边缘血液中分子机制的转录形状分析,通常由饮酒狂欢和安慰剂效应调节
Amol Carl Shetty1, John Sivinski1, Jessica Cornell1
1Institute for Genome Sciences, University of Maryland School of Medicine, 670 W. Baltimore Street, Baltimore, MD, 21201, USA.
Scientific reports
|May 10, 2024
概括
过度饮酒会动态改变基因表达,而安慰剂效应也会诱导类似途径的分子变化. 这揭示了安慰剂在大量社交饮酒者中的剂量延长分子影响.
科学领域:
- 基因组学和分子生物学
- 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.
背景情况:
- 饮酒会引起由各种因素影响的复杂,动态的分子反应.
- 对饮酒模式遗传风险的研究广泛,但对饮酒暴饮的动态分子反应,包括药理和安慰剂效应,研究不足.
研究的目的:
- 在健康的沉重社交饮酒者中调查转录组范围内的分子反应,对狂饮,中度和安慰剂饮酒的反应.
- 识别差异表达基因 (DEGs) 和受影响的生物通路.
主要方法:
- 在一个受控的,纵向的内部研究 (长达12天) 中,在17名健康的重社会饮酒者样本上使用RNA测序 (RNA-seq).
- 分析了对大量饮酒,中等饮酒和安慰剂饮酒的反应中的转录组范围的基因表达变化.
- 利用KEGG途径分析来识别受影响的生物途径.
主要成果:
- 鉴定了251个差异表达基因 (DEGs) 作为对狂饮的反应和13个DEGs作为对安慰剂的反应.
- 在过度饮酒后观察到11种蛋白质编码DEG的非常大的效应大小 (科恩d > 1).
- 过量服用显著影响了细胞因子-细胞因子受体相互作用途径 (KEGG:hsa04060).
- 安慰剂也对hsa04060产生了影响,特别是在定期饮酒后,并影响了诸如系统性红斑狼,中性细胞外细胞陷形成和酒精等途径,表明了剂量延长的安慰剂效应.
结论:
- 过度饮酒会在转录组水平上引发显著的,剂量特定的分子变化.
- 安慰剂效应可以在分子水平上表现出来,影响与酒精相似的生物学途径.
- 研究结果表明,安慰剂干预可以通过诱导类似于酒精的分子反应来产生"剂量延长效应".
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