review · Food Science & Nutrition
Luteolin is a natural plant flavonoid possessing notable antioxidant properties that counteract oxidative stress and damage caused by reactive oxygen species. It exhibits significant chemopreventive and therapeutic potential against cancer by triggering cell cycle arrest and programmed cell death. This occurs through the regulation of critical cellular proteins, including the upregulation of apoptotic markers such as caspase-3, caspase-9, and BAX, alongside the suppression of survival factors such as Bcl-2 and VEGF. In addition to oncology, luteolin influences multiple signalling pathways relevant to other major health conditions. It offers cardiovascular protection by reducing inflammation, fibrosis, and cardiac hypertrophy, while aiding diabetes management by lowering blood glucose, improving insulin sensitivity, and inhibiting alpha-glucosidase. Furthermore, its biological targets suggest potential protective roles against neurodegenerative, hepatic, and inflammatory diseases.
Oxidative stress and aberrant cellular signalling drive many chronic illnesses, including cancers, diabetes, and heart disease. Understanding how plant-derived molecules like luteolin interact with specific molecular targets highlights viable pathways for multi-disease prevention and treatment. This provides a scientific basis for developing safer, broad-spectrum therapeutic interventions derived from natural sources.
The findings position luteolin as a candidate molecule for pharmaceutical companies, nutraceutical developers, and drug discovery programmes targeting oncology, cardiology, or metabolic disorders. Because this work is a mechanistic review identifying biological targets and cellular pathways, the research remains at an early discovery stage, requiring extensive formulation, pre-clinical testing, and clinical trials before reaching commercial healthcare applications.
AI-generated from the published abstract. Always read the original work before citing.
Luteolin is widely distributed phytochemical, a flavonoid, in kingdom plantae. Luteolin with potential antioxidant activity prevent ROS-induced damages and reduce oxidative stress which is mainly responsible in pathogenesis of many diseases. Several chemo preventive activities and therapeutic benefits are associated with luteolin. Luteolin prevents cancer via modulation of numerous pathways, that is, by inactivating proteins; such as procaspase-9, CDC2 and cyclin B or upregulation of caspase-9 and caspase-3, cytochrome C, cyclin A, CDK2, and APAF-1, in turn inducing cell cycle arrest as well as apoptosis. It also enhances phosphorylation of p53 and expression level of p53-targeted downstream gene. By Increasing BAX protein expression; decreasing VEGF and Bcl-2 expression it can initiate cell cycle arrest and apoptosis. Luteolin can stimulate mitochondrial-modulated functions to cause cellular death. It can also reduce expression levels of p-Akt, p-EGFR, p-Erk1/2, and p-STAT3. Luteolin plays positive role against cardiovascular disorders by improving cardiac function, decreasing the release of inflammatory cytokines and cardiac enzymes, prevention of cardiac fibrosis and hypertrophy; enhances level of CTGF, TGFβ1, ANP, Nox2, Nox4 gene expressions. Meanwhile suppresses TGFβ1 expression and phosphorylation of JNK. Luteolin helps fight diabetes via inhibition of alpha-glucosidase and ChE activity. It can reduce activity levels of catalase, superoxide dismutase, and GS4. It can improve blood glucose, insulin, HOMA-IR, and HbA1c levels. This review is an attempt to elaborate molecular targets of luteolin and its role in modulating irregularities in cellular pathways to overcome severe outcomes during diseases including cancer, cardiovascular disorders, diabetes, obesity, inflammation, Alzheimer's disease, Parkinson's disease, hepatic disorders, renal disorders, brain injury, and asthma. As luteolin has enormous therapeutic benefits, it could be a potential candidate in future drug development strategies.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.1002/fsn3.4682
Is something wrong with this record? Report it or request removal.
Discussion
Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.
No discussion yet. Open the first thread.
New to MARATTO™? Create a free account.
