神经性疼痛的分子机制

International Conference on Informatics Education and Research for Knowledge-Circulating Society (icks 2008) Pub Date : 2008-01-17 DOI:10.1109/ICKS.2008.24

Yosuke Sawada, H. Hosokawa, Kiyoshi Matsumura, Shigeo Kobayashi

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引用次数: 14

摘要

有许多病人患有神经性疼痛。活性氧(ROS)被认为是神经性疼痛的中介。此外，低温会加重神经性疼痛。然而，ROS受体与低温的关系尚不清楚。TRPA1被疼痛产生剂如异硫氰酸烯丙酯或甲醛激活。我们推测TRPA1是ROS和低温对伤害感受器的受体。本研究的目的是利用钙离子想象膜片钳来研究这一假设的有效性。深度冷却(<17℃)和ROS激活表达TRPA1的HEK293细胞。这些结果表明TRPA1是ROS和低温的受体。

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Molecular Mechanism of Neuropathic Pain

There are many patients suffering from neuropathic pain. Reactive oxygen species (ROS) is thought to be a mediator of neuropathic pain. In addition, neuropatic pain is aggravated by low temperature. However, receptor of ROS and low temperature is unknown. TRPA1 is activated by pain- producing agents such as allyl isothiocyanate or formaldehyde. We hypothesized that TRPA1 is receptor of ROS and low temperature on nociceptor. The purpose of present study is to investigate the validity of this hypothesis using Ca2+ imagining, patch clamp. Deep cooling (<17degC) and ROS activates TRPA1 expressing HEK293 cells. These results indicate that TRPA1 is receptor of ROS and low temperature.

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International Conference on Informatics Education and Research for Knowledge-Circulating Society (icks 2008)

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