丝胶通过PI3K/Akt信号通路对受损INS-1细胞糖酵解的调控作用  

Regulatory Effects of Sericin on Glycolysis of Damaged INS-1 Cells through PI3K/Akt Signal Pathway

作　　者：李雨欣 韩思雨 易梦雅 李警耀 陈志宏 LI Yu-xin;HANSi-yu;YI Meng-ya;LI Jing-yao;CHEN Zhi-hong(School of Basic Medicine,Chengde Medical University,Chengde,Hebei,067000,China)

机构地区：[1]承德医学院基础医学院,河北承德067000

出　　处：《承德医学院学报》2024年第3期181-184,共4页Journal of Chengde Medical University

基　　金：河北省“三三三人才工程”资助项目(A2016005063);承德医学院优势学科B资助。

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。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 thesericin 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 thesericin 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 maybe that targeted Akt1 affects PI3K/Akt signal pathway and enhances glycolysis.

关 键 词：丝胶 糖尿病 INS-1细胞 PI3K/AKT信号通路 糖酵解 

分 类 号：R587.1[医药卫生—内分泌]