Abstract: Objective To investigate the molecu?lar mechanism in SAP-induced myocardial injury in mice and to explore the protective role of naringenin. Methods Animals were randomly divided into 3 groups: control group, SAP group, and Nar group (n=12 each group). Mice were subjected to intraperitoneal injection with LPS (8%,4mg/kg, pH=7) twice at 1 h intervals, to induce SAP model. Naringenin (200mg/kg) were injected intraperitoneally 0 , 12 and 48 h after LPS injection. An automatic biochemical analyzer was used to analyze the con?centration of creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I(cTnI). Real time PCR and Western blot were used to analyze mRNA and protein levels of NLRP3, Caspase-1, ASC and IL-1?. Results Compared to the control group, SAP generated not only edema, inflammatory cell infiltration and acinar cell necrosis in pancreatitis, but also the histological examination of swelled/disordered myocardial fibers and congested blood vessels in myocardium. Moreover, SAP-induced elevation of CK-MB/LDH and cTnI concentrations in serum and up-regulation NLRP3、caspase-1，ASC and IL-1? in both mRNA and protein levels in the heart tissues（p<0.05）. naringenin treatment inhibits SAP-induced elevation of CK-MB, LDH and cTnI concentrations in serum, alleviated SAP-induced pathological features. Moreover, compared to SAP group, Naringenin treated group down-regulated NLRP3, ASC, Caspase-1 and IL-1? expression in both mRNA（p<0.01） and protein levels in the heart（p<0.05）. Conclusion: Naringenin protectes severe acute pancreatitis-induced myocardial injury in mice by inhibiting NLRP3 inflammasome pathway.

Key words: Severe Acute Pancreatitis, Naringenin, Myocardial Injury, NLRP3 inflammasome