Phytate (Myo-inositol hexakisphosphate) inhibits cardiovascular calcifications in rats
Phytate (Myo-inositol hexakisphosphate) inhibits cardiovascular calcifications in rats
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DOI：
10.2741/1786
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发表时间：
2006-01-01
影响因子：
3.1
通讯作者：
Torres, JJ
中科院分区：
文献类型：
--
作者：
Grases, F;Sanchis, P;Torres, JJ
钙化是一种常见于心血管的不良疾病。一般来说，钙化性血管病变的形成涉及复杂的物理化学和分子事件。钙化（羟基磷灰石）是由损伤引发的，并通过启动子因子和/或抑制信号的缺陷进行。肌醇六磷酸（肌醇六磷酸盐，InsP（6））存在于所有哺乳动物的器官、组织和体液中，并表现出作为尿和软组织中钙盐结晶抑制剂的重要能力。发现的水平显然取决于饮食摄入量，但也可以局部吸收。在本文中，InsP 6作为心血管钙化的潜在抑制剂的能力在Wistar大鼠中进行了评估。包括三个组，对照组、InsP（6）处理组（通过维生素D和尼古丁进行钙质沉着诱导，并用含有2%InsP（6）钾盐的标准乳膏处理）和InsP（6）未处理组（仅进行钙质沉着诱导）。所有大鼠均喂食AIN 76- A饮食（其中InsP（6）不可检测的纯化饮食）。每12小时监测一次动物。钙沉着治疗60小时后，InsP 6未治疗组的所有大鼠死亡，其余大鼠处死。主动脉和心脏被切除。InsP（6）未处理大鼠的主动脉和心脏组织中的钙含量显著增加（21 +/- 1 mg钙/ g干主动脉组织，10 +/- 1 mg钙/ g干心脏组织）（1.3 +/- 0.1 mg钙/ g干主动脉组织，0.023 +/- 0.004 mg钙/ g心脏干组织）和InsP（6）处理（0.9 +/-0.2mg钙/ g干主动脉组织，0.30 +/-0.03mg钙/ g干心脏组织）动物。只有InsP（6）未处理的大鼠在主动脉和心脏中显示重要的矿物质沉积。这些发现与InsP（6）作为心血管系统钙化抑制剂的作用一致。
Calcification is an undesirable disorder, which frequently occurs in the heart vessels. In general, the formation of calcific vascular lesions involves complex physicochemical and molecular events. Calcification ( hydroxyapatite) is initiated by injury and is progressed by promoter factors and/ or the deficit of inhibitory signals. Myo- inositol hexakisphosphate ( phytate, InsP(6)) is found in organs, tissues and fluids of all mammals and exhibits an important capacity as a crystallization inhibitor of calcium salts in urine and soft tissues. The levels found clearly depend on the dietary intake but it can also be absorbed topically. In this paper, the capacity of InsP6 as a potential inhibitor of cardiovascular calcifications was assessed in Wistar rats. Three groups were included, a control group, an InsP6 treated group ( subjected to calcinosis induction by Vitamin D and nicotine and treated with standard cream with a 2% of InsP(6) as potassium salt) and an InsP(6) non-treated group ( only subjected to calcinosis induction). All rats were fed AIN 76- A diet ( a purified diet in which InsP(6) is undetectable). Animals were monitorized every 12 hours. After 60 hours of calcinosis treatment, all rats of the InsP6 non- treated group died and the rest were sacrificed. Aortas and hearts were removed. A highly significant increase in the calcium content of aorta and heart tissue was observed in the InsP(6) non- treated rats ( 21 +/- 1 mg calcium / g dry aorta tissue, 10 +/- 1 mg calcium / g dry heart tissue) when compared with controls ( 1.3 +/- 0.1 mg calcium / g dry aorta tissue, 0.023 +/- 0.004 mg calcium / g heart dry tissue) and InsP(6) treated ( 0.9 +/- 0.2 mg calcium / g dry aorta tissue, 0.30 +/- 0.03 mg calcium / g dry heart tissue) animals. Only InsP(6) non- treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP(6), as an inhibitor of calcification of cardiovascular system.