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.

Objective To screen key genes and pathways associated with tumorigenesis and progression of triple-negative breast cancer (TNBC) by using bioinformatics analysis. Methods Two gene expression profilings containing TNBC (GSE76124) and normal mammary (GSE112825) tissue samples were obtained from Gene Expression Omnibus (GEO). R software was used to identify differentially expressed genes. Gene Ontology (GO) function analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were further performed by DAVID. STRING and Cytoscape were used to construct protein-protein interaction(PPI) network. Furthermore, hub genes, core modules and seed genes were screened out. Results A total of 1,091 differentially expressed genes were screened out. The results of GO function analysis and KEGG pathway maps showed that these genes were associated with aromatic compound biosynthetic process, heterocycle biosynthetic process, and mainly enriched on the pathways in cancer and PI3K-Akt signaling pathway.We identified 10 hub genes, 2 core modules and 19 seed genes in PPI network. Conclusion A total of 10 hub genes and 19 seed genes were screened, which may play potential roles in the tumorigenesis and progression of TNBC. This study provids a bioinformatic analysis reference for further research.

Objective: To investigate the protective effects of soybean isoflavone on hippocampal cholinergic neurons of chronic cerebral ischemia rats. Methods: 30 healthy, adult female SD rats were applied in this study and randomly divided into sham operation group (n=10), model group (n=10) and treatment group (n=10). The rats in model group and treatment group were established chronic cerebral ischemia model by permanently ligating the common carotid arteries on both sides of castrated rats. In sham operation group, the bilateral ovaries and common carotid arteries were only separated without ligature. After the chronic cerebral ischemia rats' model was established, the rats in treatment group were lavaged with soybean isoflavone (9mg/kg/d) for 21 days. SP immunohistochemical staining and MiVnt image analysis system were used to detect and analyze the choline acetyltransferase (ChAT) protein expression in CA1 region of hippocampus of rats in each group. Results: The ChAT protein expression of neurons in CA1 region of hippocampus of rats in sham operation group was obvioulsy higher than model group and treatment group (P˂0.05). The ChAT protein expression of neurons in CA1 region of hippocampus of rats in treatment group was obvioulsy higher than model group (P˂0.05). Conclusions: Soybean isoflavone has protective effects on cholinergic neurons in hippocampus of rats with chronic cerebral ischemia, the mechanisms may be related to soybean isoflavone can up regulate ChAT protein expression in hippocampus.