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J. Hefei Univ. Tech. (Nat. Sci.)

合肥工业大学学报(自然科学版)

JOURNAL OF HEFEI UNIVERSITY OF TECHNOLOGY (NATURAL SCIENCE)

Competent Authorities: Ministry of Education of the People's Republic of China

Sponsor by: Hefei University of Technology

ISSN 1000-1646, CN 34-1001/N

Effects and mechanism of 5-aza-2-deoxycytidine in regulating macrophage foam cell formation

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5-氮杂-2-脱氧胞苷调控巨噬细胞泡沫化的作用和机制研究

Journal Information

J. Hefei Univ. Tech. (Nat. Sci.), Oct.2025, Vol.48 No.10: 1371-1377

DOI: 10.3969/j.issn.1003-5060.2025.10.011

Authors

GUO Wentong, YANG Xiaoxiao, PENG Ying, LIU Zhigang, WEI Lingling

(School of Food and Biological Engineering, Hefei University of Technology, Hefei 230601, China)

Abstract and Keywords

Abstract: Targeting DNA methylation modifications at specific genes has emerged as a potential strategy to ameliorate atherosclerosis development, but little is known about the relationship of methylases with macrophage foam cell formation. In this study, 5-aza-2-deoxycytidine(5-Aza) was used to treat primary mouse peritoneal macrophages collected, and the macrophage foam cell formation and inflammatory factors expression were determined. Then CD36 siRNA was used to interfere with the CD36 expression of macrophage J774 and RAW264.7 cells, and the peritoneal macrophages of macrophage specific peroxisome proliferator activated receptor(PPARγ) knockout mice were extracted to study the role and mechanism of 5-Aza in regulating macrophage foam cell formation. The results revealed that 5-Aza promoted macrophage foam cell formation by enhancing macrophage CD36 expression, membrane localization, and mRNA levels, but 5-Aza had little effect on CD36 levels in PPARγ knockout macrophages. The results suggest that 5-Aza can promote macrophage foam cell formation by enhancing the expression of CD36, which is mediated by PPARγ. This study also illustrates the new function of 5-Aza and may provide new strategy for prevention and treatment of atherosclerosis.

Keywords: 5-aza-2-deoxycytidine(5-Aza); CD36; macrophage foam cell formation; PPAR $ \gamma $; inflammatory factor

作者信息

郭文通，杨潇潇，彭颖，刘志刚，韦玲玲

（合肥工业大学食品与生物工程学院，安徽合肥230601）

摘要和关键词

摘要: 靶向特定基因的 DNA 甲基化修饰已经成为改善动脉粥样硬化发展的潜在策略,但关于甲基化酶与巨噬细胞泡沫化的关系尚不清晰。文章使用 DNA 甲基化酶抑制剂 5-氮杂-2-脱氧胞苷(5-Aza)处理小鼠腹腔原代巨噬细胞,分析巨噬细胞泡沫化水平和炎症因子的表达情况;采用 siRNA 干扰巨噬细胞系 J774、RAW264.7 细胞的 CD36 表达,提取巨噬细胞特异性敲除 PPARγ 小鼠腹腔巨噬细胞研究 5-Aza 调控巨噬细胞泡沫化的作用和机制。结果发现,5-Aza 通过上调巨噬细胞 CD36 的表达、膜定位及 mRNA 发挥促进巨噬细胞泡沫化的作用,但 5-Aza 在 PPARγ 敲除的巨噬细胞中对 CD36 的表达无诱导作用。研究结果表明,5-Aza 通过诱导 CD36 的表达加速巨噬细胞泡沫化,该过程依赖于 PPARγ。该研究阐述了 5-Aza 的新功能,为动脉粥样硬化的防治提供新思路。

关键词: 5-氮杂-2-脱氧胞苷（5-Aza）；CD36；巨噬细胞泡沫化；PPARγ；炎症因子

Funding

国家自然科学基金资助项目（81803517）；中国博士后科学基金资助项目（2020M681914）

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