Jacobs Lloydine, Vo Nam, Coelho Joao Paulo, Dong Qing, Bechara Bernard, Woods Barrett, Hempen Eric, Hartman Robert, Preuss Harry, Balk Judith, Kang James, Sowa Gwendolyn
*The Ferguson Laboratory for Orthopaedic and Spine Research †Department of Physical Medicine and Rehabilitation, Pittsburgh, PA ‡Department of Internal Medicine, Georgetown University School of Medicine, Washington, DC; and §Department of Obstetrics and Gynecology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Spine (Phila Pa 1976). 2013 May 20;38(12):984-90. doi: 10.1097/BRS.0b013e318286b31e.
Laboratory based controlled in vivo study.
To determine the in vivo effects of oral glucosamine sulfate on intervertebral disc degeneration.
Although glucosamine has demonstrated beneficial effect in articular cartilage, clinical benefit is uncertain. A Centers for Disease Control report from 2009 reported that many patients are using glucosamine supplementation for low back pain, without significant evidence to support its use. Because disc degeneration is a major contributor of low back pain, we explored the effects of glucosamine on disc matrix homeostasis in an animal model of disc degeneration.
Eighteen skeletally mature New Zealand White rabbits were divided into 4 groups: control, annular puncture, glucosamine, and annular puncture + glucosamine. Glucosamine treated rabbits received daily oral supplementation with 107 mg/d (weight based equivalent to human 1500 mg/d). Annular puncture surgery involved puncturing the annulus fibrosus of 3 lumbar discs with a 16-gauge needle to induce degeneration. Serial magnetic resonance images were obtained at 0, 4, 8, 12, and 20 weeks. Discs were harvested at 20 weeks for determination of glycosaminoglycan content, relative gene expression measured by real time polymerase chain reaction, and histological analyses.
The magnetic resonance imaging index and nucleus pulposus area of injured discs of glucosamine treated animals with annular puncture was found to be lower than that of degenerated discs from rabbits not supplemented with glucosamine. Consistent with this, decreased glycosaminoglycan was demonstrated in glucosamine fed animals, as determined by both histological and glycosaminoglycan content. Gene expression was consistent with a detrimental effect on matrix.
These data demonstrate that the net effect on matrix in an animal model in vivo, as measured by gene expression, magnetic resonance imaging, histology, and total proteoglycan is antianabolic. This raises concern about this commonly used supplement, and future research is needed to establish the clinical relevance of these findings.
基于实验室的体内对照研究。
确定口服硫酸葡萄糖胺对椎间盘退变的体内作用。
尽管葡萄糖胺已在关节软骨中显示出有益作用，但其临床益处尚不确定。美国疾病控制中心2009年的一份报告称，许多患者使用葡萄糖胺补充剂治疗腰痛，但没有显著证据支持其使用。由于椎间盘退变是腰痛的主要原因，我们在椎间盘退变动物模型中探讨了葡萄糖胺对椎间盘基质稳态的影响。
将18只骨骼成熟的新西兰白兔分为4组：对照组、环扎组、葡萄糖胺组和环扎+葡萄糖胺组。葡萄糖胺治疗的兔子每天口服补充107mg/d（按体重计算相当于人类1500mg/d）。环扎手术是用16号针穿刺3个腰椎间盘的纤维环以诱导退变。在0、4、8周、12周和20周时获取系列磁共振图像。在20周时取出椎间盘，测定糖胺聚糖含量，通过实时聚合酶链反应测量相对基因表达，并进行组织学分析。
发现接受葡萄糖胺治疗且环扎的动物损伤椎间盘的磁共振成像指数和髓核面积低于未补充葡萄糖胺的兔子的退变椎间盘。与此一致的是，通过组织学和糖胺聚糖含量测定，发现葡萄糖胺喂养的动物中糖胺聚糖减少。基因表达与对基质的有害作用一致。
这些数据表明，通过基因表达、磁共振成像、组织学和总蛋白聚糖测量，在体内动物模型中对基质的净效应是合成代谢抑制作用。这引发了对这种常用补充剂的担忧，需要进一步研究以确定这些发现的临床相关性。
