Grases Felix, Sanchis Pilar, Perello Joan, Isern Bernat, Prieto Rafel Maria, Fernandez-Palomeque Carlos, Fiol Miguel, Bonnin Oriol, Torres Jose Juan
University Institute of Health Sciences Research (IUNICS), University of Balearic Islands, Palma of Mallorca, Spain.
Front Biosci. 2006 Jan 1;11:136-42. doi: 10.2741/1786.
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, InsP6) 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 InsP6 as potassium salt) and an InsP6 non-treated group (only subjected to calcinosis induction). All rats were fed AIN 76-A diet (a purified diet in which InsP6 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 InsP6 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 InsP6 treated (0.9 +/- 0.2 mg calcium/g dry aorta tissue, 0.30 +/- 0.03 mg calcium/g dry heart tissue) animals. Only InsP6 non-treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP6, as an inhibitor of calcification of cardiovascular system.
钙化是一种不良病症,常发生于心血管中。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)由损伤引发,并因促进因子和/或抑制信号的缺乏而进展。肌醇六磷酸(植酸,InsP6)存在于所有哺乳动物的器官、组织和体液中,在尿液和软组织中作为钙盐结晶抑制剂具有重要作用。其含量显然取决于饮食摄入,但也可经局部吸收。本文在Wistar大鼠中评估了InsP6作为心血管钙化潜在抑制剂的能力。实验分为三组,一组为对照组,一组为InsP6处理组(通过维生素D和尼古丁诱导钙化,并使用含2% InsP6钾盐的标准乳膏进行处理),另一组为InsP6未处理组(仅诱导钙化)。所有大鼠均喂食AIN 76 - A饮食(一种纯化饮食,其中检测不到InsP6)。每12小时对动物进行监测。在钙化处理60小时后,InsP6未处理组的所有大鼠死亡,其余大鼠被处死。取出主动脉和心脏。与对照组(1.3±0.1毫克钙/克干主动脉组织,0.023±0.004毫克钙/克干心脏组织)和InsP6处理组(0.9±0.2毫克钙/克干主动脉组织,0.30±0.03毫克钙/克干心脏组织)相比,InsP6未处理组大鼠主动脉和心脏组织中的钙含量显著增加(21±1毫克钙/克干主动脉组织,10±1毫克钙/克干心脏组织)。只有InsP6未处理组的大鼠在主动脉和心脏中出现重要的矿物质沉积。这些发现与InsP6作为心血管系统钙化抑制剂的作用一致。