In summary, our study shows that EsA inhibits the secretion of inflammatory factors TNF-α and IL-6 by regulating the NF-κB signaling pathway and proinflammatory cell apoptosis in LPS-induced inflammatory cells and rat models of AP, respectively, providing evidence that EsA may be a novel therapeutic agent for the treatment of AP-induced intestinal inflammation and further arresting AP progression. The gene discussed is NFKB1; the disease is gastroenteritis.