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为探讨 5 -氟尿嘧啶 (5 -FU)治疗急性胰腺炎是否与其抑制高炎症细胞因子的作用有关。我们通过动物实验观察了 5 -FU对急性胰腺炎发病时的高炎症性细胞因子血症的影响。使用雄性SD大鼠 ,共分 3组。 1组 :正常对照组 (n =6 ) :2组 :胰腺炎组 (n =8)采用开腹胰管注射 5 %的牛黄胆酸钠 (1 0ml/kg)制备急性胰腺炎动物模型。以后分别于 2 ,6 ,2 4小时处死 ;3组 :5 -FU治疗组 (n =8)为胰腺炎诱导成功后 0 5小时静脉注射 5 -FU 40mg/kg ,手术后 2 ,6 ,2 4小时处死动物。分别抽血查TNF ,IL - 1,IL - 6及胰淀粉酶 ,行胰腺湿重和病理检查。结果 :在急性胰腺炎时血中的炎症性细胞因子显著增高 ,在使用 5 -FU治疗后 ,上述细胞因子均下降。在 2 ,6小时时段下降最为明显 (P <0 0 5 ) ,1,2和 3组动物 2 4小时胰腺的湿重分别为 0 5g,1 3g和 0 88g(P <0 0 5 ) ,淀粉酶分别为 374 2U/L ,1817. 2 5U/L ,797 4U/L。治疗组的病理评分也明显好于未治疗组。综上 ,5 -FU可以抑制急生胰腺炎时的高炎症细胞因子血症 ,从而可能通过抑制免疫过激的方式缓解胰腺炎的病理生理异常 ,达到治疗急性胰腺炎的目的。
To investigate whether 5 - fluorouracil (5 -FU) treatment of acute pancreatitis and its inhibition of the role of high inflammatory cytokines. We investigated the effects of 5 -FU on hyperinflammatory cytokinemia during acute pancreatitis through animal experiments. Male SD rats were used and divided into 3 groups. Group 1: Normal control group (n = 6): Group 2: Pancreatitis group (n = 8) Acute pancreatitis animal model was induced by intraperitoneal injection of 5% sodium taurocholate (10ml / kg) And then sacrificed at 2, 6 and 24 hours respectively. Group 3: 5-FU treatment group (n = 8) received intravenous injection of 5-FU 40 mg / kg 0.5 hours after successful induction of pancreatitis, Animals were sacrificed in 4 hours. Blood samples were collected for determination of TNF, IL - 1, IL - 6 and pancreatic amylase. Pancreatic wet weight and pathological examination were performed. Results: The levels of inflammatory cytokines in the blood were significantly increased in acute pancreatitis and all of the above cytokines decreased after treatment with 5-FU. (P <0 05). The wet weights of pancreas in 24 hrs in groups 1, 2 and 3 were 0 5g, 13g and 0 88g (P <0 05) respectively. Starch Enzymes were 374 2U / L, 1817. 25U / L, 797 4U / L. The pathological score of the treatment group was also significantly better than the untreated group. In conclusion, 5 -FU can inhibit hyperinflammatory cytokinesmia in acute pancreatitis, and thus may alleviate the pathophysiology of pancreatitis by means of inhibiting the immune hyperacute and achieve the purpose of treating acute pancreatitis.