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甲状腺功能低下症通过抑制BDNF促进的PI3K-Akt信号通路来促进微质M1的极化

Yuan Zhan^1,2, Lang Lang³, Fen Wang³

¹Department of Geriatric Endocrinology, The First Affiliated Hospital of Anhui Medical University, Hefei, China, zzhan192623@126.com.

Neuroendocrinology

|December 4, 2024

概括

甲状腺功能低下症通过减少来自大脑的神经营养因子 (BDNF) 来促进有害的微质M1两极分化. 通过PI3K-Akt途径恢复BDNF水平可能为相关的神经疾病提供治疗策略.

科学领域:

神经科学是一个神经科学.
内分泌学在内分泌学.
免疫学免疫学免疫学

背景情况:

甲状腺功能低下症通过神经系统疾病对患者的生活质量产生负面影响.
甲状腺功能低下症与神经退行症中的微质功能之间的确切联系仍然不清楚.

研究的目的:

为了研究甲状腺功能低下如何影响微质质的两极化.
鉴定甲状腺功能低下症引起的微质功能变化背后的调节机制.

主要方法:

使用甲基马 (methimazole) 构建了一个小鼠甲状腺功能低下症模型.
分析了微质M1偏振生物标志物和促炎细胞因子.
利用脂聚糖 (LPS) 处理的BV2细胞来研究微质偏振因子.
采用全球转录组测序 (RNA-seq) 来发现调控途径.

主要成果:

甲状腺功能低下症在小鼠中增加了M1微质偏振生物标志物和促炎细胞因子,同时降低了BDNF,TrkB和IL-10.
在BV2细胞中的LPS治疗减少了BDNF,IL-10和Arg1;BDNF过度表达逆转了LPS诱导的炎症.
过度表达BDNF调节基因表达,特别是在PI3K-Akt信号通路内,将Myc,Gdnf,Thbs1和Ccnd1确定为关键目标.

结论:

甲状腺功能低下症通过抑制BDNF表达来促进微质M1两极分化.
通过PI3K-Akt信号通路,BDNF可以抑制微质M1的两极分化.
针对BDNF-PI3K-Akt轴为甲状腺功能低下症相关的神经炎症提供了潜在的治疗策略.

关键词:

这就是为什么BDNF是BDNF.甲状腺功能低下症甲状腺功能低下症微质M1极化微质M1极化氨酸酸3酶-Akt信号通路的信号通路在RNA-seqqq.

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