纳托金酶通过激活SRF和THBS1减轻内皮炎症
Hui-Wen Chiu1, Chu-Lin Chou2, Kung-Ta Lee3
1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Medical Research, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan; Ph.D. Program in Drug Discovery and Development Industry, College of Pharmacy, Taipei Medical University, Taipei, Taiwan; TMU Research Center of Urology and Kidney, Taipei Medical University, Taipei, Taiwan.
International journal of biological macromolecules
|April 28, 2024
概括
在纳托中发现的纳托基因酶 (NK) 通过上调SRF和THBS1基因来减少血管炎症. 这种作用增强了自,并抑制了亡和炎症体,可能防止动脉样硬化进展.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 心血管研究研究心血管研究
背景情况:
- 纳托金酶 (NK) 是一种来自纳托的纤维解酶,具有已知的心血管益处.
- 在NK对血管炎症和动脉样硬化的影响背后的机制尚未完全理解.
- 血管炎症是动脉样硬化发展的关键驱动因素.
研究的目的:
- 研究NK对基因调节,自,亡和血管炎症中的炎症酶途径的影响.
- 阐明NK调节内皮细胞反应的分子机制.
- 为了验证血管炎症在体内小鼠模型中的发现.
主要方法:
- RNA测序 (RNA-seq) 用于分析用NK治疗的内皮细胞 (EC) 中的转录变化.
- 定量PCR (Q-PCR) 用于验证特定基因的mRNA表达水平 (THBS1,SRF,SREBF1).
- 在实验室中对EC和体内小鼠模型进行实验,以评估自,亡和炎症酶激活.
主要成果:
- 在EC中NK治疗上调了SRF和THBS1mRNA表达,而SREBF1没有受到影响.
- 在EC中,NK诱导了自,并抑制了NLRP3炎症和亡.
- 抑制SRF或THBS1逆转了NK的有益作用,增强了亡和炎症酶活性.
- 在小鼠模型中,NK的使用通过激活自和抑制亡和NLRP3炎症酶来减少血管炎症.
结论:
- NK上调调节SRF和THBS1,导致自的增加和亡的减少以及NLRP3炎症酶的形成.
- 这些分子作用有助于减少NK的血管炎症.
- NK显示出作为一种营养药或辅助疗法的潜力,用于控制血管炎症和动脉样硬化进展.
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