参附注射液调节兔心肺转流中高血糖的胰岛磷脂酰肌醇3激酶机制

Effect of insular phosphatidylinositol 3 kinase on shenfu injection improving hyperglycaemia in rabbits undergoing cardiopulmonary bypass

目的观察参附注射液(SFI)对兔心肺转流(CPB)中血糖的影响,探讨SFI调节兔CPB中高血糖的胰岛磷脂酰肌醇3激酶(PI3K)机制。方法健康成年新西兰大白兔30只,随机均分成三组:参附组(S组)、参附+ly294002组(SL组)和单纯CPB组(C组)。采集麻醉后即刻(T1)、主动脉阻断即刻(T2)、主动脉开放5 min(T3)、35 min(T4)和75 min(T5)动脉血液标本检测血浆血糖和胰岛素。CPB 150 min,取胰腺组织测丙二醛(MDA)和还原型谷胱甘肽(GSH)含量,免疫组织化学法测定胰岛细胞的胰岛素和PI3K p85表达。结果与T1时比较,三组T2～T5时血糖和胰岛素均增高(P<0.05);与C组比较,S组T2～T5时血糖降低,胰岛素升高(P<0.05),胰岛细胞的胰岛素和PI3K p85表达升高(P<0.05),S组和SL组胰腺MDA表达降低,GSH表达升高(P<0.05);与S组比较,SL组T2～T5时血糖升高,胰岛素降低(P<0.05),胰岛素和PI3K p85表达降低(P<0.05),胰腺MDA表达升高,GSH表达降低(P<0.05)。结论 SFI可能通过增强胰岛细胞PI3K表达而增加内源性胰岛素分泌,调节CPB中高血糖,其机制可能与SFI改善胰腺氧化和抗氧化的失衡有关。

Objective To investigate the mechanism of insular phosphatidyli- nositol 3 kinase （PI3K） for shenfu injection（SFI） improving hyperglycaemia in rabbits undergoing cardiopulmonary bypass（CPB）. Methods Thirty New Zealand white rabbits were randomly divided into there groups of CPB （group C）, SFI（group S）, SFI＋ly294002 （group SL）. Plasma concentrations of glucose and insulin were detected afer anaesthesia induction（T1 ）, after aortic cross-clamping（T2 ）, reperfused for 5 min（T3） ,35 min（Ta ） and 75 min（T5 ）, respectively. After CPB 150 min, MDA and GSH contents in the pancreas were determined, and insulin and PI3K p85 contents in islets were measured by irnmunohistochemistry. Results Plasma glucose and insulin were all significantly increased at T2 to Ts as compared with those at T1 in all groups（P〈0. 05）. Plasma glucose decreased and insulin increased at T2 to T5 ,and insulin and PI3K p85 in islets were higher in group S than those in group C（P〈 0.05）. MDA in the pancreas was lower and GSH was higher in groups of S and SL than those in group C（P〈0. 05）. The plasma glucose increased and insulin decreased at T2 to T5 and PI3K p85 expresion in islets was lower, MDA was higher and GSH was lower in group SL than those in group S （P〈0.05）. Conclusion SFI could increase insulin secretion by inceasing PI3K expresion, which can improve hyperglycaemia during CPI3. The effects were likely caused by increased PI3K contents in islets, The mechanism may be partly related to CFI reversing the disequilibrium of oxidization and antioxidation.