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.

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.