A repeated strike loading organ culture model for studying compression-associated chronic disc degeneration.

0 MEDICINE, RESEARCH & EXPERIMENTAL Biomolecules & biomedicine Pub Date : 2024-08-04 DOI:10.17305/bb.2024.10640
Baoliang Li, Xu Chen, Hongkun Chen, Fu Zhang, Jianfeng Li, Zhengya Zhu, Tao Tang, Manman Gao, Nianhu Li, Liang Ma, Zhiyu Zhou
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Abstract

Mechanical stress has been viewed as one of the key risk factors in accelerating the intervertebral disc degeneration process. The goal of the present study was to employ a repeated strike loading bovine caudal disc system to elucidate the pathophysiological impacts of cumulative mechanical stress on the disc. The discs in the model groups were subjected to two different mechanical stresses: one strike loading or repeated strike loading. The following indices were analyzed: histological morphology, glycosaminoglycan release, disc height, cell viability, apoptosis-related protein expression, and catabolism-related gene expression. Both mechanical stress modes induced degenerative changes in the discs by day 11, such as clefts and delamination of the annulus fibrosus; they increased glycosaminoglycan release. Cell viability was significantly decreased and catabolic gene expression was significantly up-regulated in the degenerative loading group and repeated strike loading group by day 9. These alterations remained evident in the annulus fibrosus tissue of the repeated strike loading group on day 11. Our data suggests that the repeated strike loading model adopted in this study could lead to degenerative changes in the disc organ model. Annulus fibrosus cells displayed a more noticeable response to mechanical stress damage and a slower recovery process, suggesting that the annulus fibrosus serves as a pivotal factor in disc degeneration due to mechanical stress injuries. The study also indicates that due to the gradual self-repair of intervertebral disc cells after injury, it is necessary to apply repeated strike loading on the disc at specific intervals when researching the repair of chronic disc injuries.

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用于研究与挤压相关的慢性椎间盘退变的重复撞击加载器官培养模型。
机械应力一直被认为是加速椎间盘退变过程的关键风险因素之一。本研究的目的是利用重复冲击加载牛尾椎间盘系统来阐明累积机械应力对椎间盘的病理生理影响。对模型组的椎间盘施加了两种不同的机械应力:一次撞击加载或重复撞击加载。对以下指标进行了分析:组织学形态、糖胺聚糖释放、椎间盘高度、细胞活力、凋亡相关蛋白表达和分解代谢相关基因表达。到第11天时,两种机械应力模式都会诱发椎间盘的退行性变化,如纤维环的裂隙和分层;它们都会增加氨基糖的释放。到第9天时,退行性加载组和重复打击加载组的细胞活力明显下降,分解代谢基因表达明显上调。这些变化在重复敲击负荷组的环状纤维组织中在第 11 天仍然明显。我们的数据表明,本研究采用的重复敲击加载模式可能会导致椎间盘器官模型发生退行性变化。椎间盘纤维环细胞对机械应力损伤的反应更明显,恢复过程更缓慢,这表明椎间盘纤维环是机械应力损伤导致椎间盘退变的关键因素。该研究还表明,由于椎间盘细胞在损伤后会逐渐进行自我修复,因此在研究慢性椎间盘损伤的修复时,有必要在特定的时间间隔内对椎间盘反复施加打击负荷。
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