel M, Fernández-Palomeque Carlos, Torres José J
Laboratory of Renal Lithiasis Research, University Institute of Health Sciences Research (IUNICS), University of Balearic Islands, Palma of Mallorca, Spain.
Circ J. 2007 Jul;71(7):1152-6. doi: 10.1253/circj.71.1152.
Pathological calcification in soft tissues (ie, ectopic calcification) can have severe consequences. Hydroxyapatite is the common mineral phase present in all tissue calcifications. In general, the development of tissue calcifications requires a pre-existing injury as an inducer (heterogeneous nucleant), whereas further progression requires the presence of other promoter factors (such as hypercalcemia and/or hyperphosphatemia) and/or a deficiency in calcification repressor factors (crystallization inhibitors and cellular defense mechanisms). The present study investigated the capacity of etidronate (a bisphosphonate used in osteoporosis treatment) and phytate (a natural product) to inhibit vascular calcification in rats.
Six male Sprague-Dawley rats in each of the 3 treatment groups were subcutaneously injected with either a placebo (physiological serum solution), etidronate (0.825 micromol x kg(-1) x day (-1)) or phytate (0.825 micromol x kg (-1) x day(-1)) for 8 days. Four days into this regimen, calcinosis was induced by subcutaneous injections of 500,000 IU/kg vitamin D at 0 h, 24 h and 48 h. Ninety-six hours after the final vitamin D injection, the rats were killed and aortas and their hearts were removed for histological and calcium analyses. The data showed that phytate-treated rats had lower levels of aortic calcium than placebo-treated rats. All groups had similar heart calcium levels.
The present study found that phytate acted as a vascular calcification inhibitor. Thus, the action of polyphosphates could be important in protecting against vascular calcification.
软组织中的病理性钙化（即异位钙化）可产生严重后果。羟基磷灰石是所有组织钙化中常见的矿物相。一般来说，组织钙化的发展需要先前存在的损伤作为诱导剂（异质成核剂），而进一步进展则需要存在其他促进因子（如高钙血症和/或高磷血症）和/或钙化抑制因子（结晶抑制剂和细胞防御机制）缺乏。本研究调查了依替膦酸（一种用于治疗骨质疏松症的双膦酸盐）和植酸（一种天然产物）抑制大鼠血管钙化的能力。
3个治疗组每组6只雄性Sprague-Dawley大鼠，分别皮下注射安慰剂（生理血清溶液）、依替膦酸（0.825微摩尔·千克⁻¹·天⁻¹）或植酸（0.825微摩尔·千克⁻¹·天⁻¹），持续8天。在该方案进行4天后，于0小时、24小时和48小时皮下注射500,000 IU/kg维生素D诱导钙质沉着。最后一次维生素D注射后96小时，处死大鼠，取出主动脉及其心脏进行组织学和钙分析。数据显示，植酸处理组大鼠的主动脉钙水平低于安慰剂处理组大鼠。所有组的心脏钙水平相似。
本研究发现植酸可作为血管钙化抑制剂。因此，多磷酸盐的作用在预防血管钙化方面可能很重要。
