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一种Nrf2激活剂TPNA10168通过调节MAPK和NF-κB通路来减轻微质中LPS诱导的炎症

Yasuhiko Izumi¹, Eri Koide¹, Fumika Kobayashi¹

¹Laboratory of Pharmacology, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Higashinada-ku, Kobe, 658-8558, Japan.

Journal of pharmacological sciences

|July 26, 2025

概括

通过抑制关键信号通路,TPNA10168可以减少初级微质细胞的炎症. 这种化合物显示出治疗神经炎症的前景,即使没有激活Nrf2通路.

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:

核因子红色素2相关因子2 (Nrf2) -抗氧化反应元素 (ARE) 途径保护细胞免受氧化应激.
Nrf2激活剂通常具有抗炎性质.
此前TPNA10168在BV-2微质细胞中表现出Nrf2独立的抗炎作用.

研究的目的:

研究TPNA10168对初级微质细胞的抗炎作用.
为了确定TPNA10168的抗炎作用是否在初级微质中依赖Nrf2.

主要方法:

主要微质细胞被用脂聚糖化物 (LPS) 和TPNA10168.8治疗.
进行了Nrf2敲击,以评估途径依赖性.
测量了炎症性基因表达 (TNF-α,IL-1β,IL-6).
通过酸化和转位分析信号通路激活 (ERK,p38 MAPK,NF-κB).

主要成果:

TPNA10168显著抑制了LPS诱导的原发性微质中的炎症基因表达.
这些抗炎作用甚至在Nrf2敲击下也被观察到.
TPNA10168抑制了LPS诱导的ERK,p38 MAPK和NF-κB p65.5的酸化.
核转移NF-κB没有受到TPNA10168.8的影响.

结论:

TPNA10168有效地减弱了微质激活和神经炎症.
它的抗炎作用通过对关键信号通路的Nrf2独立抑制来介导.
TPNA10168是神经炎症疾病的潜在治疗候选者.

关键词:

炎症炎症是一种炎症.通过MAPK路径.微质细胞中的微质细胞通过NF-κB路径.Nrf2-ARE 途径通过

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