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低温会通过TRPV4减轻神经毒性微质激活

Naoya Fukuda¹, Kohki Toriuchi¹, Rina Mimoto¹

¹Department of Pathobiology, Nagoya City University Graduate School of Pharmaceutical Sciences, 3-1 Tanabedori, Mizoho-Ku, Nagoya, Aichi, 467-8603, Japan.

Neurochemical research

|December 19, 2023

概括

治疗性低温 (TH) 通过抑制通过TRPV4通道的微质激活来减少神经炎症. 这一途径涉及AMPK-NF-κB信号传递,为神经保护提供了一个潜在的新策略,补充TH.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

治疗性低温症 (TH) 以其神经保护性益处而闻名,但其潜在的细胞机制仍然不清楚.
微质激活在各种神经系统疾病中起着至关重要的作用,使其调节成为潜在的治疗目标.
暂时受体潜在化物4 (TRPV4) 通道对温度敏感,它们在TH的神经保护作用中的参与被推测,但尚不清楚.

研究的目的:

调查低温是否会通过TRPV4通道减弱微质激活.
阐明涉及低温诱导微质活动和神经保护调节的特定分子通路.

主要方法:

培养的微质细胞用脂聚糖 (LPS) 刺激,并暴露在正常热 (37°C) 或低温 (33.5°C) 条件下.
评估了促炎性细胞因子的表达,可诱导的氧化合成酶和细胞活性.
通过使用特定的激动剂和对抗剂来检查TRPV4通道的作用,并对AMPK-NF-κB信号通路进行分析.

主要成果:

低温显著抑制了促炎性标记物的表达,并减少了细胞微质细胞的数量.
在低温条件下,AMP激活蛋白激酶 (AMPK) -NF-κB信号被抑制.
低温会减少由LPS激活的微质引起的神经元损伤,这种效应被TRPV4抗剂模仿,并被TRPV4激动剂逆转.

结论:

治疗性低温会通过TRPV4-AMPK-NF-κB通路抑制微质激活和随后的神经元损伤.
针对TRPV4通道提出了一种新的治疗策略,以增强TH的神经保护作用.
需要进一步的研究来验证这些发现在中枢神经系统的不同人口和区域背景.

关键词:

这就是AMPKK.低温症是什么意思低温症微质细胞中的微质细胞 NF-κB 神经元损伤在 TRPV4 中.

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