Abstract: Objective To detect the expression levels of six mitochondrial N-formyl peptides (NFPs) in plasma and formyl peptide receptor 1 (FPR1) in pancreas of rats with severe acute pancreatitis (SAP), and to explore the correlation between them and the progression of SAP. Methods Thirty male SD rats were divided into the sham operation group, the SAP model 3 h group and the SAP model 6 h group by random number table method, with 10 rats in each group. In the sham operation group, the pancreas was turned slightly after laparotomy, and then the abdominal cavity was closed. SAP rat model was prepared in the SAP groups by retrograde injection of 5% sodium taurocholate (50 mg/kg) into the biliary duct. The expression levels of six mitochondrial NFPs in plasma were detected by Western Blotting. The pathological changes of pancreatic tissue were observed by hematoxylin-eosin staining. Immunohistochemistry was used to detect the protein expression of FPR1 in pancreas. Results Compared with the sham operation group, pancreatic hemorrhage, acinoid cell necrosis, inflammatory cell infiltration, edema and other pathological changes occurred in the SAP model 3 h group and the SAP model 6 h group, and the pathological scores were significantly increased, especially in the SAP model 6 h group (P＜ 0.05). Immunohistochemical results showed that the expression levels of FPR1 in pancreatic tissue were significantly higher in the SAP model 3 h group and the SAP model 6 h group than that of the sham group, especially in the SAP model 6 h group (P＜0.05). The expression levels of six mitochondrial NFPs were varied. The expression levels of MT-ND1, MT-ND3 and MT-ND6 were gradually increased with the prolonging of SAP modeling time (P＜0.05), while MT-ND4 showed a decreasing trend (P＜0.05). There was no significant difference in the expression of MT-ND5 between the three groups. Conclusion FPR1 and some mitochondrial N-formyl peptides are closely associated with the progression of SAP, and which may be related to the excessive inflammatory response and amplification of inflammatory cascade in SAP.

Key words: pancreatitis, acute necrotizing, receptors, formyl peptide, DNA, mitochondrial, damage associated molecular patterns