The roles and mechanisms of p-STAT3 signaling pathway in acute pancreatitis

Abstract

To detect the expression ofsignal transducer and activator of transcription 3 (STAT3) in pancreatic tissue of the mouse model of pancreatitis, and to explore its role in the evolution of acute pancreatitis. Forty-eight healthy male balb/c mice were randomly divided into 3 groups (n=16):control group (Con) 0.09% NaCl, intraperitoneal injection; mild acute pancreatitis group (MAP) caerulein, intraperitoneal injection; severe acute pancreatitis group (SAP) caerulein plus lipopolysaccharide(LPS), intraperitoneal injection. The mice were sacrificed after 2 h and 6 h after intraperitoneall injection. Serum was isolated for amylase activity. Pancreatic was isolated and weighedto calculate the pancreatic wet weight ratio. Myeloperoxidase (MPO) activity was measured to assess the degree of inflammatory cell infiltration in lung tissue. Using HE staining, the pathological changes of pancreatic and lung were observed under the light microscope. The expression of phosphorylated STAT3 (p-STAT3) was detected by Western blot. Compared with control group, serum amylase activity, pancreatic wet weight ratio and lung MPO activity were significantlyincreased (P<0.05) in MAP and SAP group at each time point, especially SAP group showed higher levels of MPO activity than that in MAP group (P<0.01). The pathological changes of pancreas and lung were observed after modeling in 2 h. Western blot showed the expression of p-STAT3 could be detected in SAP group, the level increased most significantly after modeling 2 h, and decreased slightly after 6 h. The level of p-STAT3 was low in MAP group and negative in Con group at each time point. The expression of p-STAT3 in MAP and SAP groups are significantly different from that in control group, which indicates that STAT3 isclosely related in acute pancreatitis. Inhibition of STAT3 activity is a potential target to alleviate acute pancreatitis progression.