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基于信号通路的姜黄素抗氧化应激机制的研究进展

Research progress on the mechanism of curcumin anti-oxidative stress based on signaling pathway.

作者信息

Cui Jie, Li Haonan, Zhang Tianyi, Lin Fengli, Chen Meiyun, Zhang Guimin, Feng Zhong

机构信息

School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.

Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

出版信息

Front Pharmacol. 2025 Apr 7;16:1548073. doi: 10.3389/fphar.2025.1548073. eCollection 2025.

DOI:10.3389/fphar.2025.1548073
PMID:40260389
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12009910/
Abstract

Oxidative stress refers to an imbalance between oxidative capacity and antioxidant capacity, leading to oxidative damage to proteins, lipids, and DNA, which can result in cell senescence or death. It is closely associated with the occurrence and development of various diseases, including cardiovascular diseases, nephropathy, malignant tumors, neurodegenerative diseases, hypertension, diabetes, and inflammatory diseases. Curcumin is a natural polyphenol compound of β-diketone, which has a wide range of pharmacological activities such as anti-inflammatory, antibacterial, anti-oxidative stress, anti-tumor, anti-fibrosis, and hypolipidemic, demonstrating broad research and development value. It has a wide range of biological targets and can bind to various endogenous biomolecules. Additionally, it maintains the redox balance primarily by scavenging ROS, enhancing the activity of antioxidant enzymes, inhibiting lipid peroxidation, and chelating metal ions. This paper systematically describes the antioxidative stress mechanisms of curcumin from the perspective of signaling pathways, focusing on the Keap1-Nrf2/ARE, NF-κB, NOX, MAPK and other pathways. The study also discusses potential pathway targets and the complex crosstalk among these pathways, aiming to provide insights for further research on curcumin's antioxidant mechanisms and its clinical applications.

摘要

氧化应激是指氧化能力与抗氧化能力之间的失衡,导致蛋白质、脂质和DNA发生氧化损伤,进而可能导致细胞衰老或死亡。它与多种疾病的发生和发展密切相关,包括心血管疾病、肾病、恶性肿瘤、神经退行性疾病、高血压、糖尿病和炎症性疾病。姜黄素是一种天然的β-二酮多酚化合物,具有抗炎、抗菌、抗氧化应激、抗肿瘤、抗纤维化和降血脂等广泛的药理活性,具有广阔的研发价值。它具有广泛的生物学靶点,可与多种内源性生物分子结合。此外,它主要通过清除活性氧、增强抗氧化酶活性、抑制脂质过氧化和螯合金属离子来维持氧化还原平衡。本文从信号通路的角度系统地描述了姜黄素的抗氧化应激机制,重点关注Keap1-Nrf2/ARE、NF-κB、NOX、MAPK等通路。该研究还讨论了潜在的通路靶点以及这些通路之间复杂的相互作用,旨在为进一步研究姜黄素的抗氧化机制及其临床应用提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/9720b7992d7d/fphar-16-1548073-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/c004591aeabe/fphar-16-1548073-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/1c2a58e8c2a4/fphar-16-1548073-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/32408c5a5f9c/fphar-16-1548073-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/1341cde9c402/fphar-16-1548073-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/7249d6dad2c3/fphar-16-1548073-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/037c73dca2d8/fphar-16-1548073-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/8a8b123457ea/fphar-16-1548073-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/0e94dbb36171/fphar-16-1548073-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/9720b7992d7d/fphar-16-1548073-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/c004591aeabe/fphar-16-1548073-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/1c2a58e8c2a4/fphar-16-1548073-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/32408c5a5f9c/fphar-16-1548073-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/1341cde9c402/fphar-16-1548073-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/7249d6dad2c3/fphar-16-1548073-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/037c73dca2d8/fphar-16-1548073-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/8a8b123457ea/fphar-16-1548073-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/0e94dbb36171/fphar-16-1548073-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739f/12009910/9720b7992d7d/fphar-16-1548073-g009.jpg

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