Objective To evaluate the protective effect of taurine on renal injury induced by high energy shock wave in rabbits.Methods Twenty rabbits were divided into the experimental (n=10)and the control group (n=10) at random.Both the groups were exposed to 1500 shock waves at 12.75 KV.In the experimental group, taurine (150 mg/kg) was given intravenously during the shock, while normal saline was given in the controls. Malondialdehyde(MDA) and superoxide dismutase(SOD) in serum were measured and the histological changes, the expression of heat shock protein 70(HSP70) in kidney were determined 3 days after the shocks.Results The level of MDA was(2.2±0.4) ,(2.1±0.4)mmol/L, and the level of SOD was (56.4±9.9) ,(55.8±10.1)μU/L respectively in the experimental and the control group before the shock.There was no significant difference between the two groups(P＞0. 05). After the shock, the level of MDA and SOD was (2.7±0.7)mmol/L, (55.3±5.7)μU/L respectively in the experimental group. There was no significant difference(P＞0.05) compared with the level of before the shock's. While in the control group, the level of MDA and SOD was (5. 7±0. 7) mmol/L, (33. 3±3. 5)μU/L respectively.There was significant difference (P＜0.05) compared with the level of before the shock's. The renal tubule scores of the experimental group and the control group after shocks were 7.2±0.8 and 31.8±1.9, respectively. And the HSP70 scores were 25.2±4.1 and 6.4±0.9, respectively. There was significant difference between the two groups (P＜0.05).Conclusions Taurine can effectively protect kidney from injury induced by high energy shock wave in rabbit.The mechanism may be related with its antioxidant capacity and inducing the synthesis of HSP70 in kidney.

OBJECTIVE:To compare the relative bioavailability and pharmacokinetic parameters of domestic ciclosporin soft capsules with those of imported ciclosporin soft capsules METHODS:The drug concentration in blood were assayed by TDx after administration of a single oral dose of 300mg domestic or imported ciclosporin soft capsules to each of 12 healthy male volunteers in a randomized crossover study RESULTS:The AUC were(10 47?1 74)?g/(ml?h)and(10 71?1 45)?g/(ml?h),the Cmax were(1 91?0 31)?g/ml and(1 88?0 22)?g/ml,Tmax were(1 46?0 26)h and (1 38?0 31)h,for domestic and imported soft capsules,respectively The relative bioavailability of domestic ciclosporin soft capsules to imported ones was (97 59?9 71)% CONCLUSION:The result showed that the two soft capsules were bioequivalent

AIM: To investigate the roles of angiotensin Ⅱ and NADPH oxidase in the development of renal oxidative stress (OS) in a rat model of hyperoxaluria. METHODS:Animal model of hyperoxaluria was established in a-dult male Sprague - Dawley rats by administration of 0.8% ethylene glycol (EC) in drinking water for 4 weeks. Simultaneous treatment with apocynin (0.2g·kg~(-1)·d~(-1))or losartan (30 mg·kg~(-1)·d~(-1) ) by intragastric administration were performed in rats, respectively. At the end of the study, markers for the state of oxidative stress (OS) , urinary 8 - IP and the enzymatic activity of superoxide dismutase ( SOD) in kidney homogenates were assessed. The concentration of angiotensin H in kidney homogenates was determined using radioimmunoassay method. Expression of NADPH oxidase subunit p47phox in kidney was localized and evaluated by immunohistochemistry and real time - PCR, respectively. RESULTS: p47phox expressed widely in the kidneys of this rat model, including renal cortex, inner medulla and outer medulla. Compared with the control, OS developed significantly in rats received EG, with increased expression of p47phox mRNA in kidneys. Renal angiotensin Ⅱ also increased significantly. Treatment with apocynin or losartan significantly reduced the excretion of urinary 8 - IP, restored the SOD activity, with decrease in the expression of p47phox mRNA in kidney, but the levels of those OS markers in apocynin or losartan treated rats were still higher than those in normal controls. CONCLUSION: Results suggest that renal Ang Ⅱ and its stimulation of NADPH oxidase may partially account for the development of OS in kidney in this rat model of hyperoxaluria.

ObjectiveTo observe the interaction of the calcifying nanoparticles (CNP) with human renal tubular epithelial cells (HK-2) in vitro,to observe and investigate the mechanisms of HK-2 injury induced by CNP,and to explore the potential role of CNP in the formation of Calcium oxalate kidney stones.MethodsHuman renal tubular epithelial cells were cultured in vitro and CNP was then added to the culture medium,the cell-crystal reaction was detected by light microscopy and transmission electron microscopy (TEM).To investigate the oxidative stress,NADPH oxidase inhibitor apocynin was chosen as the intervener.The levels of LDH,MDA,HA in the mediums after 24 h were assessed. ResultsCNP could induce changes of the HK-2.Adhesion and phagocytosis of CNP by the HK-2 were observed under TEM.After 24 h,the levels of LDH,MDA,HA were significantly different among the 4 groups ( P ＜ 0.05 ). ConclusionsHK-2 has abilities of adhering and phagocyting with CNP.CNP can cause damage induced by oxidative stress of HK-2.

