OBJECTIVETo explore the role and mechanism of oxidative inflammatory cascade in pancreatic fibrosis progression of chronic pancreatitis (CP) in mice induced by dibutyltin dichloride (DBTC) plus ethanol.

METHODSThirty-six KM mice were randomly divided into 2 groups (n = 18): control group and model group (DBTC combined with ethanol). The mice in model group were intravenously injected with DBTC (8 mg/kg) in tail vein and drink 10% ethanol. After modeling 2 weeks, 4 weeks and 8 weeks, the mice were anesthetized and sacrificed, the pathological changes and the degree of fibrosis in the pancreas were observed by HE and Masson staining, the F4/80 expression level were detected by immunohistochemistry, the content of superoxide dismutase (SOD), malondialdehyde(MDA) and myeloperoxidase (MPO) were measured in the pancreatic homogenates.

RESULTSThe fibroblasts and macrophages (f4/80 positive staining) could be seen obviously in pancreas of model group at 2 weeks. At 4 weeks and 8 weeks, macrophages infiltration increased and pancreatic tissue was substituted by the proliferation of fibrosis significantly. At every time-point, in pancreatic homogenates SOD was decreased, MDA and MPO markedly increased. There was significant differences between two groups (P < 0.05).

CONCLUSIONDBTC injection joint ethanol drinking can successfully establish the model of chronic pancreatitis and pancreatic fibrosis in mice. Oxidative inflammatory cascade plays an important role in the progression of pancreatic fibrosis.