ISSN 1004-6879

CN 13-1154/R

 

Journal of Chengde Medical University ›› 2024, Vol. 41 ›› Issue (3): 181-184.

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

LI Yu-xin, HAN Si-yu, YI Meng-ya, LI Jing-yao, CHEN Zhi-hong*   

  1. School of Basic Medicine, Chengde Medical University, Chengde, Hebei, 067000, China
  • Received:2023-11-07 Online:2024-06-10 Published:2024-06-18

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

李雨欣, 韩思雨, 易梦雅, 李警耀, 陈志宏*   

  1. 承德医学院基础医学院,河北承德 067000
  • 通讯作者: *
  • 基金资助:
    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

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.

Key words: sericin, diabetes, INS-1 cells, PI3K/Akt signaling pathway, glycolysis

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。

关键词: 丝胶, 糖尿病, INS-1细胞, PI3K/Akt信号通路, 糖酵解

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