Spinal cord injury (SCI), resulting in damage of the normal structure and function of the spinal cord, would do great harm to patients, physically and psychologically. The mechanism of SCI is very complex. At present, lots of studies have reported that autophagy was involved in the secondary injury process of SCI, and several researchers also found that calcium ions (Ca²⁺) played an important role in SCI by regulating necrosis, autophagy, or apoptosis. However, to our best of knowledge, no studies have linked the spinal cord mechanical injury, intracellular Ca²⁺, and autophagy in series. In this study, we have established an in vitro model of SCI using neural cells from fetal rats to explore the relationship among them, and found that mechanical injury could promote the intracellular Ca²⁺ concentration, and the increased Ca²⁺ level activated autophagy through the CaMKKβ/AMPK/mTOR pathway. Additionally, we found that apoptosis was also involved in this pathway. Thus, our study provides new insights into the specific mechanisms of SCI and may open up new avenues for the treatment of SCI.

脊髓损伤(Spinal cord injury,SCI),导致脊髓正常结构和功能受损,对患者的身心造成极大的伤害。SCI的机制非常复杂。目前已有大量研究报道自噬参与SCI继发性损伤过程，部分研究者还发现钙离子(Ca ²⁺ )通过调节坏死、自噬或细胞凋亡在SCI中发挥重要作用。然而，据我们所知，没有研究将脊髓机械损伤、细胞内 Ca ²⁺, 和自噬系列。本研究利用胎鼠神经细胞建立 SCI 体外模型，探讨它们之间的关系，发现机械损伤可促进细胞内 Ca ²⁺浓度升高，Ca ²⁺水平升高通过CaMKKβ/AMPK/mTOR 通路。此外，我们发现细胞凋亡也参与了该途径。因此，我们的研究为 SCI 的具体机制提供了新的见解，并可能为 SCI 的治疗开辟新的途径。