Zhao Zhejun, Yang Qiuhua, Sun Yuanlong, Ruan Xiaofen
Cardiovascular Research Institute of Traditional Chinese Medicine, Shuguang Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Cardiovascular Department, Shuguang Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Pharmacol. 2025 Jul 9;16:1615294. doi: 10.3389/fphar.2025.1615294. eCollection 2025.
Syringic acid (SA), a naturally occurring phenolic acid, has garnered significant attention for its antioxidant and anti-inflammatory properties. However, the mechanisms underlying these effects and their potential therapeutic applications require further elucidation.
A comprehensive literature review was conducted using PubMed and Web of Science (1965-2024) to investigate the antioxidant and anti-inflammatory mechanisms of SA, with a focus on oxidative stress and inflammatory pathways. For insights related to traditional Chinese medicine (TCM), we referenced Chinese literature. Articles focusing on agriculture, industry, and economics are excluded.
SA exerts potent antioxidant and anti-inflammatory activities through multiple mechanisms. Specifically, it mitigates OS by scavenging free radicals, enhancing endogenous antioxidant defenses, and activating the KEAP1/NRF2 pathway. It also inhibits inflammation by downregulating key mediators, including NF-κB, TLR4, HMGB1, MyD88, and TRAF6. Crosstalk between NRF2, NF-κB, and PI3K/AKT pathways reveals SA's involvement in cellular pathophysiological processes such as apoptosis, ferroptosis, and endoplasmic reticulum stress.
SA's robust antioxidant and anti-inflammatory mechanisms underscore its promise as a therapeutic agent. Future research should address its pharmacokinetics, safety profile, and clinical potential.
丁香酸(SA)是一种天然存在的酚酸,因其抗氧化和抗炎特性而备受关注。然而,这些作用的潜在机制及其潜在治疗应用仍需进一步阐明。
使用PubMed和Web of Science(1965 - 2024)进行了全面的文献综述,以研究SA的抗氧化和抗炎机制,重点关注氧化应激和炎症途径。对于与中医相关的见解,我们参考了中文文献。排除了侧重于农业、工业和经济学的文章。
SA通过多种机制发挥强大的抗氧化和抗炎活性。具体而言,它通过清除自由基、增强内源性抗氧化防御和激活KEAP1/NRF2途径来减轻氧化应激。它还通过下调关键介质(包括NF-κB、TLR4、HMGB1、MyD88和TRAF6)来抑制炎症。NRF2、NF-κB和PI3K/AKT途径之间的相互作用揭示了SA参与细胞病理生理过程,如细胞凋亡、铁死亡和内质网应激。
SA强大的抗氧化和抗炎机制突出了其作为治疗剂的潜力。未来的研究应关注其药代动力学、安全性和临床潜力。