装载ACE2 的植物来源细胞外囊泡防治PM2.5 暴露后细胞损伤

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  • 1. 南京医科大学第一附属医院 心内科, 南京 210029; 2. 上海大学 生命科学学院, 上海 200444
周 蕾 (1970—), 女, 教授, 博士生导师, 博士, 研究方向为心衰的基础与临床研究.

网络出版日期: 2024-01-20

基金资助

国家自然科学基金面上资助项目 (81970723); 上海市教育发展基金会和上海市教委 “晨光计划” 资助项目(20CG46)

Plant-derived extracellular vesicles loaded with ACE2 prevent cell damage after PM2.5 exposure

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  • 1. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China; 2. School of Life Science, Shanghai University, Shanghai 200444, China

Online published: 2024-01-20

摘要

探究装载血管紧张素转化酶2(angiotensin converting enzyme 2, ACE2) 的植物来源 细胞外囊泡(plant-derived extracellular vesicles, PDEVs) 在保护机体抵抗空气污染颗粒物 (particulate matter, PM2.5) 引发的呼吸系统损伤过程中的作用. 基于葡萄提取PDEVs 并装 载ACE2 过表达的质粒, 通过CCK8 实验、二氢乙锭(dihydroethidium, DHE) 染色、蛋白 免疫印迹、实时荧光定量多聚酶链反应(polymerase chain reaction, PCR) 等方法, 探究改造 后的PDEVs 对PM2.5 暴露后人支气管上皮细胞(Beas-2B) 的保护效果. PM2.5 暴露会造成 Beas-2B 细胞氧化应激、细胞凋亡增加, 以及炎症因子增加, 而装载ACE2 的PDEVs 能够有 效递送ACE2, 从而缓解PM2.5 诱导的细胞损伤. 因此, PDEVs 可作为潜在的递送载体, 防 治大气PM2.5 暴露引发的细胞凋亡及损伤.

本文引用格式

叶旋, 钤嫄, 王红云, 周蕾 . 装载ACE2 的植物来源细胞外囊泡防治PM2.5 暴露后细胞损伤[J]. 上海大学学报(自然科学版), 2024 , 30(2) : 208 -217 . DOI: 10.12066/j.issn.1007-2861.2552

Abstract

To investigate the efficacy of plant-derived extracellular vesicles (PDEVs) loaded with angiotensin-converting enzyme 2 (ACE2) in mitigating respiratory system dam-age induced by particulate matter (PM2.5), we extracted PDEVs from grapes and loaded them with ACE2 overexpression plasmids. The effect of the modified PDEVs on human bronchial epithelial cells (Beas-2B) after exposure to PM2.5 was investigated using CCK8 assays, dihydroethidium (DHE) staining, western blotting, and real-time quantitative poly-merase chain reaction (PCR). Exposure to PM2.5 increases oxidative stress, apoptosis, and inflammatory factor production in Beas-2B cells. PDEVs loaded with ACE2 effectively delivered ACE2 to cells and thereby alleviated PM2.5-induced cell damage including apop-tosis, oxidative stress, and inflammation. PDEVs thus show potential for use as carriers of genes that can prevent apoptosis and damage caused by atmospheric PM2.5 exposure.
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