Abstract: 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/L STZ. In sericin group, INS-1 cells were cultured with 10 mmol/L STZ and 600 μg/mL sericin. In inhibitor group, INS-1 cells were cultured with 10 mmol/L STZ, 600 μg/mL sericin and 0.3 mmol/L Akt1 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.

Key words: sericin, type 2 diabetes mellitus, INS-1 cells, proliferation

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+600 μg/mL丝胶处理细胞）、抑制剂组（给予10 mmol/L STZ+600 μg/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。

关键词: 丝胶, 2型糖尿病, INS-1细胞, 增殖