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糖皮质激素诱导生长迟缓的机制:软骨矿化受损。

Mechanisms of glucocorticoid-induced growth retardation: impairment of cartilage mineralization.

作者信息

Silbermann M, Maor G

出版信息

Acta Anat (Basel). 1978;101(2):140-9. doi: 10.1159/000144959.

Abstract

Immature female mice were treated with daily doses of triamcinolone diacetate. Using histochemical and fluorescent methods, the mineralization pattern of the proximal epiphyseal plate of the humerus was studied at various intervals. Following 1 injection, a noticeable decrease was noted in the oxytetracycline incorporation at the mineralizing zone of the growth plate. By the 10th injection, the mineralization process was almost totally arrested. Marked accumulation of phospholipids appeared in experimental plates concomitantly with a lack of acidic glycosaminoglycans' synthesis as well as degradation. Chondroclastic activity was also inhibited resulting in an increased number of hypertrophic chondrocytes at the mineralization zone. It is suggested that the hormone's antianabolic effect led to an impairment in the activity of the chondrocytes' hydrolytic enzymes and thereby interfered with the maturation of the matrix, a prerequisite phase for normal mineralization.

摘要

对未成年雌性小鼠每日给予二醋酸曲安奈德。采用组织化学和荧光方法,在不同时间间隔研究肱骨近端骨骺板的矿化模式。注射1次后,生长板矿化区的土霉素掺入量明显减少。到第10次注射时,矿化过程几乎完全停止。实验板中出现明显的磷脂积累,同时酸性糖胺聚糖的合成及降解缺乏。破软骨细胞活性也受到抑制,导致矿化区肥大软骨细胞数量增加。提示该激素的抗合成代谢作用导致软骨细胞水解酶活性受损,从而干扰了基质成熟,而基质成熟是正常矿化的一个先决阶段。

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