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[机械应力诱导的骨重塑机制研究。新生大鼠培养长骨中压缩力诱导破骨细胞的分化]

[Study of bone remodeling mechanism induced by mechanical stress. Differentiation of osteoclasts induced by compressive force in newborn rat cultured long bone].

作者信息

Chiba M

出版信息

Nihon Kyosei Shika Gakkai Zasshi. 1989 Dec;48(6):585-600.

PMID:2640933
Abstract

The purpose of this investigation was to reveal the mechanism of differentiation of osteoclast (OC) induced by mechanical stress in long bone cultivation of new born rats. A long bone was loaded with 30 gf of continuous compressive force and cultured for 5 days in CO2 incubator. Numbers of OC increased in the long bone were counted after H-E staining and compared with the control. The study was dealt with the effects of recombinant tumor necrosis factor alpha (rTNF alpha), recombinant interleukin-1 beta (rIL-1 beta), prostaglandin E2 (PGE2) and the co-cultivation of osteoblast (OB) originated from new born rat calvariae, as to differentiation of OC. Since the bone remodeling was interacted with OB and bone marrow (BM) cells, the activity of alkaline phosphatase (ALPase) was also investigated for OB in co-cultivation with BM cells originated from new born rat long bones. In the region of diaphysis of a long bone loaded with compressive force, the bend of trabecular bones was noticed after 3 days incubation. Also, the enrichment of monocyte-macrophage (Mo-M phi) lineage cells was noticed along the trabecular bones. After 5 days incubation, the increase of the number of OC was specifically recognized. The increase of the number of OC was shown in medullary cavity of the long bone by addition of rTNF alpha to the culture medium, but any synergistic effect was not shown with the treatment of rTNF alpha and compressive force to the increase of the number of OC. Furthermore, the increase of the number of OC induced by compressive force did not suppressed by addition of anti-TNF serum. Under the treatment of rIL-1 beta or PGE2, OC slightly increased in the long bone when loaded by compressive force, but the treatment of indomethacin did not suppress it completely. However, the increase of OC in the long bone loaded by compressive force was clearly inhibited in co-cultivation with OB. On the other hand, the activity of ALPase of OB was markedly abated in co-cultivation with BM cells. These results indicated that the mechanism of differentiation of OC induced by mechanical stress was different from that induced by the general inflammation. Results also indicated that it was controlled mainly by the factor(s) or interaction between BM cells and OB and was associated with Mo-M phi lineage cells.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

本研究的目的是揭示新生大鼠长骨培养中机械应力诱导破骨细胞(OC)分化的机制。对一根长骨施加30 gf的持续压缩力,并在二氧化碳培养箱中培养5天。经苏木精-伊红(H-E)染色后,计数长骨中增加的OC数量,并与对照组进行比较。本研究探讨了重组肿瘤坏死因子α(rTNFα)、重组白细胞介素-1β(rIL-1β)、前列腺素E2(PGE2)以及源自新生大鼠颅骨的成骨细胞(OB)共培养对OC分化的影响。由于骨重塑与OB和骨髓(BM)细胞相互作用,还研究了与源自新生大鼠长骨的BM细胞共培养时OB的碱性磷酸酶(ALPase)活性。在施加压缩力的长骨干骺端区域,孵育3天后可见小梁骨弯曲。此外,沿小梁骨可见单核细胞-巨噬细胞(Mo-M phi)谱系细胞富集。孵育5天后,特异性识别出OC数量增加。向培养基中添加rTNFα可使长骨髓腔中OC数量增加,但rTNFα处理与压缩力对OC数量增加无协同作用。此外,添加抗TNF血清并未抑制压缩力诱导的OC数量增加。在rIL-1β或PGE2处理下,施加压缩力时,长骨中的OC略有增加,但吲哚美辛处理并未完全抑制。然而,与OB共培养时,施加压缩力的长骨中OC的增加明显受到抑制。另一方面,与BM细胞共培养时,OB的ALPase活性明显降低。这些结果表明,机械应力诱导OC分化的机制与一般炎症诱导的机制不同。结果还表明,它主要受BM细胞与OB之间的因子或相互作用控制,并与Mo-M phi谱系细胞有关。(摘要截于400字)

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