首页|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

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

扫码查看
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.
Regulatory Effects of Sericin on Glycolysis of Damaged INS-1 Cells through PI3K/Akt Signal Pathway
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),phosphofiuctosekinase-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 sencin 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.

sericindiabetesINS-1 cellsPI3K/Akt signaling pathwayglycolysis

李雨欣、韩思雨、易梦雅、李警耀、陈志宏

展开 >

承德医学院基础医学院,河北承德 067000

丝胶 糖尿病 INS-1细胞 PI3K/Akt信号通路 糖酵解

河北省"三三三人才工程"资助项目承德医学院优势学科B资助

A2016005063

2024

承德医学院学报
承德医学院

承德医学院学报

影响因子:0.451
ISSN:1004-6879
年,卷(期):2024.41(3)