Mechanisms for Reducing Neuropathic Pain
Mechanisms for Reducing Neuropathic Pain
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DOI：
10.1007/s12035-019-01757-9
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发表时间：
2020-01-01
影响因子：
5.1
通讯作者：
Kuffler, Damien P.
中科院分区：
文献类型：
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作者：
Kuffler, Damien P.
损伤通常会导致神经性疼痛的发生，但疼痛通常会随着伤口愈合而减轻和消失。疼痛是由驻留在损伤部位并被招募到损伤部位的细胞释放促炎细胞因子和其他介质导致促炎环境的发展并导致伤害性神经元产生慢性异位电活动而引起的，这是神经性疼痛的基础。由于一些诱导促炎症的细胞改变其表型，导致阻断促炎介质的释放，同时释放抗炎介质，并阻断伤害性神经元的慢性自发电活动，因此疼痛减轻。通常，尽管伤口明显愈合，但神经性疼痛会变成慢性。这就提出了如何消除慢性疼痛的问题。虽然已知许多有助于神经性疼痛的发生和维持的细胞和介质，但需要更好地了解如何控制损伤部位环境以永久消除促炎环境并沉默长期电活跃的伤害性神经元。本文探讨了如何通过改变局部细胞类型的组成、改变促炎和抗炎受体的活性、诱导抗炎介质的释放以及沉默长期电活跃的伤害性神经元来促进促炎损伤部位向抗炎状态转变的方法。它还检验了这样的假设：从富含血小板的血浆中释放的因子应用于慢性疼痛部位可以永久消除慢性炎症及其相关的慢性疼痛。
Injury typically results in the development of neuropathic pain, but the pain normally decreases and disappears in paralleled with wound healing. The pain results from cells resident at, and recruited to, the injury site releasing pro-inflammatory cytokines and other mediators leading to the development of pro-inflammatory environment and causing nociceptive neurons to develop chronic ectopic electrical activity, which underlies neuropathic pain. The pain decreases as some of the cells that induce pro-inflammation, changing their phenotype leading to the blocking the release of pro-inflammatory mediators while releasing anti-inflammatory mediators, and blocking nociceptive neuron chronic spontaneous electrical activity. Often, despite apparent wound healing, the neuropathic pain becomes chronic. This raises the question of how chronic pain can be eliminated. While many of the cells and mediators contributing to the development and maintenance of neuropathic pain are known, a better understanding is required of how the injury site environment can be controlled to permanently eliminate the pro-inflammatory environment and silence the chronically electrically active nociceptive neurons. This paper examines how methods that can promote the transition of the pro-inflammatory injury site to an anti-inflammatory state, by changing the composition of local cell types, modifying the activity of pro- and anti-inflammatory receptors, inducing the release of anti-inflammatory mediators, and silencing the chronically electrically active nociceptive neurons. It also examines the hypothesis that factors released from platelet-rich plasma applied to chronic pain sites can permanently eliminate chronic inflammation and its associated chronic pain.