Abstract：
The specific molecular mechanism of neuroprotective effects of wnt-3a on spinal cord injury (SCI) has not been elucidated. In our study, we evaluated the recovery of motor function after SCI by BBB, observed neuronal apoptosis by western blot and TUNEL, observed the changes of neuronal inflammation by western blot and immunofluorescence staining, and observed the changes of motoneurons and spinal cord area in the anterior horn of the spinal cord via Nissl and HE staining. We found that wnt-3a could significantly promote the recovery of motor function, reduce the loss of motor neurons in the anterior horn of the spinal cord, promote the recovery of injured spinal cord tissue, inhibit neuronal apoptosis and inflammatory response, and ultimately promote neuronal function after SCI. However, when XAV939 inhibits the wnt/β-catenin signaling pathway, the neuroprotective effects of wnt-3a are also significantly inhibited. The above results together indicated that wnt-3a exerts its neuroprotective effect on after SCI via activating the wnt/β-catenin signaling pathway.
摘要：
wnt-3a对脊髓损伤（SCI）的神经保护作用的具体分子机制尚未阐明。在我们的研究中,我们通过BBB评估SCI后运动功能的恢复，通过蛋白质印迹和TUNEL观察神经元凋亡，通过免疫印迹和免疫荧光染色观察神经元炎症的变化，并通过Nissl和HE染色观察脊髓前角运动神经元和脊髓面积的变化。我们发现wnt-3a可以显著促进运动功能的恢复，减少脊髓前角运动神经元的损失，促进受损脊髓组织的恢复，抑制神经元凋亡和炎症反应，并最终促进SCI后的神经元功能。然而,当XAV939抑制wnt/β-catenin信号通路时，wnt-3a的神经保护作用也被显著抑制。以上结果共同表明wnt-3a通过激活wnt/β-catenin信号通路对SCI后的神经保护作用。
