Chlorogenic acid alleviates the development of severe acute pancreatitis by inhibiting NLPR3 Inflammasome activation via Nrf2/HO-1 signaling.

Severe acute pancreatitis (SAP), marked by profound tissue inflammation within the pancreatic tissue, is an abrupt and intense inflammation of the pancreas. Chlorogenic acid (CGA) is one of the effective pharmacological ingredients components in JinHong Tablet (JHT). The role of CGA in protecting pancreas from severe injury in pancreatitis needs to be studied. The intervention with CGA led to a significant decline in serum amylase and lipase levels in rats with SAP, concurrently mitigating the pathological impairment within the pancreatic tissue. CGA effectively diminishes the levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in SAP rats by inhibiting the activation of NF-κB and the NLRP3 inflammasome. Additionally, in AR42J cells, the application of CGA was found to reduce the inflammatory response induced by caerulein. Mechanically, CGA alleviates the inflammatory response in SAP models by activating the Nrf2/HO-1 pathway. Together, CGA reduces the inflammatory response of SAP by activating the Nrf2/HO-1 pathway, thus alleviating the development of SAP. Our results provide a basis for the treatment of SAP.