FA促进培养软骨细胞及基质发生异常矿化

采用视黄酸（Retinoicacid，RA）、抗坏血酸（VitaminC，Vc）比较研究大骨节病病区黄腐酸（Fulvicacid，FA）对体外培养肥大软骨细胞及基质的作用，发现病区FA可促进贴壁单层培养的软骨细胞形成异常的胞外基质，促进异常矿化。病区FA刺激软骨细胞产生的活性氧[1]使近细胞膜的软骨囊内蛋白颗粒减少，细蛋白纤维消失；粗长的胶原蛋白变细，胶原蛋白连接方式由正常的束状排列变为杂乱的网状；造成蛋白多糖结构散乱，使矿化位点混乱，而在伤损基质上发生片状不均匀较大量的钙化区。这种异常矿化过程与大骨节病人软骨损伤及修复性的病理矿化有相似之处，支持了大骨节病的自由基致病机理。

FA Promoting Occurrence of Abnormal Mineralization in Chondrocytes and Matrix Cultured in vitro

A comparative study of the effects of FA with retinoic acid, vitamin C on cultured hypertrophic chondrocytes and matrix has been made. The results showed that mineralization on abnormal matrix secreted by cultured chondrocytes in adherent could be promoted by FAfrom Kashin-Beck Disease (KBD)area- Previous research showed that FA from KBD area could promote reactive-oxygen generation by the epiphyseal chondrocytes. The results showed that damaged proteins by reactive-oxygen and thin proteinic fibrils disappeared in lacuna. Collagen fibrils in matrix became thinner than those of retinoic acid or vitamin C con trols and disorder. The proteoglycan structures between collagen fibrils lost their orderness and the site of calcification became disorder and then minerals deposit in the abnormal matrix. This abnormal mineralization process might be related with KBD pathogenic process. The experimental results supported the mechanism with the reactive-oxygen species as the inducer in KBD patients.