山柰酚对重症急性胰腺炎大鼠肠黏膜屏障变化及免疫功能的影响.

Objective: To investigate the effects of kaempferol on the changes of intestinal mucosal barrier and immune function in rats with severe acute pancreatitis. Methods: The rat model of severe acute pancreatitis was established, and the rats were randomly divided into 6 groups: sham operation group, model group, kaempferol low-dose group, kaempferol medium-dose group, kaempferol high-dose group and dexamethasone group. Pathological damage of pancreatic tissue was detected by HE staining and pathological scores were obtained. Serum diamine oxidase （DAO）, serum D-lactic acid, IL-6, TNF-α and IL-1β levels were detected by ELISA. Serum amylase and lipase were detected by automatic biochemical analyzer. Mucosal thickness and villus height were measured by automatic image analyzer. NLRP3, ASC, Cleaved caspase-1/caspase-1, p-Nrf2, Nrf2, NQO1 and HO-1 expressions were detected by Western blot. Results: Compared with sham operation group, the serum levels of DAO, D-lactic acid, amylase and lipase in model group were increased （P<0.05）, the mucosal thickness and villus height were decreased （P<0.05）, and the levels of IL-6, TNF-α and IL-1β were increased （P<0.05）. NLRP3, ASC and Cleaved caspase-1/Caspase-1 expressions were increased （P<0.05）; Compared with model group, the histopathological damage of pancreas in kaempferol medium and high dose groups and dexamethasone groups were significantly improved, the histopathological score of pancreas was decreased （P<0.05）, the levels of serum DAO, D-lactic acid, amylase and lipase were decreased （P<0.05）, and the mucosal thickness and villus height were increased （P<0.05）. The levels of IL-6, TNF-α and IL-1β were decreased（ P<0.05）, and the expressions of NLRP3, ASC and Cleaved caspase-1/Caspase-1 were decreased （P<0.05）, the p-Nrf2/Nrf2 and the protein expression of NQO1 and HO-1 were increased （P<0.05）. Conclusion: Kaempferol can effectively improve the immune function of severe acute pancreatitis model rats, improve the protective function of intestinal mucosal barrier, inhibit the release of inflammatory factors, inhibit the activation of NLRP3/ASC/Caspase-1 pathway, and activate the Nrf2/NQO1/HO-1 pathway. [ABSTRACT FROM AUTHOR]