脊髓背角基质细胞衍生因子1对皮肤肌肉切口牵拉术致持续性疼痛大鼠中枢敏感化及痛觉过敏的影响

目的 观察脊髓背角基质细胞衍生因子1（SDF-1）对皮肤肌肉切口牵拉术（SMIR）致持续性疼痛大鼠中枢敏感化及痛觉过敏的影响，为探讨术后慢性疼痛的发生机制和治疗靶点提供依据。方法 采用SMIR后持续性疼痛大鼠模型。将36只雄性SD大鼠随机分为假手术组（仅切开皮肤）和SMIR后1、5、10、20 d组以及SMIR+鞘内注射SDF-1中和性抗体组，每组6只大鼠。用up-down法测定术后大鼠痛行为学，用蛋白质印迹法检测各组大鼠脊髓组织中SDF-1的表达。再取18只雄性SD大鼠随机分为假手术组、SMIR组和SMIR+脊髓表面给予SDF-1中和性抗体组（每组6只大鼠），检测3组大鼠脊髓背角C纤维诱发场电位长时程增强（LTP）的变化。结果 与假手术组大鼠相比，SMIR后第5、10、20天大鼠脊髓组织SDF-1表达均增加（P均<0.05），且SMIR后大鼠痛阈降低（P<0.01），鞘内注射SDF-1中和性抗体可部分逆转SMIR引起的痛阈下降（P<0.05）。SMIR后1 h脊髓背角LTP升高（P<0.01），脊髓表面给予SDF-1中和性抗体可抑制SMIR导致的LTP升高（P<0.01）。结论 脊髓背角SDF-1参与了SMIR致持续性疼痛大鼠中枢敏感化及痛觉过敏，但具体机制有待进一步研究。

Effects of stromal cell-derived factor 1 of spinal dorsal horn on central sensitivity and allodynia in rats with persistent pain evoked by skin/muscle incision and retraction

Objective To explore the effects of stromal cell-derived factor 1 (SDF-1) on central sensitivity and allodynia in rats with skin/muscle incision and retraction (SMIR)-induced persistent pain, so as to provide reference for elucidating the potential mechanisms and therapeutic targets of postoperative chronic pain. Methods A postoperative chronic pain rat model was induced by SMIR. Thirty-six male SD rats were randomized into sham group, 1, 5, 10, and 20 d after SMIR groups and SMIR+intrathecal injection of SDF-1 neutralizing antibody group, with six rats in each group. The mechanical allodynia was determined with up-down method, and the expressions of SDF-1 were detected by Western blotting after surgery. Furthermore, 18 male SD rats were randomly divided into sham group (n=6), SMIR group (n=6) and SMIR+anti-SDF-1 group (SDF-1 neutralizing antibody was given on the surface of the spinal cord, n=6). The long-term potentiation (LTP) of C-fiber-evoked potentials in the rat spinal dorsal horn was detected in the three groups. Results The SDF-1 expressions were significantly increased on the 5, 10 and 20 days after SMIR versus the sham group (all P<0.05). The pain threshold of rats was significantly reduced after SMIR versus the sham group (P<0.01). Compared with the sham group, intrathecal injection of SDF-1 neutralizing antibody significantly suppressed the mechanical allodynia induced by SMIR (P<0.05). The LTP was significantly increased one hour after SMIR (P<0.01), and SDF-1 neutralizing antibody given on the surface of the spinal cord significantly inhibited the increased LTP induced by SMIR (P<0.01). Conclusion SDF-1 of the spinal dorsal horn is involved in SMIR-induced central sensitivity and allodynia in rats, but the specific mechanism is still unclear.