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18β Glycyrrhetinic Acid And Pederin Intervention Mechanisms Of The Complications Of Diabetes-Encephalopathy And Ulcers

Posted on:2013-10-02Degree:MasterType:Thesis
Country:ChinaCandidate:F WangFull Text:PDF
GTID:2234330374477422Subject:Zoology
Abstract/Summary:PDF Full Text Request
According to World Health Organization survey, the number of the world with diabetes up to about246million, while China become the world’s diabetes "superpower" with92.4million the number of patients. Complications of diabetes podiatry (foot gangrene), renal disease (renal failure), eye disease (blurred), brain (cerebrovascular disease), heart disease, skin disease and peripheral microvascular disease, etc., can lead to diabetesdeath in patients with major factor. Glycyrrhetinic acid extracted from licorice, is a biological active substance, anti-inflammatory, antiviral, anticancer, antidiabetic, and immunomodulatory, and neuroprotective and enhanced memory function. The subject of the use of18β-glycyrrhetinic acid in diabetic rats to a six-week intervention, and through experimental means of the water maze and LTP, and immunehistochemistry for18p-glycyrrhetinic acid mechanism of action of anti-high blood glucose for the study of diabetes encephaloathy causes and treatment methods to provide further theoretical basis. After six weeks of intervention, treatment of rats in the Morris water maze test performance significantly better than the diabetic control group and normal control group similar to; electrophysiological LTP experiments, the treatment group were successfully guide the enhancement effect for a long time, and lasts60minutes; immunohistochemistry the a7nAChR, ChAT and aCaMK Ⅱ, GLUR2and NGF-β protein expression were higher than the diabetic control group. These experimental results show that18β-glycyrrhetinic acid caused by high blood glucose of diabetic rats, weight loss, learning memory and cognitive decline and lower a7nAChR, ChAT, aCaMK Ⅱ, GLUR2and NGF-β1protein expression has a certain role in mitigation.The surface of chronic refractory wounds (ulcers) caused by a series of injuries and diseases, including traumatic ulcers, lower extremity venous ulcers, pressure ulcersand diabetic ulcers. This type of wound, though not as dangerous, such as malignant tumors, but due to the longer duration, complications and impact on the appearance of the high cost of treatment, and caused great harm to the patient’s life and quality of work, thus causing the parties attach great importance to and competing to carry outthe study. In this study, Paederus extract pederin as confounding factors, and four weeks of the intervention treatment of diabetic skin ulcers model. After the intervention in the treatment of ulcers skin testing, and diabetic rat skin ulcers healed significantly faster than in the control group, and the healing effects oflow dose treatment group in the high dose group. The pederin on the diabetic rat skin ulcers have a certain role in therapeutic intervention, and have a better therapeutic effect in the concentration of0.1mg/ml. PDGF and VEGF, platelet-derived growth factor and vascular endothelial growth factor, and the expression of these two protein enhanced regeneration of blood vessels capacity. PDGF in clinical practice often bFGF and IGF-1and EGF combination treatment of diabetic skin ulcers, VEGF has also been reported in clinical diabetic skin ulcers, PDGF and VEGF protein expression increase in the amount, can effectively enhance the healing rate of ulcers. NGF-β is an eurotrophic factor, and Trk-A and p75NTR is two receptors of NGF-β.Their expression may reflect the ulcers of the skin nerve growth, and increased protein expression, indicating that the skin ulcers. The nerves are growing, and the wound to accelerate healing. The pederin, therefore, increase the protein expression of PDGF, VEGF, NGF-β, Trk-A and p75NTR five genes, and accelerate the blood vessels and nerve regeneration, so as to achieve the treatment of diabetic skinulcers.
Keywords/Search Tags:Diabetes, Encephalopathy, Ulcers, Water Maze, Long-term potentiation, H.E.staining, Immunohistochemistry
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