Transient receptor potential ankyrin 1 (TRPA1), the non-selective cation channel, was found that can mediate the generation of multiple sclerosis, while the mechanism is still controversial. Lysophosphatidylcholine (LPC) is a critical trigger of multiple sclerosis which results from the syndrome of neuronal inflammation and demyelination. In this work, we suggested that TRPA1 can mediate the LPC-induced oxidative stress and cytotoxicity in OLN-93 oligodendrocyte. The expression of TRPA1 in OLN-93 was detected by using quantitative real-time PCR (qRT-PCR) and immunofluorescence. The calcium overload induced by LPC via TRPA1 was detected by calcium imaging. The mechanism of LPC-induced mitochondrial reactive oxygen species (mtROS) generation, mitochondria membrane depolarization, nitric oxide (NO) increase, and development of superoxide production via TRPA1 was verified by using confocal imaging. The cell injury elicited by LPC via TRPA1 was confirmed by both CCK-8 and LDH cytotoxicity detection. These results indicate that TRPA1 plays an important role of the LPC-induced oxidative stress and cell damage in OLN-93 oligodendrocyte. Therefore, inhibition of TRPA1 may protect the LPC-induced demyelination.

瞬时受体电位锚蛋白 1 (TRPA1) 是一种非选择性阳离子通道，被发现可以介导多发性硬化症的发生，但其机制仍存在争议。溶血磷脂酰胆碱 (LPC) 是多发性硬化症的关键触发因素，多发性硬化症是由神经元炎症和脱髓鞘综合征引起的。在这项工作中，我们建议 TRPA1 可以介导 LPC 诱导的 OLN-93 少突胶质细胞的氧化应激和细胞毒性。使用定量实时PCR（qRT-PCR）和免疫荧光检测OLN-93中TRPA1的表达。通过钙成像检测 LPC 通过 TRPA1 诱导的钙超载。LPC诱导线粒体活性氧（mtROS）产生、线粒体膜去极化、一氧化氮（NO）增加的机制，通过使用共聚焦成像验证了通过 TRPA1 产生超氧化物的发展。LPC 通过 TRPA1 引起的细胞损伤通过 CCK-8 和 LDH 细胞毒性检测得到证实。这些结果表明 TRPA1 在 LPC 诱导的 OLN-93 少突胶质细胞氧化应激和细胞损伤中起重要作用。因此，抑制 TRPA1 可以保护 LPC 诱导的脱髓鞘。