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对去卵巢大鼠停止给予17β-雌二醇后,小梁骨形成出现短暂减少。

Transient reduction in trabecular bone formation after discontinuation of administration of oestradiol-17 beta to ovariectomized rats.

作者信息

Tobias J H, Chambers T J

机构信息

Department of Histopathology, St George's Hospital Medical School, London, U.K.

出版信息

J Endocrinol. 1993 Jun;137(3):497-503. doi: 10.1677/joe.0.1370497.

Abstract

While the osteopenia associated with oestrogen deficiency is thought to arise from a relative defect in bone formation with respect to resorption, oestrogen administration itself leads to a decrease, rather than an increase, in bone formation. This decrease in bone formation, which arises from oestrogen's inhibitory effect on bone turnover, presumably masks any underlying tendency of oestrogen treatment towards stimulation of bone formation. To investigate this further, we have examined the early effect of discontinuing the administration of oestradiol-17 beta (OE2; 40 micrograms/kg) on bone formation indices in ovariectomized 13-week-old rats, before the turnover-induced increase in formation occurs. Histomorphometric indices were assessed at the proximal tibial metaphysis 0, 7, 10, 13 and 16 days following discontinuation of OE2 treatment. Measurements of body weight, uterine weight and longitudinal growth rate confirmed that there were rapid effects of OE2 deficiency on these parameters. We could detect no significant increase in bone resorption, as measured by osteoclast surface and number, until 16 days after ending treatment with OE2; this was coincidental with a reduction in bone volume. Shorter periods of OE2 deficiency were associated with a marked decrease in bone formation, as assessed by dynamic histomorphometric indices. This inhibition of bone formation was largely due to a reduction in double fluorochrome-labeled trabecular surfaces, which were decreased by approximately 70%. We conclude that ending OE2 administration in ovariectomized rats caused a striking decrease in trabecular bone formation, if such indices are assessed prior to the subsequent turnover-induced increase in formation.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

虽然与雌激素缺乏相关的骨质减少被认为是由于骨形成相对于骨吸收存在相对缺陷所致,但给予雌激素本身却导致骨形成减少而非增加。这种骨形成的减少源于雌激素对骨转换的抑制作用,可能掩盖了雌激素治疗在刺激骨形成方面的任何潜在趋势。为了进一步研究这一点,我们在13周龄的去卵巢大鼠中,在由骨转换引起的骨形成增加发生之前,研究了停止给予17β -雌二醇(OE2;40微克/千克)对骨形成指标的早期影响。在停止OE2治疗后的0、7、10、13和16天,评估胫骨近端干骺端的组织形态计量学指标。体重、子宫重量和纵向生长率的测量证实,OE2缺乏对这些参数有快速影响。在用OE2治疗结束后16天之前,通过破骨细胞表面和数量测量,我们未检测到骨吸收有显著增加;这与骨体积减少同时出现。通过动态组织形态计量学指标评估,较短时间的OE2缺乏与骨形成显著减少有关。这种对骨形成的抑制主要是由于双荧光标记的小梁表面减少,减少了约70%。我们得出结论,如果在随后由骨转换引起的骨形成增加之前评估这些指标,那么在去卵巢大鼠中停止给予OE2会导致小梁骨形成显著减少。(摘要截短于250字)

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