An insight into role of amino acids as antioxidants via NRF2 activation.
Melford Chuka EgbujorOlugbemi Tope OlaniyanChigbundu N EmeruwaSarmistha SahaSarmistha SahaPaolo TucciPublished in: Amino acids (2024)
Oxidative stress can affect the protein, lipids, and DNA of the cells and thus, play a crucial role in several pathophysiological conditions. It has already been established that oxidative stress has a close association with inflammation via nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway. Amino acids are notably the building block of proteins and constitute the major class of nitrogen-containing natural products of medicinal importance. They exhibit a broad spectrum of biological activities, including the ability to activate NRF2, a transcription factor that regulates endogenous antioxidant responses. Moreover, amino acids may act as synergistic antioxidants as part of our dietary supplementations. This has aroused research interest in the NRF2-inducing activity of amino acids. Interestingly, amino acids' activation of NRF2-Kelch-like ECH-associated protein 1 (KEAP1) signaling pathway exerts therapeutic effects in several diseases. Therefore, the present review will discuss the relationship between different amino acids and activation of NRF2-KEAP1 signaling pathway pinning their anti-inflammatory and antioxidant properties. We also discussed amino acids formulations and their applications as therapeutics. This will broaden the prospect of the therapeutic applications of amino acids in a myriad of inflammation and oxidative stress-related diseases. This will provide an insight for designing and developing new chemical entities as NRF2 activators.
Keyphrases
- oxidative stress
- amino acid
- induced apoptosis
- signaling pathway
- diabetic rats
- ischemia reperfusion injury
- dna damage
- transcription factor
- nuclear factor
- anti inflammatory
- pi k akt
- epithelial mesenchymal transition
- toll like receptor
- small molecule
- inflammatory response
- cell proliferation
- current status
- cancer therapy
- drug induced