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.

ObjectiveTo investigate the effects of type H hypertension on prognosis of intravenous thrombolysis in patients with acute cerebral infarction.Methods182 cases of acute cerebral infarction patients receiving intravenous thrombolysis with at-PA were divided into type H hypertension+cerebral infarction group (group A), hypertension+cerebral infarction group (group B), hyperhomocysteinemia+cerebral infarction group (group C) and cerebral infarction group without HHcy and hypertension (group D). The blood pressure, serum Hcy level and prognosis of patients in 4 groups were compared; And the influencing factors of poor prognosis after thrombolytic therapy were also analyzed.ResultsThe systolic pressure, serum Hcy level of patients in group A were obviously higher than group B, C, D (P<0.05). Compared with other 3 groups, the incidence of poor prognosis of group A was the highest (P<0.05). Logistic regression analysis showed that age, Hcy and systolic pressure are independent risk factors of recent poor prognosis of intravenous thrombolysis after acute cerebral infarction.ConclusionsType H hypertension is an important risk factor for the prognosis of intravenous thrombolysis in patients with acute cerebral infarction.

Objective: To investigate the changes and significance of plasma fibrinogen (FIB) and D-dimer level in patients with different types small vessel disease (CSVD). Methods: The plasma FIB and D-dimer level of 134 CSVD patients and 75 controls were detected and the risk factors of CSVD were analyzed. Results: The ratio of hypertension, plasma FIB level and plasma D-dimer level of CSVD and its subtypes (lacunar infarction/LI, white matter lesions/WML, LI combined WML) patients were all obviously higher than controls (P<0.05). Logistic regression analysis showed that D-dimer was risk factor for CSVD, LI, WML and LI combined WML (P<0.05); FIB was risk factor for CSVD, LI and LI combined WML (P<0.05). Conclusions: As risk factors for CSVD, FIB and D-dimer involve in the development of CSVD, but the risk factors for subtypes of CSVD are different.

Objective: To explore the correlations between serum lipid level and severity of white matter lesions (WML). Methods: The clinical data of 214 WML patients were retrospectively analyzed, and 61 healthy examined people at the same term were taken as control. The blood lipid correlation indexes of all the subjects were detected; and Logistic regression was used to analyze the risk factors of WML. Results: The difference of total cholesterol (TC) and low-density lipoprotein cholesterin between control group and WML group with different severity was statistically significant (P<0.05), which was related to the severity of WML. Logistic regression showed that age, hypertension and TC are risk factors of WML. Conclusions: Clinicians can prevent the occurrence of WML or delay the course of WML by controlling the risk factors of WML, such as hypertension and high TC level.