4-Octyl itaconate通过激活Nrf2在小鼠骨髓衍生的巨细胞中部分抑制了聚I:C诱导的干扰素-β分泌
Ying-Xing Yue1, Bing-Bing Jia1, Ji-Rong Wang1
1Zhejiang Provincial Key Lab of Geriatrics and Geriatrics Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, 1229 Gudun Road, Hangzhou, China.
Heliyon
|December 11, 2023
概括
4-octyl itaconate (4-OI) 抑制了巨细胞中抗病毒干扰素-β (IFN-β) 的分泌. 这种免疫反应调节部分通过Nrf2信号通路的调节来调节.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- 病毒对人类健康构成重大威胁,需要强有力的抗病毒反应.
- 干扰素-β (IFN-β) 对于抗病毒防御至关重要,可提高对抗病毒感染的基因的调节.
- 伊塔可纳酸衍生物,如4-octyl itaconate (4-OI),调节免疫反应,但它们对IFN-β分泌的影响尚不清楚.
研究的目的:
- 为了研究4-octyl itaconate (4-OI) 对双链RNA刺激的巨细胞中干扰素-β (IFN-β) 分泌的作用.
- 阐明4-OI对抗病毒反应影响的分子机制.
主要方法:
- 鼠标骨髓衍生巨细胞 (BMDM) 用聚I:C和4-octyl itaconate (4-OI) 进行治疗.
- 使用ELISA和定量PCR分别量化IFN-β分泌和mRNA表达.
- 进行了转录组测序,基因本体学 (GO) 和KEGG通路分析.
- 使用siRNA和化学抑制剂调节了nrf2的表达.
主要成果:
- 4-octyl itaconate (4-OI) 在BMDM中显著抑制了多I:C诱导的IFN-β分泌和mRNA表达.
- 转录组分析显示,4-OI降低了抗病毒基因的调节和升高了代谢基因的调节.
- Nrf2抑制部分逆转了4-OI对IFN-β分泌的抑制作用.
结论:
- 4-octyl itaconate (4-OI) 抑制了巨细胞中的抗病毒干扰素-β (IFN-β) 反应.
- 这种抑制部分通过对Nrf2信号的调节来调节.
- 研究结果表明,4-OI可能会影响先天的抗病毒免疫力.
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