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论文摘要

蝉花提取物促进酿酒酵母寿命延长的机制研究

Study on the mechanism of Cordyceps cicadae extracts promote longevity in Saccharomyces cerevisiae

作者:杨力(四川大学生命科学学院 生物资源与生物环境重点实验室);闫孟利(四川大学生命科学学院 生物资源与生物环境重点实验室);刘科(四川大学生命科学学院 生物资源与生物环境重点实验室)

Author:YANG Li(Key Laboratory of Bio-Resources and Eco-Environmentof Ministry of Education, College of Life Sciences,Sichuan University);YAN Meng-Li(Key Laboratory of Bio-Resources and Eco-Environmentof Ministry of Education, College of Life Sciences,Sichuan University);LIU Ke(Key Laboratory of Bio-Resources and Eco-Environmentof Ministry of Education, College of Life Sciences,Sichuan University)

收稿日期:2019-02-25          年卷(期)页码:2020,57(1):169-173

期刊名称:四川大学学报: 自然科学版

Journal Name:Journal of Sichuan University (Natural Science Edition)

关键字:蝉花;活性氧;寿命;抗氧化

Key words:Cordyceps cicadae; ROS; Lifespan; Anti-oxidant

基金项目:国家自然科学基金项目(31870849)

中文摘要

本实验探究蝉花提取物(Cordyceps cicadae extracts,CCE)促进酿酒酵母抵抗H2O2诱导的氧化胁迫并延长其时序性寿命的机制.实验使用不同浓度的CCE处理酿酒酵母细胞,检测细胞的时序性寿命.然后通过H2O2诱导酿酒酵母细胞氧化胁迫,检测CCE处理组和不加药对照组的抗氧化胁迫能力以及细胞内的活性氧(ROS)水平的变化.酿酒酵母细胞经CCE处理后,通过实时荧光定量实验在mRNA水平检测抗氧化基因SOD2、GPX2、CTT1的表达量.结果显示CCE能够延长酿酒酵母时序性寿命,并且其作用随 CCE 浓度的增加而增强.此外,在H2O2诱导的氧化应激下,CCE预处理的细胞抗氧化胁迫能力增强,细胞内ROS水平显著降低.这些结果表明CCE延长了酿酒酵母的时序性寿命并通过上调CTT1和SOD2从而抵抗H2O2诱导的氧化胁迫.

英文摘要

This study aims to explore the role of Cordyceps cicadae extracts (CCE) in resistance against H2O2 -induced oxidative stress and chronological lifespan extension in Saccharomyces cerevisiae. The experiments are performed with various concentrations of CCE to test the chronological lifespan extension. Then, the resistance against H2O2 induced oxidative stress was measured in terms of intracellular ROS accumulation. The mRNA levels of SOD2, GPX2 and CTT1 were measured by real -time PCR. The results indicate that CCE can prolong yeast chronological lifespan in a dose dependent manner. Furthermore, the CCE pre-treated cells accumulate significantly lower ROS in the case of H2O2-induced oxidative stress. Taken together these results suggest that CCE extends chronological lifespan and develops resistance against H2O2 induced oxidative stress through upregulation of CTT1 and SOD2.

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