Effects Of Chitooligosaccharide On The Mice Hyperuricemia Model Induced By Yeast And Adenine

High intake of food that contens high amounts of nucleic acid greatly increase purine contents in the body after they are degradated. Among these metabolites, adenine is transformed into uea acid after the oxidation by xanthine oxidase (XOD).Uric acid is poorly dissolved in water, and will separate out as crystalline from water at high concentration. Uricase in mammalian animal body can transform uric acid into allantoin and evacuate.Unfortunatey the gene encode the uricase in human body mutated thousands years ago, so adenine is degradated into Uric acid. Two thirds uric acid it is excreted by the kidney and the rest is eliminated via the gastrointestinal tract. The uric acid level in the body is determined by the degradation speed of adenine as well as the speed of being excreted by kidneys and gastrointestinal. When Uric acid is produced more than it can be excreted sufficiently, hyperuricemia occurs in the body. The rate of hyperuricemia is increasing rapidly these yearspartly due to the modern lifestyle. Hyperuricemia is colsely related to gout, high uric acid nephropathy, hypertension, hyperlipidemia, high insulin deficiency and becomes a disease threating our health.Chitin is the second most abundant biopolymer on earth after cellulose, and chitooligosaccharide(COS) is the derivative of chitin after degradation and deacetylation. COS has good physical and biological characteristics of low molecular weight, good water-solubility, good absorbability and avirulence and is becoming more attractive to researchers. COS has been reported to have unique biological functions such as immunity enhancing, regulating plasma liquid and antitumor effects. COS has also been found to have the function of liver and acute renal failure protection. Because of its various biological activities, COS has become a potential consideration to be utilized in many fields.In the present study, mice hyperuricemia model is established by intragastrically administration of ademine and yeast. Hyperuricemia mice were treated with different doses of COS to investigate its uric acid lowering properties. Serum biochemical factors including creatinine(Cr), urea nitrogen(BUN),Uric acid(UA) and XOD activities of liver homogenate are detected to evaluate the therapeutic function of COS. Kidney histopathology were conducted to futher analyze the protection of COS to kidney tissue.It is revealed from the data of serum Cr, BUN and UA that the model of mice hyperuricemia is established successfully. On the 14th day after treatment with COS, serum Scr,BUN and UA values were decreased to 70.22%,64.78%,69.08% of model group. XOD is the most key enzyme controlling the UA synthesis. XOD activity assay of liver homogenate showed that COS can inhibit XOD activity of liver homogenate which were inceased in model group. Histological observation results showed that glomerular of negative group becomes loose, renal parenchymal presences interval, tubular expands. The kidney in COS protection groups develop better than negative group with complete glomerular structure, neat tubular epithelial cells. In a conclusion. our results indicate that COS has good protective effects on kidney in hyperuricemia mice.