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内炎性刺激诱导脊柱疼痛行为和脊椎间盘退化 in vivo
Lauren E Lisiewski1,2, Hayley E Jacobsen2, Dan C M Viola2
1Department of Biomedical Engineering, Columbia University, New York, New York, USA.
概括
炎症,而不是结构损伤,可以导致椎间盘 (IVD) 疼痛. 这项研究使用脂聚糖 (LPS) 显示炎症激活了大鼠IVD的疼痛通路,为疼痛研究提供了新模式.
科学领域:
- 生物医学研究的研究.
- 疼痛机制 疼痛机制
- 脊柱退行症 脊柱退行症
背景情况:
- 椎间盘 (IVD) 退化与疼痛有关,但炎症的作用尚不清楚.
- 穿孔模型造成结构损伤,而不是模仿自然的IVD退化.
- 需要一个精确的模型来研究炎症在IVD疼痛中的作用.
研究的目的:
- 为了研究炎症是否能单独引发大鼠尾部IVDs的疼痛.
- 使用脂聚糖 (LPS) 建立一个新的IVD损伤模型,而不会造成身体损伤.
- 探索与炎症诱导的IVD疼痛相关的分子和细胞变化.
主要方法:
- 用细针将脂聚糖化物 (LPS) 内滴注入大鼠尾部IVD中.
- 对促炎性细胞因子和巨细胞标记物的基因表达的分析.
- 针对巨细胞,神经元标记物的免疫化,以及IVD结构完整性和疼痛行为的评估.
主要成果:
- 在IVD中,LPS注射诱导了促炎性细胞因子和巨细胞标志物表达.
- 组织学分析揭示了LPS后的IVD结构破坏和生化变化.
- 内性炎症导致机械过敏症,并改变了 nociceptive 标记物的表达,表明疼痛产生.
结论:
- 内部炎症刺激,独立于结构损伤,可以启动IVDs的疼痛.
- 这种LPS诱导的老鼠IVD模型表明炎症和疼痛行为之间存在直接联系.
- 这些发现表明,炎症介导的途径有助于IVD疼痛,需要进一步调查.
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