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运动可增加化学诱导的关节软骨损伤后的骨赘形成,并减少纤维化。

Exercise increases osteophyte formation and diminishes fibrillation following chemically induced articular cartilage injury.

作者信息

Williams J M, Brandt K D

出版信息

J Anat. 1984 Dec;139 ( Pt 4)(Pt 4):599-611.

Abstract

The present study shows that a treadmill exercise regimen imposed on guinea-pigs whose articular cartilage has been damaged by intra-articular injection of IA reduces chondrocyte depletion, results in an increase in pericellular Safranin-O staining around surviving chondrocytes, and prevents fibrillation of the articular surface. The data suggest that exercise protected, or facilitated recovery of, chondrocytes subjected to chemical injury, and that the surviving cells then synthesised a matrix which was sufficiently normal to withstand impulsive joint loading. On the other hand, the exercise regimen accelerated osteophyte formation, and led to formation of osteophytes in sites at which they did not develop in animals which received intra-articular IA but which were not exercised.

摘要

本研究表明,对关节内注射碘乙酸(IA)致使关节软骨受损的豚鼠实施跑步机运动方案,可减少软骨细胞耗竭,使存活软骨细胞周围的细胞周番红O染色增加,并防止关节表面纤维化。数据表明,运动对遭受化学损伤的软骨细胞起到了保护作用或促进其恢复,且存活细胞随后合成了足够正常的基质以承受脉冲式关节负荷。另一方面,运动方案加速了骨赘形成,并导致在接受关节内IA注射但未运动的动物中未形成骨赘的部位形成了骨赘。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1619/1164972/0bf73233bdae/janat00200-0017-a.jpg

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