硫化物和多硫化物作为前感受媒介:专注于Ca3.2功能增强和TRPA1激活
Fumiko Sekiguchi1, Maho Tsubota1, Atsufumi Kawabata1
1Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan.
Journal of pharmacological sciences
|May 26, 2024
概括
硫化物和多硫化物等反应性硫种显著影响疼痛信号. 硫化物增强Cav3.2通道,而聚硫化物激活TRPA1通道,这两者都有助于疼痛,并提供潜在的治疗点.
科学领域:
- 生物化学 生物化学
- 神经科学是一个神经科学.
- 身体生理学 身体生理学
背景情况:
- 活性硫种 (RSS) 在生物过程中至关重要.
- RSS通过金属相互作用,二硫化物键裂解和S-过硫化调节蛋白质功能.
- RSS在健康和疾病状态中都起着重要作用.
研究的目的:
- 研究硫化物和多硫化物在疼痛信号通路中的作用.
- 阐明RSS通过哪些机制影响涉及 nociception 的离子通道.
- 确定潜在的治疗目标来管理病态疼痛.
主要方法:
- 对Cav3.2 T型Ca2+通道进行电生理学研究.
- 通过聚硫化物对TRPA1通道激活的研究.
- 对硫化物和多硫化物对 nociceptors 疼痛信号的影响的分析.
主要成果:
- 硫化物通过去除抑制性Zn2+来增强Cav3.2通道活性,增加 nociceptor刺激性并促进体质和内脏疼痛.
- 多硫化物通过囊S-化激活TRPA1通道,促进体质疼痛.
- 硫化物增强的Cav3.2和多硫化物激活的TRPA1的联合作用协同加速体质疼痛信号.
结论:
- 硫化物/Ca3.2系统是病理性疼痛的关键贡献者,特别是神经病变和炎症性疼痛.
- 聚硫化物激活TRPA1有助于体质疼痛.
- 准硫化物/Cav3.2通路为各种疼痛条件提供了一个有希望的治疗策略,包括内脏疼痛.
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