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人乳来源外泌体在坏死性小肠结肠炎中的治疗潜力

Therapeutic potential of human breast milk-derived exosomes in necrotizing enterocolitis.

作者信息

Di Si-Jia, Cui Xue-Wei, Liu Tian-Jing, Shi Yong-Yan

机构信息

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, 110004, China.

出版信息

Mol Med. 2024 Dec 19;30(1):243. doi: 10.1186/s10020-024-01010-7.

Abstract

Necrotizing enterocolitis (NEC) is a severe inflammatory and necrotizing disease of the intestine that primarily affects the neonates, particularly premature infants. It has a high incidence of approximately 8.9% in extremely preterm infants, with a mortality rate ranging from 20 to 30%. In recent years, exosomes, particularly those derived from breast milk, have emerged as potential candidates for NEC therapy. Human breast milk-derived exosomes (BME) have been shown to enhance intestinal barrier function, protect intestinal epithelial cells from oxidative stress, promote the proliferation and migration of intestinal epithelial cells, and reduce the severity of experimental NEC models. As a subset of extracellular vesicles, BME possess the membrane structure, low immunogenicity, and high permeability, making them ideal vehicles for the treatment of NEC. Additionally, exosomes derived from various sources, including stem cells, intestinal epithelial cells, plants, and bacteria, have been implicated in the development and protection of intestinal diseases. This article summarizes the mechanisms through which exosomes, particularly BME, exert their effects on NEC and discusses the feasibility and obstacles associated with this novel therapeutic strategy.

摘要

坏死性小肠结肠炎(NEC)是一种严重的肠道炎症和坏死性疾病,主要影响新生儿,尤其是早产儿。在极早产儿中,其发病率约为8.9%,死亡率在20%至30%之间。近年来,外泌体,尤其是源自母乳的外泌体,已成为NEC治疗的潜在候选物。人母乳来源的外泌体(BME)已被证明可增强肠道屏障功能,保护肠道上皮细胞免受氧化应激,促进肠道上皮细胞的增殖和迁移,并降低实验性NEC模型的严重程度。作为细胞外囊泡的一个子集,BME具有膜结构、低免疫原性和高通透性,使其成为治疗NEC的理想载体。此外,源自各种来源的外泌体,包括干细胞、肠道上皮细胞、植物和细菌,都与肠道疾病的发生和保护有关。本文总结了外泌体,特别是BME,对NEC发挥作用的机制,并讨论了这种新型治疗策略的可行性和障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3de/11656790/813de570cb45/10020_2024_1010_Fig1_HTML.jpg

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