食品科学 ›› 2023, Vol. 44 ›› Issue (17): 86-93.doi: 10.7506/spkx1002-6630-20220909-085

• 营养卫生 • 上一篇    下一篇

咖啡酸苯乙酯对HepG2细胞氧化应激和脂质代谢的调节作用

刘畅,常超,陈瑞达,林萌慧,孙蓉,蔡成岗,赵敏洁,蔡海莺   

  1. (1.浙江科技学院生物与化学工程学院,浙江省农业生物资源生化制造协同创新中心,浙江省农产品化学与生物加工技术重点实验室,浙江 杭州 310023;2.浙江大学生物系统工程与食品科学学院,浙江 杭州 310058;3.美欣达集团有限公司,浙江 湖州 313002)
  • 出版日期:2023-09-15 发布日期:2023-09-29
  • 基金资助:
    国家自然科学基金面上项目(31972079;32172214);浙江省自然科学基金一般项目(LQ19E030001;LY18C200006)

Regulatory Effect of Caffeic Acid Phenethyl Ester on Oxidative Stress and Lipid Metabolism in HepG2 Cells

LIU Chang, CHANG Chao, CHEN Ruida, LIN Menghui, SUN Rong, CAI Chenggang, ZHAO Minjie, CAI Haiying   

  1. (1. Zhejiang Provincial Collaborative Innovation Center of Agricultural Biological Resources Biochemical Manufacturing, Zhejiang Key Lab for Chem & Bio Processing Technology of Farm Product, School of Biological and Chemical Engineering, Zhejiang University of Science and Technology, Hangzhou 310023, China; 2. College of Biosystems Engineering and Food Science, Zhejiang University, Hangzhou 310058, China; 3. Mizuda Group Co., Ltd., Huzhou 313002, China)
  • Online:2023-09-15 Published:2023-09-29

摘要: 咖啡酸苯乙酯(caffeic acid phenethyl ester,CAPE)是来源于蜂胶中的一种天然多酚物质,具有良好的调节脂代谢生物活性,但其调节脂代谢的分子机制尚不明确,本研究利用CAPE处理油酸诱导的人肝脏肿瘤细胞HepG2,通过转录组学探讨其在细胞水平上改善脂代谢的作用与机制。结果表明,与高脂肪组相比,经过CAPE干预后的细胞脂质积累情况得到明显的改善,转录组水平上共筛选出3 270 个差异表达基因(differentially expressed genes,DEGs),其中表达上调的DEGs有1 351 个,表达下调的DEGs有1 919 个。经京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)功能注释分析发现,CAPE处理后的DEGs显著注释到脂质代谢相关通路上。由KEGG信号通路富集分析显示,富集较显著的信号通路为HIF-1α通路和脂肪酸分解代谢通路,其中CAPE组HIF-1α、PPARα、CPT1A、FABP5等基因表达水平比高脂肪组分别提高了0.326、0.661、1.039、1.598 倍。综上,CAPE可能通过HIF-1α通路改善高脂细胞氧化应激,并通过PPARα和脂肪酸氧化分解途径改善高脂诱导细胞的脂代谢紊乱。本实验可为CAPE调节脂代谢的分子机制及调节高脂膳食脂代谢紊乱的深入研究提供一定的理论参考。

关键词: 咖啡酸苯乙酯;HepG2细胞;脂代谢;转录组;信号通路

Abstract: Caffeic acid phenethyl ester (CAPE), a natural polyphenol derived from propolis, has a good regulatory effect on lipid metabolism, but its molecular mechanism is not clear. In the present study, the ameliorative effect of CAPE on lipid metabolism in oleic acid-induced HepG2 human liver cancer cells and its mechanism at the cellular level were investigated. The results showed that compared with the high fat group, lipid accumulation in the cells was significantly improved after CAPE intervention, and a total of 3 270 differentially expressed genes (DEGs) were selected at the transcriptomic level; 1 351 of them were up-regulated and the rest were down-regulated. The functional annotation analysis using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database showed that the DEGs caused by CAPE intervention were significantly annotated to lipid metabolism-related pathways. The KEGG signaling pathway enrichment analysis showed that the HIF-1α pathway and the fatty acid catabolism pathway were significantly enriched. The expression levels of gene HIF-1α, PPARα, CPT1A and FABP5 were 1.326, 1.661, 2.039 and 2.598 times higher in the CAPE group than the high fat group. It is suggested that CAPE can improve lipid metabolism disorder in oleic acid-induced cells possibly by reducing oxidative stress and regulating the PPARα and fatty acid oxidative catabolic pathways. This study provides a theoretical reference for future research on the molecular mechanism of lipid metabolism regulation by CAPE and the regulation of lipid metabolism disorder induced by a high-fat diet.

Key words: caffeic acid phenethyl ester; HepG2 cells; lipid metabolism; transcriptome; signaling pathway

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