通过调节Ccr2/Akt/Gsk-3β通路,GAS减少了激活的微质中的炎症反应
Haolong Shi1, Jinsha Shi1, Zhao Wang1
1Department of Anatomy and Histology & Embryology, Faculty of Basic Medical Sciences, Kunming Medical University, 1168 West Chunrong Road, Kunming, Yunnan, 650500, PR China.
Molecular brain
|May 6, 2025
概括
加斯特罗丁 (GAS) 通过减少神经炎症来保护免受缺氧缺血性脑损伤 (HIBD). 它调节Ccr2/Akt/Gsk-3β通路,减少炎症因素,并在新生儿脑损伤模型中提供神经保护.
科学领域:
- 神经科学是一个神经科学.
- 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:
- 缺氧缺血性脑损伤 (HIBD) 是新生儿死亡率和长期神经缺陷的主要原因.
- 激活的微质细胞有助于HIBD诱导的神经炎症.
- 素 (GAS) 是一种天然化合物,具有抗氧化和抗炎性质.
研究的目的:
- 在HIBD小鼠模型和氧-葡萄糖剥夺 (OGD) 治疗的BV2细胞中研究Gastrodin (GAS) 的神经保护作用.
- 阐明涉及Ccr2/Akt/Gsk-3β信号通路和炎症媒介的潜在分子机制.
主要方法:
- 建立HIBD小鼠模型和OGD诱导的BV2细胞模型.
- 评估Ccl2,Ccr2,Akt,p-Akt,Gsk-3β,p-Gsk-3β,TNF-α和IL-1β的表达,使用西式涂抹,免疫光和qRT-PCR.
- 使用RS102895对Ccr2进行药理抑制,以探索途径相互作用.
主要成果:
- GAS治疗显著降低了Ccl2和Ccr2的表达,同时增加了HIBD小鼠和OGD治疗的BV2细胞中的Akt和Gsk-3β酸化.
- GAS的使用降低了促炎性细胞因子TNF-α和IL-1β的表达.
- 抑制Ccr2增强了p-Akt和p-Gsk-3β水平和减弱了炎症介质的产生,与GAS结合时没有添加作用.
结论:
- 加斯特罗丁 (GAS) 通过减轻神经炎症,对HIBD产生神经保护作用.
- GAS可能通过对Akt/Gsk-3β信号通路进行上调来起作用,这种信号通路可能通过Ccr2受体进行介导.
- 这些发现表明GAS是新生儿缺氧缺血性脑损伤的潜在治疗剂.
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