薄荷驱动的TRPM8热生成:预防感冒伤害的机制
Yujie Li1,2, Yuanyuan Song3, Xin Yang1
1Department of Endocrinology, General Hospital of Northern Theater Command, No. 83 Wenhua Road, Shenyang, 110000, Liaoning Province, China.
Journal of physiology and biochemistry
|September 13, 2025
概括
薄荷醇通过在棕色脂肪组织中激活TRPM8 (短暂受体潜在阴离子通道亚家族M成员8) 来保护寒冷损伤,促进热生成并改善小鼠的寒冷耐受性.
科学领域:
- 生理学 生理学 生理学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 寒冷伤害对健康构成重大风险,导致因极度寒冷暴露而导致组织损伤.
- 了解热生成的机制对于制定有效的预防感冒伤害策略至关重要.
研究的目的:
- 为了研究薄荷醇对寒冷伤害的保护作用.
- 探索短暂受体潜在阴离子通道亚家族M成员8 (TRPM8) 在薄荷介导热生成和寒冷耐受性中的作用.
主要方法:
- 网络药理学确定TRPM8作为一个关键目标.
- 分子对接和途径分析证实了TRPM8在棕色脂肪组织 (BAT) 热生成中的作用.
- 实验包括薄荷治疗,寒冷暴露 (-20°C),TRPM8抑制,以及对小鼠核心体温,活动和寒冷伤害严重程度的测量.
主要成果:
- 薄荷醇治疗显著增加了核心体温和耐寒性,同时减少了寒冷伤害的严重程度.
- 网络药理学确定了PKA/UCP1通路是TRPM8调节的BAT热生成的核心.
- 抑制TRPM8减弱了薄荷醇的有益作用,证实了其至关重要的作用.
结论:
- 薄荷醇在棕色脂肪组织中激活TRPM8,增强热生成并提供对寒冷伤害的保护.
- TRPM8是薄荷醇发热效应和耐寒性的关键调解者.
- 薄荷醇作为预防感冒伤害的天然剂显示出希望,TRPM8作为潜在的治疗点.
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