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The Study On Effect Of Officinalisininion Hypoglycemic Action And Neuroprotective Mechanisms

Posted on:2017-02-18Degree:MasterType:Thesis
Country:ChinaCandidate:J LiuFull Text:PDF
GTID:2284330485474144Subject:Biochemistry and Molecular Biology
Abstract/Summary:PDF Full Text Request
ObjectiveTo study the effect of Officinalisinin I on blood glucoselevel, discuss the mechanism of hypoglycemic and diabetes nerve injury protection.Methods(1) Experimental diabetic mouse model was induced by giving alloxan, and to observe the reducing blood sugar effects of Officinalisinin I.(2)To test the inhibiting ability of α- glycosidase with an in vitro α- glycosidase inhibitors screening model that has been established.(3) Use the preparation alloxan diabetes mice model, Observe GLP-1 change under the condition of different concentrations Officinalisinin I.(4) After long-term drug delivery, detection the change of blood sugar, BNDF and GSH-PX activity change(5)MTT was used to find the optimum concentration and reactive time of high glucose DMEM to PC12 cells, in the meantime, th the consumption of glucose and LDH leakage and SOD activity in PC12 cells were determind.(6) Application signal blocking agent SB203580 and BEZ235 to valuate the mechanism of Officinalisinin I.Results(1) Officinalisinin I can improve the glucose tolerance of diabetic mice.(2) Officinalisinin I can not inhibit the action of the α- glycosidase(3) Officinalisinin I can effectively improve the formation of GLP-1, and use this way to reduce blood glucose.(4) Officinalisinin I can effectively reduce the blood glucose levels of diabetic mice with long-term medication., and improve the formation of BNDF and GXH-PX activity(5) Officinalisinin I can significantly improve the damage caused by high glucose PC12 cell survival rate, and reduce the leakage rate of LDH.(6) Officinalisinin I can effectively improve the glucose consumption of PC12 cells and MAPK signal blocking reduced survival of PC 12 cells, PI3K inhibitor had no significant effect on PC 12 cells protection, but glucose consumption strengthen.Conclusion(1)Officinalisinin I by promoting glp-1 can effectively improve diabetes glucose tolerance in mice.(2) Long-term drug delivery of Officinalisinin I can significantly reduce the blood sugar of diabetic mice, and protect the nerve from diabetic damage(3) Officinalisinin I can improve the PC 12 damage and survival caused by high glucose, and improve the antioxidant ability of the cells.(4) Officinalisinin I can protect PC 12 cells significantly through MAPK signal pathway and may be through the PI3K signaling pathway to strengthen its glucose utilization.
Keywords/Search Tags:Diabetes, Glucose tolerance, Diabetic nerve injury, PC12
PDF Full Text Request
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