1.Influence of donepezil hydrochloride and hyperbaric oxygen on cognitive function in patients with vascular dementia
Chinese Journal of Primary Medicine and Pharmacy 2016;23(15):2301-2303,2304
Objective To investigate the influence of donepezil hydrochloride and hyperbaric oxygen on cognitive function in patients with vascular dementia.Methods 61 cases of patients with vascular dementia were chosen to research,and were divided into research group(31 cases)and control group(30 cases),the control group was treated with piracetam,the research group was treated with donepezil hydrochloride and hyperbaric oxygen,after 12 weeks of treatment congnitive function,daily life quality and adverse reaction between two group were compared. Results The ADL score and MMSE score between the two group had no significant difference before treatment(all P <0.05).The MMSE score of the research group were higher than the control group[(18.71 ±3.29)points vs (15.83 ±3.45)points]after treatment,the difference was statistically significant (t =3.337,P <0.05).The ADL score of the research group were lower than control group[(37.12 ±7.13)points vs (42.53 ±6.74)points],the difference was statistically significant (t =3.026,P <0.05).4 cases of mild to moderate earache and 1 case of mild diarrhea occurred in the research group,and 1 case of upper abdominal pain occurred in the control group,there was no significant difference in the incidence of adverse reactions between the two groups (χ2 =0.803,P >0.05 ). Conclusion Donepezil hydrochloride combined with hyperbaric oxygen could effectively improve the cognitive function of patients with vascular dementia,and with good safety.
4.Gecko crude peptides inhibit migration and lymphangiogenesis by down regulating the expression of VEGF-C in human hepatocellular carcinoma cells and human lymphatic endothelial cells
GUO MENG-LI ; WANG CAI-E ; DUAN YI-MENG ; WANG JIAN-GANG
Chinese Journal of Pharmacology and Toxicology 2017;31(10):958-959
OBJECTIVE To explore the role of gecko crude peptides (GCPs) in the proliferation, apoptosis, migration and lymphangiogenesis of human hepatocellular carcinoma cells (HepG2) and human lymphaticendothelial cells (HLECs) in vitro. METHODS The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate the anti- proliferative effect of GCPs and siRNA-VEGF-C on HepG2 cells, Hoechst 33258 staining and flow cytometry were performed to analyze cycle and apoptosis. The migration and invasion ability of cells were assayed by transwell chamber experiment and wound-healing assay. The protein and mRNA expressions of vascular endo?thelial growth factor-C (VEGF-C) and CXC chemokine receptor-4 (CXCR4) were detected by q-PCR, immunofluorescence, Western blot. The protein expressions of the extracellular signal regulated kinase (ERKI/2), c-Jun N-terminal kinase (JNK), p38-mitogen activated protein kinases (p38 MAPK), serine/threonine kinase (Akt) and phosphatidylinositol- 3- kinase (PI3K) were detected by western blot. The anti-lymphangiogenesis effect of GCPs on the HLECs was analyzed using an in vitro tube-formation assay. The protein and mRNA expressions of vascular endothelial growth factor receptor-3 (VEGFR-3) and stromal cell-derived factor-1 (SDF-1) were detected by q-PCR, Western blot. RESULTS GCPs and siRNA-VEGF-C inhibited HepG2 proliferation, invasion and migration, and the most obvious inhibitory effect was both synergistic effects. Thus, GCPs suppressed HLECs proliferation, migration and tube-like structure formationin a dose- dependent manner, and had inhibitory effect of tumor- induced lymphangiogenesis in vitro. Additionally, we found that GCPs and siRNA- VEGF- C decreased the expressions of MMP-2, MMP-9, VEGF-C, CXCR4, phospho-ERK1/2, phospho-P38, phospho-JNK and PI3K in HepG2 cells. Moreover, GCPs had a dose-dependent depressive effecton the expressions of VEGFR- 3, SDF- 1 in HLECs. CONCLUSION The low expression of VEGF- C mediated by siRNA-VEGF-C and GCPs inhibit tumor proliferation, invasion and migrationby suppressing the MAPK signaling pathway through reduced levels of VEGF-C, and GCPs inhibit tumor lymphangiogenesis by suppressing the CXCR4/SDF-1 signaling pathway through suppressed VEGF-C/VEGFR-3.