From nature to therapy: Luteolin's potential as an immune system modulator in inflammatory disorders.
Md Sadique HussainGaurav GuptaAhsas GoyalRiya ThapaWaleed Hassan Al-MalkiImran KazmiSami I AlzareaShivkanya FuloriaDhanalekshmi Unnikrishnan MeenakshiVikas JakhmolaManisha PandeySachin Kumar SinghKamal DuaPublished in: Journal of biochemical and molecular toxicology (2023)
Inflammation is an essential immune response that helps fight infections and heal tissues. However, chronic inflammation has been linked to several diseases, including cancer, autoimmune disorders, cardiovascular diseases, and neurological disorders. This has increased interest in finding natural substances that can modulate the immune system inflammatory signaling pathways to prevent or treat these diseases. Luteolin is a flavonoid found in many fruits, vegetables, and herbs. It has been shown to have anti-inflammatory effects by altering signaling pathways in immune cells. This review article discusses the current research on luteolin's role as a natural immune system modulator of inflammatory signaling mechanisms, such as its effects on nuclear factor-kappa B, mitogen-activated protein kinases, Janus kinase/signal transducer and activator of transcription, and inflammasome signaling processes. The safety profile of luteolin and its potential therapeutic uses in conditions linked to inflammation are also discussed. Overall, the data point to Luteolin's intriguing potential as a natural regulator of immune system inflammatory signaling processes. More research is needed to fully understand its mechanisms of action and possible therapeutic applications.
Keyphrases
- nuclear factor
- oxidative stress
- toll like receptor
- immune response
- signaling pathway
- cardiovascular disease
- transcription factor
- induced apoptosis
- multiple sclerosis
- human health
- risk assessment
- metabolic syndrome
- bone marrow
- papillary thyroid
- epithelial mesenchymal transition
- coronary artery disease
- big data
- electronic health record
- climate change
- protein kinase
- dendritic cells
- endoplasmic reticulum stress
- artificial intelligence
- cardiovascular events