Naringenin inhibits spinal cord injury-induced activation of neutrophils through miR-223.

Naringenin (NR), a flavonoid abundant in citrus fruits has been reported to possess anti-inflammatory properties. The present study aimed to investigate the protective of naringenin in rats after spinal cord injury (SCI) and the underlying mechanisms associated with neuroinflammation. Adult male Sprague-Dawley rats were subjected to laminectomy at T9-T11 and compression with a vascular clip. The spinal cords spanning the injury site about 0.8cm were collected for testing. There were five groups (n=7 in each group): (a) Control group; (b) sham group group; (c) SCI+saline; (d) SCI+NR (50mg/kg, p.o.) group and (e) SCI+NR (100mg/kg, p.o.) group. Different doses of NR (50mg/kg, p.o. and 100mg/kg, p.o.) or saline were administered once daily for 11 consecutive days, from 3days prior to surgery to 7days after surgery. The expression level of miR-223, NLRP3 and IL-1β were measured by RT- qPCR. The accumulation of neutrophils at the site of compression, as evaluated by measuring the tissue myeloperoxidase activity, significantly increased with time following the compression, peaking at 24h post compression. The expression of miR-223 was significant elevated in (b). However, spinal cord myeloperoxidase activity and the expression of miR-223 did not increase in sham-operated animals. NR significantly inhibited a SCI-induced activation of neutrophils through repressed miR-223 in group (d) and (e). There was a better effect in group (e) than group (d). miR-223 is thought to act as a fine-tuner of granulocyte production and the inflammatory response. Our findings suggested that repeated administration of naringenin (100mg/kg, p.o) may provide the protective effect of the spinal cord injury in rats, possibly through inhibiting neuroinflammation.