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天然化合物靶向程序性细胞死亡(PCD)信号机制治疗溃疡性结肠炎:综述

Natural compounds target programmed cell death (PCD) signaling mechanism to treat ulcerative colitis: a review.

作者信息

Chen Bo, Dong Xinqian, Zhang Jin Long, Sun Xitong, Zhou Lin, Zhao Kangning, Deng Hualiang, Sun Zhen

机构信息

Shandong University of Traditional Chinese Medicine, Jinan, China.

Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China.

出版信息

Front Pharmacol. 2024 Feb 9;15:1333657. doi: 10.3389/fphar.2024.1333657. eCollection 2024.

DOI:10.3389/fphar.2024.1333657
PMID:38405669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10885814/
Abstract

Ulcerative colitis (UC) is a nonspecific inflammatory bowel disease characterized by abdominal pain, bloody diarrhea, weight loss, and colon shortening. However, UC is difficult to cure due to its high drug resistance rate and easy recurrence. Moreover, long-term inflammation and increased disease severity can lead to the development of colon cancer in some patients. Programmed cell death (PCD) is a gene-regulated cell death process that includes apoptosis, autophagy, necroptosis, ferroptosis, and pyroptosis. PCD plays a crucial role in maintaining body homeostasis and the development of organs and tissues. Abnormal PCD signaling is observed in the pathological process of UC, such as activating the apoptosis signaling pathway to promote the progression of UC. Targeting PCD may be a therapeutic strategy, and natural compounds have shown great potential in modulating key targets of PCD to treat UC. For instance, baicalin can regulate cell apoptosis to alleviate inflammatory infiltration and pathological damage. This review focuses on the specific expression of PCD and its interaction with multiple signaling pathways, such as NF-κB, Nrf2, MAPK, JAK/STAT, PI3K/AKT, NLRP3, GPX4, Bcl-2, etc., to elucidate the role of natural compounds in targeting PCD for the treatment of UC. This review used (ulcerative colitis) (programmed cell death) and (natural products) as keywords to search the related studies in PubMed and the Web of Science, and CNKI database of the past 10 years. This work retrieved 72 studies (65 from the past 5 years and 7 from the past 10 years), which aims to provide new treatment strategies for UC patients and serves as a foundation for the development of new drugs.

摘要

溃疡性结肠炎(UC)是一种非特异性炎症性肠病,其特征为腹痛、血性腹泻、体重减轻和结肠缩短。然而,由于其高耐药率和易复发,UC难以治愈。此外,长期炎症和疾病严重程度增加可导致部分患者发生结肠癌。程序性细胞死亡(PCD)是一个基因调控的细胞死亡过程,包括凋亡、自噬、坏死性凋亡、铁死亡和焦亡。PCD在维持机体稳态以及器官和组织的发育中起关键作用。在UC的病理过程中观察到PCD信号异常,如激活凋亡信号通路促进UC进展。靶向PCD可能是一种治疗策略,天然化合物在调节PCD关键靶点以治疗UC方面已显示出巨大潜力。例如,黄芩苷可调节细胞凋亡以减轻炎症浸润和病理损伤。本综述重点关注PCD的具体表达及其与多种信号通路的相互作用,如NF-κB、Nrf2、MAPK、JAK/STAT、PI3K/AKT、NLRP3、GPX4、Bcl-2等,以阐明天然化合物靶向PCD治疗UC的作用。本综述以(溃疡性结肠炎)(程序性细胞死亡)和(天然产物)为关键词,检索了过去10年PubMed、Web of Science和中国知网数据库中的相关研究。这项工作共检索到72项研究(过去5年65项,过去10年7项),旨在为UC患者提供新的治疗策略,并为新药开发奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8135/10885814/fa633cadddb1/fphar-15-1333657-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8135/10885814/bc0d1c0ec684/fphar-15-1333657-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8135/10885814/fa633cadddb1/fphar-15-1333657-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8135/10885814/bc0d1c0ec684/fphar-15-1333657-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8135/10885814/fa633cadddb1/fphar-15-1333657-g002.jpg

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