Luteolin in Inflammatory Bowel Disease and Colorectal Cancer: A Disease Continuum Perspective

被引:0
作者
Liu, Fang [1 ,2 ]
Guo, Cui [1 ]
Liu, Xue [2 ]
Gu, Zhili [2 ]
Zou, Wenxuan [2 ]
Tang, Xuegui [2 ]
Tang, Jianyuan [1 ]
机构
[1] Chengdu Univ Tradit Chinese Med, Clin Sch Med, Chengdu 610072, Peoples R China
[2] North Sichuan Med Coll, Clin Med Coll Integrated Chinese & Western Med, Nanchong 637100, Peoples R China
基金
中国国家自然科学基金;
关键词
luteolin; inflammatory bowel disease; colorectal cancer; ulcerative colitis; natural products; MOLECULAR-MECHANISMS; NETWORK PHARMACOLOGY; URSOLIC ACID; COLITIS; CELLS; INVOLVEMENT; QUERCETIN; APOPTOSIS; APIGENIN; KINASE;
D O I
10.3390/cimb47020126
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition that may progress to colorectal cancer (CRC), presenting significant challenges to global health. With shifts in lifestyle, the incidence of both conditions continues to rise, underscoring the urgent need for effective treatments. While traditional therapies can be effective, their high recurrence rates and associated adverse reactions limit their broader application. Luteolin, a flavonoid derived from natural plants, has emerged as a promising focus in both IBD and CRC research due to its multi-target therapeutic potential. This article reviews the molecular mechanisms and signaling pathways through which luteolin regulates immune cell differentiation, mitigates inflammation and oxidative stress, modulates gut microbiota, and restores intestinal mucosal barrier function in IBD. In the context of CRC, luteolin demonstrates significant anti-tumor effects by inhibiting cancer cell proliferation, inducing apoptosis, and suppressing cell migration and invasion. Notably, luteolin has demonstrated significant improvements in IBD symptoms by influencing the differentiation of T cell subsets, decreasing the expression of inflammatory mediators, activating antioxidant pathways, and enhancing the structure of gut microbiota. Furthermore, advancements in formulation technology, such as the use of polymer micelles and responsive nanoparticles, have greatly improved the bioavailability and efficacy of luteolin. However, further investigation is needed to address the bioavailability and potential toxicity of luteolin, particularly in the critical transition from IBD to CRC. This article emphasizes the potential of luteolin in the treatment of IBD and CRC and anticipates its promising prospects for future clinical applications as a natural therapeutic agent.
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页数:15
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共 71 条
[31]  
Tang L., Gao J., Li X., Cao X., Zhou B., Molecular Mechanisms of Luteolin Against Atopic Dermatitis Based on Network Pharmacology and in vivo Experimental Validation, Drug Des. Dev. Ther, 16, pp. 4205-4221, (2022)
[32]  
Tan C., Fan H., Ding J., Han C., Guan Y., Zhu F., Wu H., Liu Y., Zhang W., Hou X., Et al., ROS-responsive nanoparticles for oral delivery of luteolin and targeted therapy of ulcerative colitis by regulating pathological microenvironment, Mater. Today Bio, 14, (2022)
[33]  
Dorrington M.G., Fraser I.D.C., NF-κB Signaling in Macrophages: Dynamics, Crosstalk, and Signal Integration, Front. Immunol, 10, (2019)
[34]  
Xue L., Jin X., Ji T., Li R., Zhuge X., Xu F., Quan Z., Tong H., Yu W., Luteolin ameliorates DSS-induced colitis in mice via suppressing macrophage activation and chemotaxis, Int. Immunopharmacol, 124Pt B, (2023)
[35]  
Wan Y., Yang L., Jiang S., Qian D., Duan J., Excessive Apoptosis in Ulcerative Colitis: Crosstalk Between Apoptosis, ROS, ER Stress, and Intestinal Homeostasis, Inflamm. Bowel Dis, 28, pp. 639-648, (2022)
[36]  
Li Y., Shen L., Luo H., Luteolin ameliorates dextran sulfate sodium-induced colitis in mice possibly through activation of the Nrf2 signaling pathway, Int. Immunopharmacol, 40, pp. 24-31, (2016)
[37]  
Yang W., Wang Y., Zhang C., Huang Y., Yu J., Shi L., Zhang P., Yin Y., Li R., Tao K., Maresin1 Protect Against Ferroptosis-Induced Liver Injury Through ROS Inhibition and Nrf2/HO-1/GPX4 Activation, Front. Pharmacol, 13, (2022)
[38]  
He L., He T., Farrar S., Ji L., Liu T., Ma X., Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species. Cell, Physiol. Biochem, 44, pp. 532-553, (2017)
[39]  
Suga N., Murakami A., Arimitsu H., Nakamura T., Nakamura Y., Kato Y., Luteolin suppresses 5-hydroxytryptamine elevation in stimulated RBL-2H3 cells and experimental colitis mice, J. Clin. Biochem. Nutr, 69, pp. 20-27, (2021)
[40]  
Lavelle A., Sokol H., Gut microbiota-derived metabolites as key actors in inflammatory bowel disease, Nat. Rev. Gastroenterol. Hepatol, 17, pp. 223-237, (2020)