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Aspirin Causes Lipid Accumulation and Damage to Cell Membrane by Regulating DCI1/OLE1 in Saccharomyces cerevisiae.
Microbial Drug Resistance ( IF 2.6 ) Pub Date : 2020-07-31 , DOI: 10.1089/mdr.2019.0200
Pan Zhu 1 , Ming Li 1 , Chongjia Yan 1 , Jing Sun 2 , Min Peng 2 , Zhiwei Huang 3 , Ping Shi 1
Affiliation  

Aspirin is one of the most commonly used nonsteroidal anti-inflammatory drugs. Various potential pharmacological effects of aspirin, such as anticancer, antibacterial activity, and prolonging life expectancy have been discovered. However, the mechanism of aspirin is not fully elucidated. Herein, the effects of aspirin on fatty acid metabolism in yeast cell model Saccharomyces cerevisiae were studied. The results showed that aspirin can induce lipid accumulation and reduce the unsaturated fat index in cells. The assessment of cell membrane integrity demonstrated that aspirin caused damage to the cell membrane. These effects of aspirin were attributed to the alterations of the expression of DCI1 and OLE1. Similarly, aspirin was able to cause lipid accumulation and damage to the cell membrane by interfering with the expression of OLE1 in Candida albicans. These findings are expected to improve current understanding of the mode of action of aspirin and provide a novel strategy for antifungal drug design.

中文翻译:

阿司匹林通过调节酿酒酵母中的DCI1 / OLE1引起脂质蓄积并破坏细胞膜。

阿司匹林是最常用的非甾体抗炎药之一。阿司匹林具有多种潜在的药理作用,例如抗癌,抗菌活性和预期寿命的延长。但是,阿司匹林的机制尚未完全阐明。在此,研究了阿司匹林对酵母细胞模型酿酒酵母中脂肪酸代谢的影响。结果表明,阿司匹林可以诱导脂质蓄积并降低细胞中的不饱和脂肪指数。细胞膜完整性的评估表明阿司匹林对细胞膜造成了损害。阿司匹林的这些作用归因于DCI1OLE1表达的改变。类似地,阿司匹林是能够通过与表达干扰引起脂质积聚而损坏细胞膜OLE1白色念珠菌。这些发现有望增进当前对阿司匹林作用方式的了解,并为抗真菌药物设计提供一种新颖的策略。
更新日期:2020-08-08
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