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.

Objective To explore the protective effects of sericin on streptozotocin(STZ)-induced injury rats’ INS-1 cells. Methods INS-1 cells were cultured in vitro and randomly divided into five groups. Normal control group (culture under conventional conditions), model group (10mmol/L STZ), low sericin group (STZ+150μg/mL sericin), medium sericin group (STZ+300μg/mL sericin), high sericin group (STZ+600μg/mL sericin). The cells in five groups were cultured respectively with corresponding drugs for 24h. The protein and mRNA expressions of BCL-2 and P53 were detected by Western blotting and real-time PCR. Cell apoptosis was detected by flow cytometry. Results Compared with the normal control group, the expression of BCL-2 protein and mRNA of INS-1 cells in the model group were remarkably decreased, while the expression of P53 protein and mRNA were remarkably increased (P<0.05), as well as the early apoptosis rate was remarkably increased (P<0.05). Compared with the model group, the expression of BCL-2 protein and mRNA in 3 sericin groups were remarkably increased, while the expression of P53 protein and mRNA were remarkably decreased (P<0.05), and the early apoptosis rate was remarkably decreased (P<0.05). Moreover, there were statistically remarkable differences among the 3 sericin groups (P<0.05). Conclusion The protective effects of sericin on STZ-induced injury INS-1 cells is related to the regulation of apoptotic proteins and inhibition of INS-1 cell apoptosis.

Objective To investigate whether sericin can protect streptozotocin (STZ) induced INS-1 cells injury by affecting autophagy and oxidative stress. Methods INS-1 cells were randomly divided into group A, B, C, D and E. In group A (normal group), INS-1 cells were cultured under conventional conditions for 24h without other treatments. In group B(STZ induced injury group), INS-1 cells were cultured with 10 mmol/L STZ for 24h. In group C, D and E, INS-1 cells were respectivly cultured with 10mmol/L STZ and different dose sericin (150μg/mL, 300μg/mL, 600μg/mL) for 24h. Western blot and real-time fluorescence quantitative PCR were used to detect the expressions of autophagy related gene protein and mRNA, and the reactive oxygen species(ROS) content in INS-1 cellswas detected by DCFH-DA ROS fluorescence probe. Results The expressions of LC3B-II/I, SIRT1, ATG5, BECLIN1, PINK1 proteins and mRNA in group C, D and E were all significantly higher than those in group B (P<0.05). The expression levels of each index in the three groups were group E>group D>group C, and the differences were statistically significant (P<0.05). The ROS content of INS-1 cells in group C, D and E were all obviously lower than that in group B (P<0.05). The ROS content of the three groups was in the order of group E<group D<group C, and the difference was statistically significant(P<0.05). Conclusions ericin can protect STZ induced INS-1 cells injury, and the protective mechanism is related to sericin's ability to reduce oxidative stress and enhance autophagy.