Antioxidants in Inflammatory Diseases

Le résumé fourni par la source

Damage to tissues and abnormal function of organs are hallmarks of inflammatory disorders, which are characterized by an overactive and inadequately controlled immune response. Inflammation and chronic diseases can result from microbial infections, tissue damage, and autoimmune dysregulation. These stimuli trigger macrophages and neutrophils, releasing ROS and RNS. ROS/RNS overwhelm the body's antioxidant defenses, causing oxidative assault and inflammatory signaling cascades. NF-кβ and AP-1 activate amid oxidative assault. These transcription factors regulate the expression of pro-inflammatory genes that create cytokines (TNF, ILs), chemokines, and adhesion molecules, which enhance inflammation and recruit immune cells to damaged areas. Antioxidants oversight several inflammatory signaling cascades. They're able to block the production of pro- inflammatory genes by reducing NF-кβ and AP-1 activation. Crucial inflammatory MAPK pathways like ERK, JNK, and p38 MAPK can be modulated by antioxidants. Antioxidants can decrease pro-inflammatory mediator synthesis because they interfere with these pathways. Directly scavenging and neutralizing ROS/RNS is how antioxidants do their job. Scavenging protects lipids, proteins, and DNA against oxidative damage. Antioxidants enhance SOD, catalase, and glutathione peroxidase, which are body-produced antioxidant enzymes. Thus, increasing enzyme expression and activity strengthens cells’ antioxidant defenses. Antioxidants can induce an anti-inflammatory phenotype in macrophages and T cells. They are capable of shifting macrophages from M1 to M2. M2 macrophages aid tissue repair and immunomodulation. Antioxidants also promote the formation of regulatory T cells, which regulate the immune system by inhibiting other immune cells. In conclusion, this abstract emphasizes the crucial role of oxidative assault in inflammatory diseases and the potential of antioxidants as therapeutic agents.

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