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目的:观察背根节慢性压迫(chronic compression of dorsal root ganglion,CCD)大鼠脊髓内高迁移率蛋白-1(high mobility group box-1,HMGB1)的变化,探讨其参与痛觉信息传递的机制,为慢性痛的治疗提供新的思路和靶点。方法:(1)24只SD大鼠随机分成4组,为正常大鼠组、假手术组、CCD 3 d组、7 d组。检测大鼠脊髓HMGB1 mRNA的表达情况。(2)24只SD大鼠分成4组,行CCD手术。术后7 d鞘内给予生理盐水、HMGB1的中和抗体10、30、100μg,检测大鼠各时间点机械性缩足阈值。(3)24只SD大鼠分成4组(n=6),鞘内给予生理盐水、HMGB1的中和抗体10、30、100μg,检测大鼠的运动功能。(4)30只SD大鼠分成5组(n=6)。在CCD术后7 d鞘内给予saline、HMGB1的中和抗体10、30、100μg,检测大鼠脊髓TNF-α、IL-1β和IL-6 mRNA的表达。结果:(1)CCD术后3 d和7 d,脊髓内HMGB1 mRNA的表达明显上调(P<0.05)。(2)鞘内给予HMGB1的中和抗体30、100μg后可以明显逆转CCD大鼠术后7 d的机械性痛敏,且其作用可以持续24 h(P<0.05)。(3)鞘内给予HMGB1的中和抗体没有引起大鼠的运动功能损伤(P>0.05)。(4)鞘内给予HMGB1的中和抗体30、100μg可以显著抑制CCD大鼠术后7 d组脊髓内的TNF-α、IL-1β、IL-6 mRNA的表达(P<0.05)。结论:脊髓内HMGB1的上调可能参与了CCD大鼠痛敏状态的形成。
OBJECTIVE: To observe the changes of high mobility group box-1 (HMGB1) in the spinal cord of chronic compression of dorsal root ganglion (CCD) rats and to explore the mechanism involved in the transmission of pain information. Provide new ideas and targets for the treatment of chronic pain. Methods: (1) Twenty-four SD rats were randomly divided into 4 groups: normal group, sham operation group, CCD 3 d group and 7 d group. Detection of rat spinal cord HMGB1 mRNA expression. (2) Twenty-four SD rats were divided into 4 groups and underwent CCD surgery. At 7 days after operation, NS, 10 and 100μg HMGB1 neutralizing antibody were given intrathecally, and the threshold of mechanical contractions were measured at each time point. (3) Twenty-four SD rats were divided into 4 groups (n = 6). The rats were given normal saline and 10, 30 and 100μg of neutralizing antibody of HMGB1 respectively to detect the motor function of rats. (4) 30 SD rats were divided into 5 groups (n = 6). Neonatal antibodies of saline and HMGB1 were given intrathecally at 10, 30 and 100μg after 7 days of CCD surgery. The expression of TNF-α, IL-1β and IL-6 mRNA in spinal cord of rats were detected. Results: (1) The expression of HMGB1 mRNA in the spinal cord was significantly up-regulated at 3 d and 7 d after operation (P <0.05). (2) The neutralization antibody of HMGB1 administered intrathecally could obviously reverse the mechanical hyperalgesia of CCD rats 7 days after exposure to 100 and 100μg of retinol, and the effect could be sustained for 24 hours (P <0.05). (3) Neutralizing antibodies administered intrathecally to HMGB1 did not cause motor function impairment in rats (P> 0.05). (4) The neutralizing antibody 30 and 100μg administered intrathecally to HMGB1 significantly inhibited the expression of TNF-α, IL-1β and IL-6 mRNA (P <0.05) in the spinal cord of the 7th day after the operation in the CCD. Conclusion: Upregulation of HMGB1 in spinal cord may be involved in the formation of pain-sensitive state in CCD rats.