Protective effects of thalidomide on rats with acute necrotizing pancreatitis / 中华胰腺病杂志

ABSTRACT

Objective To investigate the protective effects of thalidomide on rats with acute necrotizing pancreatitis (ANP) and its mechanism. Methods Fifty four SD rats were randomly divided into the three groups; ANP group, thalidomide group and control group with 18 rats in each group. The model of ANP was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. Rats in thalidomide group received thalidomide 200 mg/kg body weight gastric lavage 1 h after ANP induction. The rats were sacrificed 3 h, 6 h, and 12 h after ANP induction, and the amount of intraperitoneal ascites was quantified. The serum levels of TNF-α, IL-6, IL-18 were measured by EUSA. The proportion of CD4 + T cell, CD8 + T cell in peripheral blood was determined by flow cytometry. The expression of TNF-α mRNA in pancreatic tissue were measured by RT-PCR. The expression of ICAM-1 protein in pancreatic tissue was measured by immunohistochemistry. Pancreatic tissue underwent pathologic examination. Results Six hours after surgery, the amount of ascite, serum levels of TNF-α, IL-6, IL-18, CD4 + T cell, CD,+ T cell, pancreatic TNF-α mRNA and ICAM-1 protein expression, pathologic score in control group was (1.03 ±0.31)ml,(57.17±11.29)pg/ml, (24.45 ±4.14)pg/ml, (64.23 ±21.85)pg/ml, (47.58 ±9.21)% , (40.88 ± 2.96)%, 0.07 ±0.02, 0.57 ±0.30, 0.67 ±0.81, respectively, and the corresponding values were (3.63 ± 0.38)ml, (107.54 ±33.05) pg/ml, (47.30 ± 11.40) pg/ml, (367.76 ± 108.43 ) pg/ml, (54.90 ± 7.15)%, (17.17 ±3.12)%, 0.65 ±0.26, 3.20 ±0.57, 11.50 ±1.87 in ANP group; and (1.45 ±0.53)ml, (80.60 ±20.48) pg/ml, (26.61 ±10.85) pg/ml, (321.82 ±85.20) pg/ml, (29.80 ±2.19)% , (15.52± 1.96)%, 0.35 ±0.23, 2.37 ±0.67, 8.00 ±3.03. Besides the value of CD8 + T cell was significantly decreased, all other values were significantly increased when compared with control group (P <0.05). Conclusions Thalidomide can decrease the release of inflammatory mediator, and reduce the pathological damage of pancreas of ANP rats by inhibiting TNF-α mRNA expression.