Hydroxyproline Lead To Kidney Damage And Kidney Stone Model In Rats

Objective: Determine in SD rat models, hydroxyproline (HP) diet can causekidney damage and kidney stones, and the analysis of the composition of stones.Do the process of the formation of lithogenic preliminary in this paper. Thepurpose is further study of kidney damage mechanism and stone formationmechanism of experimental basis.Methods:24male and female SD rats were randomly divided into large dosefeeding hydroxyproline group tendency for19.1/kg (2.5g/kg), small dosefeeding hydroxyproline group tendency for9.6/kg (1.25g/kg) and blankcontrol group (distilled water), adopt the method of filling the stomach to feedfour weeks. Before feeding to weigh each rat body weight, weighing again indrug withdrawal rat body weight, and detection of SD rat serum creatinine,blood urea nitrogen and observed under light microscopy in the rat kidneypathological changes, and if there is a stone formation into stone analysis wascarried out on the stone.Results: Use hydroxyproline preparation liquid lavage after4weeks, A group ofeight SD rats form mental weariness, acupuncture reaction is A bit slow, activityless, eat less, and there are four rats appear brown yellow hair, and A controlgroup appear slightly smaller size. Group B in lavage after4weeks,5rats inacupuncture only slow, activity less, eat less, and there is only1rats appear hairbrown yellow, and smaller slightly compared with controls. Control group to observe group C has no obvious abnormalities. Medication before each weight(176.6±9.1,174.9±11.5,169.4±14.9) g, dosing after4weeks according toweight each SD rats (166.0±9.5,169.5±9.5,172.5±14.2) g, the control groupC rats weight gain, there is a decrease in the group B part of the body weight ofrats, statistical analysis, there was no statistically significant difference. Group A,on average, losing weight is about10.6g, the weight and dosing changes beforeline statistical analysis of the difference was statistically significant (P <0.05).Experimental animals eat hydroxyproline preparation after fluid, group A andgroup B were no death of SD rats, observed the kidney pathological, group Bdid not see have kidney crystallization, group A were renal crystal form, crystalis relatively more, but did not see have stone, no death and no control group Crenal crystal formation.4weeks after the treatment, each value of blood ureanitrogen (43.0±11.1,13.0±3.0,7.2±0.4) the tendency for l, groups of serumcreatinine value is (167.0±19.7,62.0±5.6,49.0±4.9) umol/l, A set of eight SDrats blood urea nitrogen and serum creatinine were higher than reference range;Group A, blood urea nitrogen and serum creatinine compared with the controlgroup C difference was statistically significant (P <0.05). Group B7SD ratsblood urea nitrogen is higher than the reference range, the difference wasstatistically significant compared with the control group C (P <0.05), group B3only SD rats serum creatinine is higher than the reference range, compared withthe control group C difference was statistically significant (P <0.05), comparedwith group B, group A difference in the comparison of serum creatinine and ureanitrogen had statistical significance (P <0.05).8group A only2in the SD ratrenal biopsy only see around the renal tubules tan crystal, spread out in A tubularepithelial shedding necrosis, interstitial small amounts of neutrophil infiltration, renal tubular cell edema. Another5group A rat renal biopsy small district seelittle crystals, cortex, not seen in inflammatory cells infiltration, local necroticinflammatory cell infiltration, renal tubular expansion, loosely arranged cells.Group A last1rat renal biopsy only see the collection tube crystals, visiblestromal hyperplasia of fibre involving renal tubules, tubular cell edema, Ahandful of glomerular necrosis. In group B8only SD rats4rat renal biopsy onlysee partial necrotic inflammatory cells infiltration fiber hyperplasia, visiblefibrous hyperplasia involving renal tubules, tubular epithelial edema, necrosisand inflammatory cells infiltration is light, not seen. B group and the other4SDrat renal biopsy did not see crystallization, renal interstitial less granulocyteinfiltration, mild edema, a small amount of interstitial cell hyperplasia.Malpighian tube cavity expansion, wall thinning, interstitial fibrosis, part of theglomerulus atrophy. Group C8SD rat renal cortex and medulla no crystals form,did not see epithelial cells degeneration, no inflammatory cell infiltration,glomerular morphology was normal, normal renal tubular form.Conclusions:1、4weeks after feeding large doses of hydroxyproline, kidney ofrats can appear obvious pathological damage and stone of crystallization.2、Renal tubular and glomerular pathological damage, and renal tubules have stonecrystal forms, as the hydroxyproline intake increase, the severity of thepathological damage and deepening of crystallization.3、To SD rats fedhydroxyproline can effectively establish the experimental model of kidneydamage and renal calculi.