It achieves this by inhibiting key inflammatory mediators such as nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), all of which play central roles in the inflammatory pathways driving the pathogenesis of AP (Wang et al., 2023; Nagy-Pénzes et al., 2022). This evidence concerns the gene IL1B and alkaline phosphatase measurement.