评价氨基葡萄糖对实验性大鼠骨关节炎模型的影响。
Evaluation of the effect of glucosamine on an experimental rat osteoarthritis model.
机构信息
Department of Orthopaedic Surgery, Juntendo University Shizuoka Hospital, 1129 Nagaoka, Izunokuni, Shizuoka 410-2295, Japan.
出版信息
Life Sci. 2010 Mar 27;86(13-14):538-43. doi: 10.1016/j.lfs.2010.02.015. Epub 2010 Feb 24.
AIMS
To investigate the in vivo effect of glucosamine on articular cartilage in osteoarthritis (OA), we evaluated serum biomarkers such as CTX-II (type II collagen degradation) and CPII (type II collagen synthesis) as well as histopathological changes (Mankin score, toluidine blue staining of proteoglycans in an experimental OA model using rats.
MAIN METHODS
OA was surgically induced in the knee joint by anterior cruciate ligament transection (ACLT) in rats. Animals were divided into three groups: sham-operated group (Sham), ACLT group without GlcN administration (-GlcN) and ACLT group with oral administration of glucosamine hydrochloride (+GlcN; 1000mg/kg/day for 56days).
KEY FINDINGS
ACLT induced macroscopic erosive changes on the surfaces of articular cartilage and histological damages such as increase of Mankin score. Of note, glucosamine administration substantially suppressed the macroscopic changes, although the effect on Mankin score was not significant. In addition, serum CTX-II levels were elevated in -GlcN group compared to that in Sham group after the operation. Of importance, the increase of CTX-II was significantly suppressed by GlcN administration. Moreover, serum CP-II levels were substantially increased in +GlcN group compared to those in Sham and -GlcN groups after the operation.
SIGNIFICANCE
GlcN has a potential to exert a chondroprotective action on OA by inhibiting type II collagen degradation and enhancing type II collagen synthesis in the articular cartilage.
目的
为了研究氨基葡萄糖(GlcN)对骨关节炎(OA)关节软骨的体内作用,我们评估了血清生物标志物,如 CTX-II(II 型胶原降解)和 CPII(II 型胶原合成),以及组织病理学变化(Mankin 评分、甲苯胺蓝染色法检测软骨蛋白聚糖),在使用大鼠的 OA 实验模型中。
主要方法
通过前交叉韧带切断术(ACLT)在大鼠膝关节中诱导 OA。动物分为三组:假手术组(Sham)、未给予 GlcN 处理的 ACLT 组(-GlcN)和给予盐酸氨基葡萄糖口服处理的 ACLT 组(+GlcN;每天 1000mg/kg,共 56 天)。
主要发现
ACLT 引起关节软骨表面的宏观侵蚀性变化和组织学损伤,如 Mankin 评分增加。值得注意的是,氨基葡萄糖的给予显著抑制了大体变化,尽管对 Mankin 评分的影响不显著。此外,与 Sham 组相比,-GlcN 组术后血清 CTX-II 水平升高。重要的是,氨基葡萄糖的给予显著抑制了 CTX-II 的增加。此外,与 Sham 组和 -GlcN 组相比,+GlcN 组术后血清 CPII 水平显著升高。
意义
GlcN 通过抑制 II 型胶原降解和增强关节软骨中 II 型胶原合成,对 OA 具有潜在的软骨保护作用。