| 吕晓敏,陈 红,薛朝霞,王丽斯,刘 奇.褪黑素通过改善神经元树突棘可塑性在瑞芬太尼诱发大鼠痛觉过敏机制中的作用[J].,2021,(9):1633-1638 |
| 褪黑素通过改善神经元树突棘可塑性在瑞芬太尼诱发大鼠痛觉过敏机制中的作用 |
| The Role of Melatonin in Improving the Plasticity of Neuronal Dendritic Spines in the Mechanism of Remifentanil Induced Hyperalgesia in Rats |
| 投稿时间：2020-11-24 修订日期：2020-12-18 |
| DOI：10.13241/j.cnki.pmb.2021.09.007 |
| 中文关键词: 褪黑素 神经元树突棘 瑞芬太尼 痛觉过敏 |
| 英文关键词: Melatonin neuronal dendritic spines Remifentanil Hyperalgesia |
| 基金项目:内蒙古自治区自然科学基金项目（2019MS08088） |
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| 中文摘要: |
| 摘要 目的：探究褪黑素通过改善神经元树突棘可塑性在瑞芬太尼诱发大鼠痛觉过敏机制中的作用。方法：30只8~10周龄的SD大鼠（175~200 g），根据研究目的随机分为三组：对照组（（大鼠足底进行切口手术，生理盐水处理，n=10），模型组（大鼠足底进行切口手术，静脉滴注瑞芬太尼，n=10），治疗组（在模型组的基础上行褪黑素处理，n=10）。通过机械诱发痛和热缩足检测不同组处理后2 h、2 d、3 d和7 d大鼠的爪缩回阈值，通过RT-qPCR分析大鼠中IL-1、TNF-α和IL-1β的mRNA表达，通过蛋白印迹检测大鼠体内AMPA和Kalirin-7的蛋白表达，通过观察组织切片比较不同组大鼠的脊柱密度和长度，通过低感光电荷耦合设备的摄像头监视器分析单个神经元的电生理。结果：在第2 h、2 d、3 d和7 d的测试中，相比于对照组，模型组痛缩足阈降低（P<0.05），热缩足潜伏时间缩短（P<0.05），IL-1、TNF-α、IL-1β的mRNA表达、AMPA和Kalirin-7的蛋白表达均升高（P<0.05），脊柱密度、脊柱长度升高（P<0.05），电流幅度升高（P<0.05），电流间隔降低（P<0.05）。治疗组较模型组的痛缩足阈升高（P<0.05），热缩足潜伏时间延长（P<0.05），IL-1、TNF-α和IL-1β的mRNA表达、AMPA和Kalirin-7的蛋白表达均降低（P<0.05），脊柱密度、脊柱长度降低（P<0.05），电流幅度降低（P<0.05），电流间隔升高（P<0.05）。结论：褪黑素通过抑制AMPA和Kalirin-7的蛋白表达改善神经元树突棘可塑性，从而降低瑞芬太尼诱发的大鼠痛觉过敏。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the role of melatonin in the mechanism of remifentanil-induced hyperalgesia in rats by improving the plasticity of neuronal dendritic spines. Methods: Purchase 30 SD rats (175~200 g) aged 8-10 weeks. According to the purpose of the study, all rats were randomly divided into three groups: control group (rats undergoing incision surgery on the soles of rats, treated with saline, n=10), model group (rats undergoing incisions on the soles of rats, sutured intravenously remifentanil, n=10), treatment group (melatonin treatment on the basis of the model group, n=10). Shrinkage feet reflection of rats in different groups at 2 h, 2 d, 3 d and 7 d after treatment was detected by the paw withdrawal threshold and the paw withdrawal latency time. The mRNA expression of IL-1, TNF-α and IL-1β in rats was analyzed by RT-qPCR. The protein expression of AMPA and Kalirin-7 in rats was detected by Western blot. The heat sensitivity of rats was evaluated by a hot-plate biological instrument. The density and length of the spine of rats in different groups were compared by observing tissue sections. The electrophysiology of a single neuron is analyzed by the camera monitor of a low-sensitivity charge-coupled device. Results: In the 2 h, 2 d, 3 d and 7 d tests, comparing with the control group, the paw withdrawal threshold was lower (P<0.05), the paw withdrawal latency time was shorter(P<0.05), the mRNA expression of IL-1, TNF-α, IL-1β and the protein expression of AMPA and Kalin-7 was higher(P<0.05) in the model group. And the spine density and length and the current amplitude was higher(P<0.05), the current interval was lower(P<0.05) in the model group. Comparing with the model group, the paw withdrawal threshold was higher(P<0.05), the paw withdrawal latency time was longer(P<0.05), the mRNA expression of IL-1, TNF-α, IL-1β and the protein expression of AMPA and Kalin-7 was lower(P<0.05) in the treatment group. And the spine density and length and the current amplitude was lower(P<0.05), the current interval was increased(P<0.05) in the model group. Conclusion: Melatonin improves the plasticity of neuronal dendritic spines by inhibiting the protein expression of AMPA and Kalirin-7, thereby reducing remifentanil-induced hyperalgesia in rats. |
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