丝胶靶向Akt1调控PI3K/Akt信号通路促进STZ致损伤INS-1细胞增殖  

Sericin Targeting Akt1 Regulates PI3K/Akt Signaling Pathway to Promote Proliferation of INS-1 Cells Damaged by STZ

作　　者：韩思雨 李雨欣 易梦雅 李警耀 陈志宏 HAN Si-yu;LI Yu-xin;YI Meng-ya;LI Jing-yao;CHEN Zhi-hong(School of Basic Medical Sciences,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2期96-100,共5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：目的探讨丝胶是否通过靶向Akt1调控磷酸肌醇-3-激酶(PI3K)/蛋白激酶B(protein kinase B,Akt)信号通路促进链脲佐菌素(STZ)致损伤大鼠胰岛素瘤细胞(INS-1细胞)增殖。方法INS-1细胞随机分为4组:对照组(不予任何处理)、模型组(给予10 mmol/L STZ处理细胞)、丝胶组(给予10 mmol/L STZ+600μg/mL丝胶处理细胞)、抑制剂组(给予10 mmol/LSTZ+600μg/mL丝胶+0.3 mmol/L的Akt1抑制剂A-674563处理细胞)。药物作用时间均为24 h。CCK-8法检测各组INS-1细胞存活率。免疫蛋白印迹法(western blot)检测PI3K/Akt信号通路相关蛋白PI3K、p-Akt和增殖相关蛋白增殖细胞核抗原(PCNA)、细胞核增殖相关抗原Ki67(Ki67)的表达情况。结果与对照组相比,模型组INS-1细胞存活率下降(P<0.05),PI3K、p-Akt1、PCNA和Ki67的蛋白表达显著下降(P<0.05);与模型组相比,丝胶组INS-1细胞存活率上升(P<0.05),PI3K、p-Akt1、PCNA和Ki67的蛋白表达显著增多(P<0.05);与丝胶组相比,抑制剂组INS-1细胞存活率下降(P<0.05),p-Akt1、PCNA和Ki67的蛋白表达显著下降(P<0.05)。结论丝胶具有促进STZ致损伤INS-1细胞增殖的作用,其作用机制与丝胶通过靶向Akt1调控PI3K/Akt信号通路有关。Objective To investigate whether sericin promotes proliferation of streptozotocin(STZ)damaged insulinoma cells(INS-1 cells)through targeting Akt1 regulates PI3K/Akt signaling pathway.Methods INS-1 cells were randomly divided into four groups.In control group,INS-1 cells were cultured under conventional conditions without other treatments.In model group,INS-1 cells were cultured with 10 mmol/LSTZ.In sericin group,INS-1 cells were cultured with 10 mmol/LSTZ and 600μg/mLsericin.In inhibitor group,INS-1 cells were cultured with 10 mmol/LSTZ,600μg/mLsericin and 0.3 mmol/LAkt1 inhibitor A-674563.The cells in four groups were cultured with corresponding drugs respectively for 24h.The survival rate of INS-1 cells in each group was detected by CCK-8 method.Western blot was used to detect the expression of PI3K/Akt signaling pathway related proteins PI3K and p-Akt,and proliferation related proteins PCNA and Ki67.Results The survival rate,and the protein expressions of PI3K,p-Akt1,PCNA,and Ki67 of INS-1 cells in model group significantly decreased compared with control group(P<0.05).The survival rate,and the protein expressions of PI3K,p-Akt1,PCNA,and Ki67 of INS-1 cells in sericin group significantly increased compared with model group(P<0.05).The survival rate,and the protein expressions of PI3K,p-Akt1,PCNA,and Ki67 of INS-1 cells in inhibitor group significantly decreased compared with sericin group(P<0.05).Conclusion Sericin can protect proliferation of INS-1 cells damaged by STZ,and the protective mechanisms may related to target Akt1 regulates PI3K/Akt signaling pathway.

关 键 词：丝胶 2型糖尿病 INS-1细胞 增殖 

分 类 号：R587.1[医药卫生—内分泌]