乌司他丁调控PI3K/AKT通路对大鼠心脏术后心脏收缩及舒张功能的影响及其机制研究

Influence and mechanism of ulinastatin on cardiac systolic and diastolic functions through regulating PI3K/AKT pathway in rats after cardiac surgery

目的探究乌司他丁调控肌醇磷脂-3-激酶/蛋白激酶B(PI3K/AKT)通路对大鼠心脏术后心脏收缩及舒张功能的影响和机制。方法将大鼠分为对照组、心脏手术组、心脏手术+乌司他丁组(每组各15只)。心脏手术组、心脏手术+乌司他丁组构建心脏手术模型,心脏手术+乌司他丁组以乌司他丁腹腔内注射(100kU/kg),1/d,连续7d。通过检测左心室射血分数(LVEF)和左心室缩短分数(LVFS)评估心脏功能。比较各组炎性细胞因子水平、PI3K和AKT蛋白的表达量。结果三组大鼠的LVEF、LVFS、炎性细胞因子水平、PI3K和AKT蛋白的表达量差异显著(P<0.05)。心脏手术组的LVEF、LVFS、PI3K和AKT蛋白的表达量显著低于对照组,白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)显著高于对照组(P<0.05)。心脏手术+乌司他丁组的LVEF、LVFS、PI3K和AKT蛋白的表达量显著高于心脏手术组,IL-1β和IL-6显著低于心脏手术组(P<0.05)。结论乌司他丁可提高心脏手术大鼠的心功能,并促进PI3K/AKT通路。

Objective To investigate the influence and mechanism of ulinastatin on cardiac systolic and diastolic functions through regulating PI3K/AKT pathway in rats after cardiac surgery.Methods All rats were divided into control group,cardiac surgery group and cardiac surgery+ulinastatin group(each n=15).The model of cardiac surgery was established in cardiac surgery group and cardiac surgery+ulinastatin group,and surgery+ulinastatin group was given intraperitoneal injection of ulinastatin(100kU/kg)once a day for 7d.The heart function was reviewed through detecting left ventricular ejection fractions(LVEF)and left ventricular fraction shortening(LVFS).The levels of inflammatory cytolines and protein expressions of PI3K and AKT were compared in all groups.Results The levels of LVEF,LVFS and inflammatory cytolines and protein expressions of PI3K and AKT had significant differences among 3 groups(P<0.05).The levels of LVEF and LVFS and protein expressions of PI3K and AKT were significantly lower,and levels of interleukin-1(IL-1β)and interleukin-6(IL-6)were significantly higher in cardiac surgery group than those in control group(P<0.05).The levels of LVEF and LVFS and protein expressions of PI3K and AKT were significantly higher,and levels of IL-1βand IL-6 were significantly lower in cardiac surgery+ulinastatin group than those in cardiac surgery group(P<0.05).Conclusion Ulinastatin can improve heart function and promote PI3K/AKT pathway in rats undergone cardiac surgery.