【摘要】 目的 观察丝胶对链脲佐菌素(STZ)致损伤大鼠胰岛素瘤细胞(INS-1细胞)PI3K/Akt信号通路和糖酵解的调控作用。方法 实验以体外培养的INS-1细胞为研究对象随机分为五组，正常对照组、模型组、丝胶组、Akt1抑制剂组、Akt1激动剂组。运用蛋白印迹和实时荧光定量PCR法检测各分组细胞的磷脂酰肌醇-3-激酶(PI3K)，蛋白激酶B(Akt)，磷酸果糖激酶-1(PFK1)，6-磷酸果糖-2,6-二磷酸酶(PFKFB2)的蛋白及mRNA的表达情况。结果 与正常对照组相比，模型组PI3K，p-Akt，PFK1，PFKFB2的蛋白表达显著下降(P<0.05)；丝胶组与模型组相比PI3K，p-Akt，PFK1，PFKFB2的蛋白表达显著增高(P<0.05)；Akt1抑制剂组与丝胶组相比，p-Akt，PFK1，PFKFB2的蛋白表达显著降低(P<0.05)；Akt1激动剂组与丝胶组相比，p-Akt，PFK1，PFKFB2的蛋白呈现上升的趋势。各组INS-1细胞中PI3K，Akt，PFK1，PFKFB2 mRNA的变化趋势与蛋白一致。结论 丝胶对STZ致损伤INS-1细胞发挥保护作用的机制可能是，靶向Akt1影响PI3K/Akt信号通路增强糖酵解。更多还原

【Abstract】 Objective To observe the regulatory effects of sericin on PI3K/Akt signal pathway and glycolysis of INS-1 cells injured by streptozotocin (STZ).Methods INS-1 cells cultured in vitro were randomly divided into five groups.Normal control group,model group,sericin group,Akt1 inhibitor group and Akt1 agonist group.Western blotting and real-time fluorescence quantitative PCR were used to detect the expression of phosphatidylinositol-3-kinase (PI3K),protein kinase B (Akt),phosphofructosekinase-1 (PFK1),6-phosphofructose-2,6-diphosphatase (PFKFB2) protein and mRNA.Results Compared with the normal control group,the protein expression of PI3K,p-Akt,PFK1,PFKFB2 of INS-1 cells in the model group decreased significantly (P<0.05).The protein expression of PI3K,p-Akt,PFK1,PFKFB2 of INS-1 cells in the sericin group were significantly higher than that in the model group (P<0.05).The protein expression of p-Akt,PFK1,PFKFB2 of INS-1 cells in the Akt1 inhibitor group were significantly lower than that in the sericin group (P<0.05).Compared with sericin group,the protein expression of p-Akt,PFK1 and PFKFB2 showed an upward trend in the Akt1 agonist group.The change trend of PI3K,Akt,PFK1,PFKFB2 mRNA expression in INS-1 cells of each group were consistent with that of protein.Conclusion The protective mechanism of sericin on STZ-induced injury of INS-1 cells may be that targeted Akt1 affects PI3K/Akt signal pathway and enhances glycolysis.更多还原