In the AP model, BA treatment significantly inhibited the degradation of the IκBα protein and the translocation of NF-κB p65 to the nucleus, resulting in decreased levels of IL-1β, IL-6, TNF-α, and CCL2; in a mouse model, acinar cell necrosis and pancreatic tissue edema in mice are alleviated, and the activities of serum amylase and lipase are decreased in response to BA [46]. The gene discussed is NFKB1; the disease is alkaline phosphatase measurement.