Effect Of Hyperlipidemia On Rodent Model Of Renal Calcium Oxalate Crystal Deposition

Background:Kidney stones is a clinincal common and frenquently occurring disease whichseriously influence the health of human body,Although technology of kidney stones’diagnosis and treatment made a great progress in the past deccades,the rate of incidenceand recurrence still matains high.The main reason is that at present the pathogenesis ofkidney stones is not clear and relevant research progress is relatively slow.So theConvenient and stability experiment of animal calcium oxalate stone model is animportant tools and ways in the clinical and basic research of kidney stones,which made aimportant significance to exporing the kidney stones and controling mechanismIn recent years, large epidemiological studies found that metabolic factor such asobese, insulin resistance and type2diabetes, urine pH lower and Hypertension not only isthe risk of deeloping kidney stones, but also closely related to the evolution of the stone.At present the metabolic syndrome factor of a single concrete how to take part in stoneformation process relatively weak. At present in metabolic syndrome the factor of singleconcrete how to take part in the progress of stone formation is relatively weak.Dyslipidemia as the key component of the metabolic syndrome,which has not seen basicresearch on the influence of stones generation.From ingredients of kidney stones, the priority of Human kidney stones mainlycontains calcium stones,i n which calcium oxalate stones contains the most about80%ofthe total number of stones. The mainstream view believe that the main mechanism ofcalcium oxalate stone formation is calcium oxalate crystal of nucleation, growth, gatheredin in the renal tubules,urine composition supersaturated separation is just one condition ofstone formation. In normal physiological state, due to the effect of urine flushing thecrystal of calcium oxalate which in Renal rubualr cannot be form stone in renal tubular.Only in the injury of renal tubular epithelial, The crystal of Urine calcium oxalate canstick, growth and gathered in the renal in or form "ShiBan on the surface of kidneynipple,after a series of reactions and create the calcium oxalate stone.Therefore, the deposition of calcium oxalate crystallization is considered as gererated important basis ofcalcium oxalate stone, Establish a mature, stable calcium oxalate crystallization modelplays an important role in researching early generating mechanism.of calcium oxalatestone.Objective:by intraperitoneal injection of glyoxylate to increase urinary oxalate excretion, withthe renal tubular injury factors, Establish a model calcium oxalate crystal in short time.Hyperlipidemia which induced by apolipoprotein E gene defects in mice or low densitylipoprotein receptor deficient mice increase the glyoxylate-induced renal calculi; oxidant/antioxidant balance disorders, systemic systemic promote calcification factor is thepossible mechanism.Research methods:.the first part to give of C57BL/6, BABL-c,129S three strains of mice byintraperitoneal injection in vivo metabolism of ethylene glycol intermediates glyoxylate toincrease urinary oxalate excretion, supplemented by renal tubular epithelial cell agentschlorine ammonium to establish a model of murine renal calcium oxalate crystallization.HE staining of mouse renal calcium oxalate crystallization generated, and each group ofmice renal tissue calcium content for quantitative detection. The second and third partswere used ApoE-deficient mice and LDLR-deficient mice induced the hyperlipidemiamouse model. hyperlipidemia mouse model to establish the crystallization of calciumoxalate model. HE staining of mouse renal tissue calcium oxalate crystals to generate, anddetermination of renal tissue and serum calcium and vitamin E content. and correlationanalysis of renal tissue calcium content and lipid levels, and monitoring of renal tissue ofOPN expression.Results:The three strains of mice by intraperitoneal injection of glyoxylic acid method,supplemented with1%ammonium chloride drinking water successfully established renal calcium oxalate crystallization model in7day. Hyperlipidemic induced by defective ApoEand LDLR deficient mice to increase the formation of glyoxylate-induced kidney calciumoxalate crystallization. Immunohistochemical detection of significantly increased relativeto the control group, hyperlipidemia mouse renal tissue with tubular and interstitial renalpieces of OPN expression. Detection of calcium and vitamin E levels, low levels ofvitamin E in the mouse model of hyperlipidemia in renal tissue, blood, high levels ofperformance. Conclusions:(1) by intraperitoneal injection of glyoxylate, and supplementedwith ammonium chloride-water method successful create a renal calcium oxalatecrystallization mode in7daysl, which combines the characteristics of acute kidney injuryand chronic fibrosis.2This study demonstrated that mice hyperlipidemia caused by apoEdeficiency and LDLR defects can increase the formation of glyoxylate-induced kidneycalcium oxalate crystallization; oxidant/antioxidant balance disorders, systemic factors ofsystemic promote calcification The dyslipidemia mice induced the possible mechanism ofstone.