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一种来自传统中药的天然肽，通过激活胃干细胞，有潜力治疗慢性萎缩性胃炎。

A Natural Peptide from A Traditional Chinese Medicine Has the Potential to Treat Chronic Atrophic Gastritis by Activating Gastric Stem Cells.

机构信息

Institute of Traditional Chinese Medicine and Stem Cell Research, College of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.

Bio-X Institutes, Shanghai Jiao Tong University, Shanghai, 200240, China.

出版信息

Adv Sci (Weinh). 2024 May;11(20):e2304326. doi: 10.1002/advs.202304326. Epub 2024 Mar 27.

DOI:10.1002/advs.202304326
PMID:38544338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11132046/
Abstract

Chronic atrophic gastritis (AG) is initiated mainly by Helicobacter pylori infection, which may progress to stomach cancer following the Correa's cascade. The current treatment regimen is H. pylori eradication, yet evidence is lacking that this treatment is effective on later stages of AG especially gastric gland atrophy. Here, using AG mouse model, patient samples, gastric organoids, and lineage tracing, this study unraveled gastric stem cell (GSC) defect as a crucial pathogenic factor in AG in mouse and human. Moreover, a natural peptide is isolated from a traditional Chinese medicine that activated GSCs to regenerate gastric epithelia in experimental AG models and revitalized the atrophic gastric organoids derived from patients. It is further shown that the peptide exerts its functions by stabilizing the EGF-EGFR complex and specifically activating the downstream ERK and Stat1 signaling. Overall, these findings advance the understanding of AG pathogenesis and open a new avenue for AG treatment.

摘要

慢性萎缩性胃炎（AG）主要由幽门螺杆菌感染引起，可能会沿着 Correa 级联反应发展为胃癌。目前的治疗方案是根除幽门螺杆菌，但缺乏证据表明这种治疗对 AG 的后期阶段（特别是胃腺体萎缩）有效。本研究通过 AG 小鼠模型、患者样本、胃类器官和谱系追踪，揭示了胃干细胞（GSC）缺陷是导致小鼠和人类 AG 的关键致病因素。此外，从一种中药中分离出一种天然肽，该肽可激活 GSC 在实验性 AG 模型中再生胃上皮，并使源自患者的萎缩性胃类器官恢复活力。进一步表明，该肽通过稳定 EGF-EGFR 复合物并特异性激活下游 ERK 和 Stat1 信号通路发挥作用。总的来说，这些发现推进了对 AG 发病机制的理解，并为 AG 的治疗开辟了新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/7fa97540f079/ADVS-11-2304326-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/340674de58fa/ADVS-11-2304326-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/50261efc6e7e/ADVS-11-2304326-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/e01a615e142c/ADVS-11-2304326-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/9d20ac9063dd/ADVS-11-2304326-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/7fa97540f079/ADVS-11-2304326-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/340674de58fa/ADVS-11-2304326-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/cea7bed41911/ADVS-11-2304326-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/9ba11d5b900e/ADVS-11-2304326-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/50261efc6e7e/ADVS-11-2304326-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/e01a615e142c/ADVS-11-2304326-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/9d20ac9063dd/ADVS-11-2304326-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f38e/11132046/7fa97540f079/ADVS-11-2304326-g004.jpg

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