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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Eugenol Inhibits ATP-induced P2X Currents in Trigeminal Ganglion Neurons
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Eugenol Inhibits ATP-induced P2X Currents in Trigeminal Ganglion Neurons

机译：丁香酚抑制三叉神经节神经元中ATP诱导的P2X电流。

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Eugenol is widely used in dentistry to relieve pain. We have recently demonstrated voltage-gated Na+ and Ca2+ channels as molecular targets for its analgesic effects, and hypothesized that eugenol acts on P2X3, another pain receptor expressed in trigeminal ganglion (TG), and tested the effects of eugenol by whole-cell patch clamp and Ca2+ imaging techniques. In the present study, we investigated whether eugenol would modulate 5'-triphosphate (ATP)-induced currents in rat TG neurons and P2X3-expressing human embryonic kidney (HEK) 293 cells. ATP-induced currents in TG neurons exhibited electrophysiological properties similar to those in HEK293 cells, and both ATP- and α ,β-meATP-induced currents in TG neurons were effectively blocked by TNP-ATP, suggesting that P2X3 mediates the majority of ATP-induced currents in TG neurons. Eugenol inhibited ATP-induced currents in both capsaicin-sensitive and capsaicin-insensitive TG neurons with similar extent, and most ATP-responsive neurons were IB4-positive. Eugenol inhibited not only Ca2+ transients evoked by α ,β-meATP, the selective P2X3 agonist, in capsaicin-insensitive TG neurons, but also ATP-induced currents in P2X3-expressing HEK293 cells without co-expression of transient receptor potential vanilloid 1 (TRPV1). We suggest, therefore, that eugenol inhibits P2X3 currents in a TRPV1-independent manner, which contributes to its analgesic effect.
机译：丁香酚被广泛用于牙科以减轻疼痛。我们最近证明了电压门控的Na + 和Ca 2 + 通道作为其镇痛作用的分子靶标，并假设丁子香酚对P2X 3 是另一种在三叉神经节（TG）中表达的疼痛受体，并通过全细胞膜片钳和Ca 2 + 成像技术测试了丁香酚的作用。在本研究中，我们研究了丁子香酚是否会调节5'-三磷酸（ATP）诱导的大鼠TG神经元和表达P2X 3 的人胚肾（HEK）293细胞中的电流。 TG神经元中的ATP诱导电流表现出与HEK293细胞相似的电生理特性，而TNP-ATP有效地阻断了TG神经元中的ATP-和α，β-meATP诱导电流，表明P2X 3 介导TG神经元中大多数ATP诱导的电流。丁香酚在对辣椒素敏感和对辣椒素不敏感的TG神经元中均抑制ATP诱导的电流，并且大多数ATP响应神经元都具有IB4阳性。丁香酚不仅抑制了辣椒素不敏感的TG神经元中由α，β-meATP（选择性P2X 3 激动剂）引起的Ca 2 + 瞬变，而且还抑制了ATP诱导的电流。表达P2X 3 的HEK293细胞，而不共表达瞬时受体电位香草酸1（TRPV1）。因此，我们建议丁子香酚以不依赖TRPV1的方式抑制P2X 3 电流，这有助于其止痛作用。

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