Objective To investigate the effects of complement component 1q subcomponent B(C1QB) on neural repair and the phosphatidylinositol 3-kinase/protein kinase B(PI3K/AKT) signaling pathway in rats with spinal cord injury(SCI).Methods From March 2024 to October 2024, experiments were conducted in the laboratory of Xuzhou Medical University. An SCI rat model was established, and successfully modeled rats were randomly assigned to the model group(SCI group), si-NC group, si-C1QB group, and si-C1QB + PI3K/AKT signaling pathway inhibitor group(si-C1QB + LY294002 group), with 12 rats in each group. Additionally, 12 normal healthy SD rats were used as the blank control group(Control group). At the end of the treatment, the BBB score was assessed. Enzyme-linked immunosorbent assay(ELISA) was used to detect inflammatory factors in spinal cord tissue. Hematoxylin-eosin(HE) staining was used to observe pathological damage in spinal cord tissue. Terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) staining was used to detect apoptosis of spinal cord neurons. Immunohistochemistry was used to detect the expression of ionized calcium-binding adapter molecule 1(IBA-1) and glial fibrillary acidic protein(GFAP). Western blot was used to detect the expression of proteins related to the PI3K/AKT signaling pathway.Results Compared with the Control group, the spinal cord tissue structure in the SCI group was more disordered, with extensive cavitation due to loss of integrity, severe neuronal damage, disorganized nerve fiber arrangement, and prominent inflammatory cell infiltration. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were decreased(t/P=23.859/<0.001, 13.739/<0.001, 13.418/<0.001, 13.191/<0.001), while TNF-αand IL-6 levels, neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were increased(t/P=14.325/<0.001, 14.820/<0.001, 18.653/<0.001, 13.191/<0.001, 12.269/<0.001, 13.168/<0.001, 14.795/<0.001). Compared with the si-NC group, the si-C1QB group showed better structural and morphological repair of spinal cord tissue, with noticeable reduction in cavitation, relatively clear gray and white matter boundaries, orderly nerve fiber arrangement, and reduced inflammatory cell infiltration. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were increased(t/P=21.430/<0.001, 11.692/<0.001, 11.393/<0.001, 13.182/<0.001), while TNF-αand IL-6 levels, neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were decreased(t/P=11.889/<0.001, 12.385/<0.001, 3.846/0.003,12.187/<0.001, 9.242/<0.001, 12.050/<0.001, 11.900/<0.001). Compared with the si-C1QB group, the si-C1QB+LY294002 group showed more severe spinal cord tissue damage. The BBB score, IL-10 level, and p-PI3K/PI3K and p-AKT/AKT expression were decreased(t/P=14.543/<0.001, 9.647/<0.001, 10.735/<0.001, 12.187/<0.001), while TNF-αand IL-6 levels,neuronal apoptosis rate, and expression of C-caspase-3, C-caspase-9, IBA-1, and GFAP were increased(t/P=10.708/<0.001,10.678/<0.001, 3.149/0.010, 10.694/<0.001, 8.832/<0.001, 10.681/<0.001, 10.614/<0.001).Conclusion Silencing C1QB can promote neural repair in rats with spinal cord injury, which is associated with activation of the PI3K/AKT signaling pathway.
Key words:Spinal cord injury ; Complement component 1q subcomponent B ; PI3K/AKT signaling pathway ; Neural repair ; Rat

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