知识与财富的链接
目的 探讨重症急性胰腺炎急性肺损伤中磷脂酰肌醇3-激酶/蛋白激酶B(P13K/PKB)信号转导通路的活性变化规律.方法 健康成年雄SD大鼠40只,随机分为SO组(n=10)、SAP组(n=30),BD针胰胆管逆行注入牛磺胆酸法建立重症急性胰腺炎急性肺损伤大鼠模型.SAP组3、6、12h检测血淀粉酶、血气分析、肺含水量,肺组织髓过氧化物酶(MPO)活性,光镜下进行胰腺和肺组织病变程度评分.免疫组化法检测肺组织ICAM-1和P-PKB的表达,蛋白印迹(Western blot)法检测PI3K/PKB信号通路的活性变化.SO组在术后12h检测上述相关指标.结果 肺损伤程度逐渐加重,组织含水量及MPO活性逐渐升高(P<0.05),PaO_2明显降低(P<0.05).制模后3h随p-PKB的活性逐步增强,ICAM-1表达逐渐增多,两者呈正相关(r=0.910,P<0.05);PI3K/PKB信号通路逐步被激活,至12h达到峰值,与肺损伤程度呈正相关(r=0.871,P<0.05).结论 P13K/PKB信号传导通路被激活是重症急性胰腺炎急性肺损伤的重要发病机制之一.
Objective To study the signal transduction pathway activity changes of PI3K/PKB in rats of acute lung injury with severe acute pancreatitis.Methods 40healthy adult male SD rats were randomly divided into 2 groups, SO group (n = 10), SAP group (n = 30), inject taurocholate retrograde biliopancreatic ducts by using BD Intravenous Catheters to establish the rat model of acute lung injury with severe acute pancreatitis.When the SAP model were induced in 3h, 6h and 12h, detect the blood amylase, blood gas analysis, lung water content, lung tissue MPO activity, and the pathological score of pancreas and lung strueture.The expression of ICAM -1 and p -PKB in lung tissue by immunohistochemistry and the activity change of PI3K/PKB signal pathway by protein blot (Western blot) assay were detected.The relative data mentioned as above also detected in SO group after 12h.Results The lung injury becomes more and more serious, water content and MPO activity also increased gradually (P <0.05).Meanwhile PaO_2 decreased evidently (P < 0.05).3h after modeling with the p -PKB activity gradually increased, ICAM -1 expression is also gradually increased, which were positively correlated (r = 0.910, P < 0.05) ; PI3 K/PKB signaling pathway is activated gradually to reach its peak while modeling in 12h, correlating with the lung injury positively(r =0.871 ,P <0.05).Conclusion The activation of PDK/PKB is one of the important pathogenesis in rats of acute lunginjury with severe acute pancreatitis.
