Objective To explore the possible anti-inflammatory mechanism of intensive insulin therapy (IIT) by studying the effect of IIT on the levels of TNF-?,IL-6,C-reactive protein (CRP) and APACHE Ⅱ score in biliary pyemia.Methods Twenty eight patients with biliary pyemia who were admitted by our department and given an operation within 24 h form Jan.2005 to Dec.2008 were randomly divided into two groups by using random number table numbers:one group treated with IIT (IIT group,n=14) and another group treated with routine insulin therapy (RIT group,n=14).The inflammatory factors,such as TNF-?,IL-6 and CRP were detected dynamically and the APACHEⅡ score was calculated.Results The level of CRP and APACHEⅡ score on day 5 and 7 and the levels of TNF-? and IL-6 on day 3,5 and 7 after operation in IIT group were significantly lower than those in RIT group (P

Objective: To establish the model of palatine mucoperiosteal expansion and observe a new possible treatment approach to soft tissue defect of cleft palate. Methods: Expanders of 10ml were implanted beneath the palatine mucoperiosteum in 4 dogs and injected 1.0ml 0.9% NaCl at the same time. 20 days after the placement of the expander, the expander was expanded by 1.0-1.5ml every 7 days again. The dogs were killed after the expanders reached their capacity. All the specimens were performed histomorphometric and histological examinations. Results: Histological results showed the increase in the layer of cell and the number of collagen fibra and blood vessel. All the specimens of expanded tissue showed the formation of extra palatine mucoperiosteal tissue. Conclusion: Expansion technique is able to form extra palatine mucoperiosteal tissue,which could be a new restoration approach to soft tissue defect of cleft palate and others.

OBJECTIVE: To determine the neuro-protective effects of albiflorin against MPP+-induced PC12 cells death and related molecular mechanisms. METHODS: PC12 cells were treated with 4 mmol·L-1 MPP+ to establish apoptotic cell models. MTT method, DCFH-DA staining, JC-1 staining and Western Blot were used to determine the changes of cell viability, intracellular ROS concentration, mitochondrial membrane potential and the expression of Bel-2 and Bcl-X1, and the phosphoration of Akt/GSK3β in PC12 cells. RESULTS: Albiflorin showed significantly neuro-protective effects against MPP+-induced cell damage. Results showed that albiflorin enhanced the cell viability, reduced intracellular ROS level and caspase 3 activation, restored the mitochondrial membrane potential, increased the expression of Bcl-2 and Bcl-X1, and enhanced the phosphoration of Akt/GSK3β. CONCLUSION: Albiflorin shows neuro-protective effects against MPP+-induced PC12 cells damage via mitochondrial-dependent pathway and Akt/GSK3β signaling.

OBJECTIVE: To investigate the anti-hepatocellular carcinoma effect and underlying mechanisms. METHODS: In PLC/PRF/5 and HepG2, after treatment with Grifola frondosa extract, MTT method, chemical method, JC-1 staining and Western Blot were applied to determine cell viability, caspase 3 activity, mitochondrial membrane potential, the expression of Bcl-2 and Bax, and the phosphorylation of Akt/GSK3β. The anti-tumor activity of Grifola frondosa extract was further confirmed in PLC/PRL/5-xengrafted mice model. RESULTS: Grifola frondosa extract significantly reduced cell viability, mitochondrial membrane potential, the expression of Bcl-2 and the phosphorylation of Akt/GSK3β, and enhanced LDH release, caspase 3 activity and the expression of Bax in both PLC/PRF/5 and HepG2 cells. 12-day Grifola frondosa extract treatment significantly inhibited the PLC/PRF/5-xenografted tumor growth without influence the body weight of mouse. CONCLUSION: All these data indicate that Grifola frondosa extract-mediated anti-hepatocellular carcinoma effects are related to its modulation of the activations of Akt/GSK3β and mitochondrial pathway.

Objective: To study the structures of ginseng glycopeptides, and to explore the protective effect on the apoptosis of PCI 2 cells treated with amyloid beta25-35 (Aβ25-35), and to lay a theoretical foundation for the development of ginseng anti-Alzheimer' s disease (AD) drugs. Methods: The structures of ginseng glycopeptides were analyzed by reversed-phase high performance liquid chromatography coupled with Q Exactive Orbitrap mass spectrometry. The PCI2 cells were divided into 6 groups, and treated with the medium including different concentrations 0, 6. 25, 12. 50, 25. 00, 50. 00, and 100. 00 mol • L_ 1 ) of Aβ25-35 , and the survival rates of PC12 cells were measured by cell counting kit-8 (CCK-8) method. The PC12 cells were divided into blank control group, model group, and ginseng glycopeptides administration group. The medium including 50. 00 jumol • L_ 1 Aβ25-35, was added in model group, and different concentrations 0. 03, 0.10, 0. 30, and of 1. 00 g • L_ 1 ) ginseng glycopeptides+ 50 jumol • L_ 1 Aβ25-35 were added in administration groups. The survival rates of PC12 cells were measured by CCK-8 method. The apoptotic rates of PCI 2 cells after treated with glycopeptides and Aβ25-35, were detected by Annexin V-FITC/PI method. The PCI 2 cells were divided into blank control group, model group (50.00 jumol • L_ 1 Aβ25-35) and different concentrations (0 . 1 0 and 0.30 g • L_ 1 ) of ginseng glycopeptides administration groups; the percentages of PCI 2 cells in different cell cycles were tested by flow cytometry. Results: More than 20 glycopeptide structures were obtained, such as the peptide chain was NLSHYHSGSS, the glycosyl group was Nl-HexNAc, and the peptide chain was SGSSSSSSSEDDGMGR, the glycosyl group was S6-HexNAc. When the concentration of Aβ25-35 was 50 jumol • L_ 1 , the survival rate of PC12 was (55. 45 + 2. 3 4) % and the survival rate was significantly lower than that in blank control group (P < 0 . 0 1) . Compared with blank control group, the survival rate of the PC12 cells in model group was significantly decreased (P < 0 01); compared with model group, the survival rates of the PCI2 cells in administration groups were significantly increased (P< 0. 05). Compared with blank control group, the apoptotic rate of the PC12 cells in model group were increased (P < 0. 01); compared with model group, the apoptotic rates of the PC12 cells in administration groups were decreased (P < 0 . 05). Compared with blank control group, the percentage of PC12 cells in S phase in model group was increased (P