Objective Based on the CXC chemokine receptor 4-focal adhesion kinase (CXCR4-FAK) signaling pathway, to explore the improvement of neuromotor function after intrathecal injection of dexmedetomidine (DHI) after spinal cord ischemia-reperfusion injury (SCIRI) in rats.
Method 60 SPF male SD rats aged 10-12 weeks were randomly divided into 4 groups (n=15): sham group, model group, DHI group, and DPA group. The model group, DHI group, and DPA group opened the chest and clamped the aortic arch for 15 minutes to construct the SCIRI model. The sham group only opened the chest and freed the aortic arch without clamping. The rats in the DHI and DPA groups were injected intrathecal DHI and Diprotin A 72 hours before ischemia. The injection dose was 30 μL at a concentration of 5 μmol/L. The sham group and the model group were injected with the same amount of normal saline, once a day. Continuous 3d. Modified Tarlov scoring method, Evans blue (EB) staining, wet and dry method, electron microscopy, YUNEL staining, DCFH-DA staining and kits, Western bllot to detect neuromotor function scores, The structural integrity of the blood-spinal cord barrier (BSCB), spinal cord tissue water content, spinal cord ultrastructural changes, cell apoptosis, oxidative stress, and expression levels of CXCR4 and p-FAK proteins.
Results Compared with the sham group, the neuromotor function score, superoxide dismutase (SOD) activity, water content of spinal cord tissue, EB red fluorescence intensity, cell apoptosis rate, and reactive oxygen species (ROS) green were significantly reduced in the model group. Fluorescence intensity, malondialdehyde (MDA) content, CXCR4 and p-FAK expression levels increased significantly. Compared with the model group, the neuromotor function score, SOD enzyme activity, CXCR4 and p-FAK expression levels in the spinal cord tissues of the DHI and DPA groups were significantly increased, and the water content of the spinal cord tissue, EB red fluorescence intensity, and apoptosis Rate, ROS green fluorescence intensity, and MDA content are significantly reduced. The differences were statistically significant (P<0.05). Compared to the DHI group and the DPA group, the difference was not significant (P<0.05) and was not statistically significant.
Conclusion The protective effect of dexmedetomidine on SCIRI rats may be through activating the CXCR4-FAK signaling pathway to reduce cell oxidative stress damage, so as to play a protective effect on the spinal cord tissue of SCIRI rats.