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血清补体的激活抑制器官培养中胎鼠骨骼的胶原蛋白合成。

Activation of serum complement inhibits collagen synthesis in fetal rat bone in organ culture.

作者信息

Kream B E, Raisz L G, Sandberg A L

出版信息

Calcif Tissue Int. 1982 Jul;34(4):370-5. doi: 10.1007/BF02411270.

Abstract

Activation of rabbit serum complement caused a marked reduction in collagen synthesis but a much smaller change in noncollagen protein synthesis in fetal rat calvaria maintained in organ culture. In the periosteum of the fetal rat calvarium, both collagen and noncollagen protein synthesis were reduced, whereas in the central bone, presumably enriched in osteoblasts, only collagen synthesis was inhibited. This large decrease in bone collagen synthesis could not be attributed to enhanced degradation of newly synthesized collagen or its release into the culture medium. Activation of complement also stimulated the production of PGE in fetal rat calvaria. Antagonists of prostaglandin cyclooxygenase decreased prostaglandin synthesis but did not restore collagen synthesis in complement-treated bones, suggesting that complement decreases osteoblast collagen synthesis by a mechanism largely independent of prostaglandin production.

摘要

兔血清补体的激活导致器官培养的胎鼠颅骨中胶原蛋白合成显著减少,但非胶原蛋白合成的变化要小得多。在胎鼠颅骨的骨膜中,胶原蛋白和非胶原蛋白的合成均减少,而在可能富含成骨细胞的中央骨中,仅胶原蛋白合成受到抑制。骨胶原蛋白合成的大幅下降并非归因于新合成胶原蛋白的降解增强或其释放到培养基中。补体的激活还刺激了胎鼠颅骨中前列腺素E(PGE)的产生。前列腺素环氧化酶拮抗剂减少了前列腺素的合成,但并未恢复补体处理过的骨骼中的胶原蛋白合成,这表明补体通过一种很大程度上独立于前列腺素产生的机制降低成骨细胞胶原蛋白的合成。

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