神经病理性疼痛（neuropathic pain, NP）是由躯体感觉神经系统的损伤或疾病直接造成的疼痛，是外周和中枢神经系统之间复杂机制相互作用的结果，是疼痛综合征中最难治愈的。瞬时受体电位通道A1（transient receptor potential cation channel, subfamily A, member 1, TRPA1）参与NP的形成，在伤害性信号的传递整合中起着至关重要的作用。NP过程中产生的大量氧化应激产物等作用于TRPA1，引起痛觉过敏。TRPA1特异性抑制剂有望用于NP的治疗。文章主要对TRPA1的激活与调节机制、在NP方面的研究进展等内容进行综述，为疼痛治疗提供新的思路。
Neuropathic pain (NP) is a direct pain caused by a lesion or disease of the somatosensory nervous system, which is the consequence of a complex interplay of mechanisms in the peripheral and central nervous systems and the most intractable pain syndrome. Transient receptor potential cation channel, subfamily A, member 1 (TRPA1) is involved in the formation of neuropathic pain and plays a crucial role in the integration of nociceptive signals. During NP, a large amount of oxidative stress products are released to cause hyperalgesia. TRPA1-specific antagonists are expected to be used in the treatment of neuropathic pain. This review summarizes the mechanism of TRPA1 activation and regulation and research progress in TRPA1 in NP, so as to provide new insights for pain management.
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