Abstract
Many diseases, such as hypertension, obesity, diabetes, arthritis, and cancer, are caused by inflammation resulting from oxidative stress and dysbiosis. Oxidative stress is triggered by reactive oxygen species (ROS), and long-term inflammation contributes to aging. Inflammation damages DNA, carbohydrates, proteins, and lipids at the cellular and tissue levels. Cytokines such as IL-1β, IL-6, tumor necrosis factor-alpha (TNF-α), and COX-2 are produced through nuclear factor-kappa B (NF-κB) mediation, and ROS is associated with NF-κB activation. Angiogenesis is initiated by the release of angiogenic growth factors and cytokines, including vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), TNF-α, prostaglandin E2 (PGE2), nitric oxide (NO), IL-1, IL-6, and IL-8 from macrophages, affecting endothelial cells. Fibroblasts are activated by TGF-β, which is secreted by macrophages and leads to fibrosis. Prolonged oxidative stress caused by ROS is a major contributor to aging. To delay the aging process, it is important to reduce oxidative stress and NF-κB activation. Celecoxib and symbiosis have the potential to prevent aging by regulating NF-κB activation. Additionally, maintaining a healthy lifestyle with regular exercise and a balanced diet can help reduce oxidative stress and delay aging. It is important to consider a range of anti-aging strategies, including both pharmaceutical interventions and lifestyle changes.
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