炎症介质与急性坏死性胰腺炎大鼠的肺损伤

Inflammatory mediators and lung injury in murine acute necrotizing pancreatitis

目的 探讨急性坏死性胰腺炎 (ANP)大鼠并发肺损伤的机制。方法 逆行性胰胆管注射 3 5 %牛磺胆酸钠建立ANP大鼠模型。观察肺组织学改变 ,测定血中淀粉酶、磷脂酶A2 (PLA2 ) ,用ELISA法测定血中肿瘤坏死因子α(TNFα)水平 ,并用免疫组织化学技术观察肺组织TNFα、细胞间粘附分子 1和淋巴细胞功能相关性抗原的表达。结果 ANP组大鼠的血中TNFα及PLA2 水平明显升高 ,分别为 (6 8 7± 1 8)pg/ml和 (2 30± 34 )U/L ,正常组为 (4 1 5± 5 7)pg/ml和 (71± 14)U/L ,两组相比 ,P均 <0 0 1,同时肺组织中TNFα和粘附分子也有高表达。

Objective To study the pathogenesis of lung injury associated with murine acute necrotizing pancreatitis (ANP).Methods Murine ANP model was established by retrograde injection of 35% sodium taurocholate into bilio-pancreatic duct. Amylase and serum inflammatory mediators (PLA_2 and TNFα) were measured and the expressions of TNFα and adhesion factors (ICAM-1 and LFA) were observed by ABC immunohistochemistry. Results TNFα and PLA_2 level increased significantly in ANP rats as compared with that in normal contrals 〔(687±18)*!pg/ml,and (230±34) U/L vs. (415±57)*!pg/ml and (71±14) U/L, all P<001〕. TNFα and adhesion factors were overexpressed in lung tissue in ANP model also. Conclusion The increase of inflammatory mediators in blood and the overexpression of TNFα and adhesion factors in lung tissue may play an important role in the development of ANP.