Jin Yongming, Mao Guangfeng, Yang Chen, Xia Chen, Chen Chuyong, Shi Fangfang, Chen Qi
Department of Orthopedic Surgery, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, People's Republic of China.
Department of Orthopedic Surgery, The Third People's Hospital of Zhuji, Shaoxing, Zhejiang, People's Republic of China.
Global Spine J. 2023 May;13(4):984-994. doi: 10.1177/21925682211012323. Epub 2021 Apr 28.
A prospective study.
Intervertebral disc degenerative disease is a common and frequently-occurring disease in adults and is the main cause of lower back pain. However, there is a lack of universal animal models to study disc degeneration.
Forty-two male New Zealand white rabbits aged 12 months were used in this study. We established an endplate ischemic disc degeneration model though surgical ligation of rabbit lumbar vertebral body segment arteries. Two weeks after surgery, 6 experimental animals were randomly selected for follow-up tests. First, ischemia and lumbar disc degeneration were confirmed using imaging techniques. Then, immunohistochemical staining was performed to observe the growth of the annulus fibrosus. Finally, quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, and western blotting were used to detect mRNA expression and protein content of IL-1α, TNFα, collagen II, MMP-3, aggrecan, and PLA2 in the nucleus pulposus of the disc.
Imaging examination confirmed the successful construction of a lumbar disc degeneration model. Histological analysis and biochemical analysis showed a damaged intervertebral disc structure, and collagen II and aggrecan, the key extracellular matrix components of intervertebral discs, were reduced in synthesis and content. The synthesis and expression of IL-1α, TNFα, PLA2, and MMP-3 related to disc catabolism and inflammatory response were enhanced.
We successfully constructed a lumbar disc degeneration ischemia model, which provides a novel approach to study the pathological mechanisms involved in discogenic low back pain and to prevent and treat discogenic low back pain.
前瞻性研究。
椎间盘退行性疾病是成年人常见且多发病，是下腰痛的主要原因。然而，缺乏用于研究椎间盘退变的通用动物模型。
本研究使用了42只12月龄雄性新西兰白兔。通过手术结扎兔腰椎椎体节段动脉建立终板缺血性椎间盘退变模型。术后两周，随机选取6只实验动物进行随访检测。首先，使用成像技术确认缺血和腰椎间盘退变情况。然后，进行免疫组织化学染色以观察纤维环的生长情况。最后，采用定量聚合酶链反应、酶联免疫吸附测定和蛋白质印迹法检测椎间盘髓核中IL-1α、TNFα、胶原蛋白II、MMP-3、聚集蛋白聚糖和PLA2的mRNA表达和蛋白质含量。
影像学检查证实成功构建了腰椎间盘退变模型。组织学分析和生化分析显示椎间盘结构受损，椎间盘关键细胞外基质成分胶原蛋白II和聚集蛋白聚糖的合成及含量降低。与椎间盘分解代谢和炎症反应相关的IL-1α、TNFα、PLA2和MMP-3的合成及表达增强。
我们成功构建了腰椎间盘退变缺血模型，为研究椎间盘源性下腰痛的病理机制以及预防和治疗椎间盘源性下腰痛提供了一种新方法。
