2023, Vol. 27 ›› Issue (11): 1744-1749

Abstract: BACKGROUND: Apelin/APJ exhibits functions in regulating cell proliferation, apoptosis, inhibiting inflammatory responses and vascular remodeling. Therefore, it is speculated that Apelin has similar functions in spinal cord injury.
OBJECTIVE: To evaluate the effects of Apelin in rats with spinal cord injury.
METHODS: A rat model of spinal cord transection was used in an in vivo experiment. Forty-five female Sprague-Dawley rats were randomly divided into sham group, spinal cord injury group and Apelin-13 group. Rats in the latter two groups were submitted to make animal models of spinal cord transection. Rats were given the intraperitoneal injection of 0.2 mg/kg Apelin-13 in the Apelin group or the same amount of normal saline in the other two groups for 14 consecutive days. The motor function of rat’s hind limbs was assessed by Basso, Beattie, Bresnahan locomotor rating scale at the 1st, 3rd, 7th, and 14th days after modeling. The spinal cord tissues were collected at the 14th day after spinal cord injury and used for immunohistochemical, immunofluorescence and RT-PCR analyses. In in vitro experiments, H2O2 was used to induce PC12 cell injury followed by treatment with different concentrations (1, 2, 4 μmol/L) of Apelin-13. We then used cell counting kit-8 to detect the effect of Apelin-13 on the viability of injured PC12 cells, thereby exploring the neuroprotective effect of Apelin.
RESULTS AND CONCLUSION: (1) After spinal cord injury, the hindlimb function of the rats was completely lost and motor recovery was observed 3 days after injury. However, there was no significant difference in the spinal cord injury group at different time points. Apelin promoted motor function recovery post spinal cord injury. (2) Spinal cord injury disrupted the local continuity of the spinal cord, and Apelin restored the injured morphology induced by spinal cord injury. (3) There were only a few cells positive for ionized calcium binding adapter protein 1 in the sham group. Spinal cord injury led to a sharp increase in the number of local positive cells and astrocytes. Apelin could alleviate the local activation of astrocytes and microglia (P < 0.05). (4) Severe demyelination occurred after spinal cord injury and the positive area of Luxol Fast Blue staining was significantly reduced. Apelin could attenuate demyelination caused by spinal cord injury. (5) The expression of growth-related protein 43 was significantly increased after spinal cord injury (P < 0.001). Apelin could further promote the expression of growth-related protein 43 (P < 0.05). (6) Apelin increased the cell viability of H2O2-stimulated PC12 cells in vitro (P < 0.05). To conclude, Apelin promotes locomotor recovery and spinal cord morphology repair in rats after spinal cord injury.
Key words: spinal cord injury, Apelin, microglia, PC12 cell, astrocyte, growth-related protein 43, demyelination, inflammation