Chang Hengrui, Kang Shaomeng, Li Chenchen, Wu Lihui, Liu Hongran, Zhang Di, Chang Yanzhong
Department of Spinal Surgery, The Third Hospital of Hebei Medical University, No.139 Ziqiang Road, Shijiazhuang, 050051, Hebei, People's Republic of China.
College of Life Science, Hebei Normal University, No.20 Road East. 2nd Ring South, Shijiazhuang, 050051, Hebei, People's Republic of China.
Sci Rep. 2025 Jun 2;15(1):19323. doi: 10.1038/s41598-025-04388-4.
Clinical studies have reported that anemic patients with lower back pain exhibit significantly more severe lumbar intervertebral disc (IVD) degeneration compared to non-anemic individuals. Given that iron deficiency (ID) is the leading cause of anemia, we hypothesized that ID may disrupt IVD metabolism-particularly extracellular matrix synthesis-thereby contributing to aberrant disc development and degeneration. To investigate this, we established an iron-deficiency anemia (IDA) rat model via an iron-deficient diet and induced IVD degeneration through needle puncture. Degenerative changes were assessed using MRI, while morphological alterations were evaluated via O-fast green and hematoxylin-eosin (H&E) staining. The gene expression was measured by quantitative reverse transcription PCR (RT-qPCR). Immunofluorescence staining was employed to observe the protein expression. Additionally, TUNEL (TdT-mediated dUTP nick end labeling) was performed to assess apoptosis in nucleus pulposus cells. Our findings revealed that iron deficiency significantly impaired the development of rat caudal intervertebral discs characterized by reduced MRI signal intensity, diminished notochordal cell populations in the nucleus pulposus, thinning of the cartilage endplate, and Impaired type II collagen synthesis. However, despite these developmental abnormalities, iron deficiency did not exacerbate puncture-induced disc degeneration. MRI and histological analyses showed no significant differences in degenerative severity between IDA and control groups following needle injury. Additionally, TUNEL assays indicated no marked increase in apoptotic activity in IDA rats.
临床研究报告称，与非贫血个体相比，患有下背部疼痛的贫血患者腰椎间盘（IVD）退变明显更严重。鉴于缺铁（ID）是贫血的主要原因，我们推测缺铁可能会扰乱IVD代谢，尤其是细胞外基质合成，从而导致椎间盘异常发育和退变。为了对此进行研究，我们通过缺铁饮食建立了缺铁性贫血（IDA）大鼠模型，并通过针刺诱导IVD退变。使用MRI评估退变变化，通过固绿和苏木精-伊红（H&E）染色评估形态学改变。通过定量逆转录PCR（RT-qPCR）测量基因表达。采用免疫荧光染色观察蛋白质表达。此外，进行TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）以评估髓核细胞中的细胞凋亡。我们的研究结果表明，缺铁显著损害大鼠尾椎间盘的发育，其特征为MRI信号强度降低、髓核中脊索细胞数量减少、软骨终板变薄以及II型胶原合成受损。然而，尽管存在这些发育异常，缺铁并未加剧针刺诱导的椎间盘退变。MRI和组织学分析显示，针刺损伤后IDA组和对照组在退变严重程度上无显著差异。此外，TUNEL检测表明IDA大鼠的细胞凋亡活性没有明显增加。
