Abstract

Objective To evaluate the effect of exogenous resolvin D2 on radicular pain in a rat model of non-compressive lumbar intervertebral disc herniation. Methods Thirty-six clean-grade healthy male Sprague-Dawley rats, aged 8 weeks, weighing 230-270 g, were divided into 3 groups (n=12 each) using a random number table method: sham operation group (group S), radicular pain induced by non-compressive lumbar intervertebral disc herniation group (group P) and exogenous resolvin D2 group (group R). The right L5 dorsal root ganglions were covered by autologous nucleus pulposus tissues to establish the model of non-compressive lumbar disc herniation in P and R groups.The corresponding surgical site was only exposed in group S. The corresponding drugs were intrathecally injected within 3 days after establishing the model, phosphate buffer solution 10 μl was injected in group P, 1 ng/μl resolvin D2 solution 10 μl was injected in group R, and normal saline 10 μl was given for pipe washing after administration in the three groups.The mechanical paw withdrawal threshold (MWT) was measured on 1 day before establishing the model and 1-7 days after establishing the model.The spinal dorsal horns of lumbar enlargement segments were removed on day 7 after establishing the model for determination of the expression of glial fibrillary acidic protein (GFAP) (by Western blot) and co-expression of G-protein-coupled receptor 18 with GFAP (by double-label immunofluorescence). Results Compared with group S, the MWT was significantly decreased at 1-7 days after establishing the model, and the expression of GFAP was up-regulated in group P (P<0.05). Compared with group P, the MWT was significantly increased at 3-7 days after establishing the model, and the expression of GFAP was down-regulated in group R (P<0.05). G-protein-coupled receptor 18 was co-expressed with GFAP. Conclusion Exogenous resolvin D2 can reduce radicular pain in a rat model of non-compressive lumbar intervertebral disc herniation, and the mechanism is related to inhibiting activation of astrocytes in the spinal dorsal horns. Key words: Docosahexaenoic acids; Neuralgia; Intervertebral disc displacement; Glial fibrillary acidic protein

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