ZNF667 通过依赖mTOR的有氧糖解调节抑制LPS诱导的巨细胞炎症
Yong-Zhen Li1, Ru Chao1, Shun-Lin Qu1
1Key Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, People's Republic of China.
Current pharmaceutical design
|June 1, 2023
概括
指667 (ZNF667) 蛋白通过调节mTOR依赖的有氧糖解抑制巨细胞的炎症. 这项研究揭示了ZNF66767的存在.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 巨细胞是炎症反应的关键参与者,过度的媒介释放与不受控制的炎症有关.
- 指667 (ZNF667) 蛋白是一种新型的DNA结合蛋白,涉及氧化应激,但其在巨细胞中的作用尚不清楚.
研究的目的:
- 为了研究ZNF667对巨细胞中脂聚糖 (LPS) 诱导的炎症的影响.
- 阐明ZNF667在巨细胞中的抗炎作用背后的分子机制.
主要方法:
- 使用RAW264.7巨细胞系作为模型系统.
- 评估炎症基因表达和PI3K/AKT/mTOR通路的酸化,使用RT-PCR和西部涂抹.
- 研究ZNF667过度表达和缺乏对细胞代谢和炎症标志物的影响.
主要成果:
- 通过LPS治疗,可以提高巨细胞中ZNF667的表达.
- 过度表达ZNF667显著抑制了LPS诱导的促炎媒介 (iNOS,IL-1β,IL-6,TNF-α) 和PI3K/AKT/mTOR过酸化.
- 通过降低HK2和PFKFB3的调节,ZNF667抑制了有氧糖解,减少了葡萄糖消耗和乳酸盐生产.
结论:
- 在RAW264.7巨细胞中,ZNF667作为LPS刺激的炎症的负调节剂.
- ZNF667通过调节mTOR依赖的有氧糖解路径来发挥其抗炎作用.
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