Objective To investigate the protective effect of apocynin against renal oxidative injury in a rat model of hyperoxaluria. Methods Animal model of hyperoxaluria was established by administration of 0.8% ethylene glycol (EG) to adult male Sprague-Dawley rats in administration were performed in the rats. Markers of oxidative stress(OS) state, urinary H2O2 and 8-(so-prostaglandin IP), and renal injury were assessed at the end of the study. Expression and localization of NADPH oxidase subunits (p47phox, gp91phox, Nox-1) in kidneys were examined by immunohistochemistry, real-time PCR and Western blot, respectively. Results p47phox expressed widely in kidneys of model rats, including renal cortex, inner medulla and outer medulla. Compared with the control, OS and renal injury occurred in rats receiving EG, in accordance with the up-regulated expression of NADPH oxidase subunits in kidneys. Treatment with apocynin significantly reduced the excretion of urinary H2O2 and 8-IP, improved the creatinine clearance and the kidney/body weight, with the down-reguLated expression of NADPH oxidase subunits (except gp91phox mRNA) in kidneys, but the levels of OS markers in apocynin-treated rats were still higher than thoset of normal controls. Conclusions The increased expression of NADPH oxidase subunits is suggested to be partially accounted for the development of renal OS in this rat model of hyperoxaluria. Apocynin treatment is effective for renal protection in this model.

BACKGROUND: Acellular amniotic membrane used widely in treating ocular surface disease as well as extensive burn wounds due to its low antigenicity and excellent histocompatibility. However, it is poorly understood whether it can be used in repairing urethral defects.OBJECTIVE: To evaluate role and the feasibility of human acellular amniotic membrane (HAAM) in the rabbit urethral reconstruction.DESIGN, TIME AND SETTING: The randomized control experiment of animals was performed at the Laboratory Center of Guangxi Medical University between April and June 2007.MATERIALS: Thirty-two New Zealand rabbits were supplied by animal center of Guangxi Medical University. The human HAAM was obtained from Department of Obstetrics, First Affiliated Hospital of Guangxi Medical University.METHODS: HAAM was prepared by detergent-enzymatic approach. Firstly, the fresh amniotic membrane was protected with cross linking of 1% formaldehyde- 0.2% glutaral, digested with 0.125% trypsogen- 0.05 mol/L EDTA, followed by washing with 0.5% Triton X-100. Totally 32 New Zealand male rabbits were assigned into 3 groups: experimental group (n=12), control group (n=12) and sham operation group (n=8). Rabbits were prepared for urethral defects models in the experimental and control groups, which were repaired with HAAM or anastomosised directly. There was no urethral operation in the sham operation group.MAIN OUTCOME MEASURES: The growth of epithelial cells and smooth muscle cells, as well as inflammatory cell infiltration was observed by histopathologic examination at days 10, 21 and 42 after operation. The urethral pressure changes and urinary bladder was examined by retrograde urethrography at day 42 after operation.RESULTS: ①The prepared HAAM was translucent, there was no residual cells or fragments. ②The pathological section examination showed that in the experimental group, some epithelial cells has grown without acute rejection at day 10 after operation, and several layers of urothelium covered HAAM at day 21 with reduced inflammatory cell infiltration. At day 42, a sprinkle of smooth muscle grew in HAAM with few inflammatory cells. Urodynamic studies indicated that there were no significant difference among 3 groups in the bladder volume, maximum urethral pressure and minimum urethral pressure (P > 0.05). The weight of bladder had obvious difference between the sham operation and control groups (P < 0.05).CONCLUSION: HAAM is an ideal biomaterial with well histocompatibility, biocompatibility and low antigenicity. HAAM is a good choice for urethral reconstruction.

Objective To investigate the mechanisms of calculus crystal transport by macro-phage in kidney. Methods Hyperoxaluria rat model was established by administration of 1% ethyl-ene glycol and 1% ammonium chloride in drinking water. 24 h rat urine was collected, urinary oxalate were analyzed by ion chromatography. The expression and location of osteopontin and macrophage in kidney were observed by immunohistochemistry. Macrophage and calculus crystal at the basement membrane of renal tubular epithelial cells and interstitium were observed. Results The urinary ox-slate concentration were (0.22±0.13), (0.29±0.08), (0. 50±0.26), (0. 41±0. 22), (0.25±0. 12) ng/ml among these 5 groups. The osteoponitin expression was 0.16±0.04, 0.25±0.09, 0.37±0.10, 0.23±0.08, 0.19±0.02 respectively. The expression of osteopontin was positively correlated with urinary oxlate concentration(r=0.887, P<0.05). The macrophage at the basement membrane of renal tubular epithelial cells was 0.12±0.08, 0.19±0.06, 0.27±0.04, 0.16±0.03, 0.18±0.03 respectively. The macrophage distribution was positively correlated with the expression of osteopontin (r= 0.596, P<0.05). The macrophage moved from vessel to the basement membrane of loops of Henle, then disrupted and released the calculus crystal. Conclusions The macrophage might take part in the calculus crystal transport in kidney at the basement membrane of loops of Henle, which may be the source of Randall plaque. This process may be mediated by osteopontin.

Objective To investigate the mechanism of melamine-induced renal damage in rats.Methods 48 male SD rats were randomly divided into 4 groups with 12 in each group and feed for 3 months.Group A were the control group,feed with standard granule feedstuff and drinking tap water.Group B were stone-induced group,feed with granule feedstuff containing 3％ Mel and drinking tap water.Group C were feed with granule feedstuff containing 3％ Mel and drinking water containing 2％ taurine.Group D were feed with standard granule feedstuff and drinking water containing 2％ taurine.Every week 24 h urine was collected to test PH,SCr,uric acid,protein,8-IP,H2O2 and Mel level.All rats were sacrificed at the end of 3 months.Blood creatinine detection,renal pathology analysis ( HE and Oil ep-red O dyeing,immunohistochemical) and mitochondria separation and detection were undertaken. ResultsMel was not detedted in urine of Group A and Group D.The urine concentration of Mel in Group B and Group C in 1 week,2 weeks,3 weeks,4 weeks were 3.16 ±0.45,4.39 ±0.213,5.40 ±0.28,5.50 ±3.26 and 3.52 ±0.49,4.32 ± 0.135,5.34 ± 0.40,5.46 ± 2.99 mg/ml,respectively.Compared with Group A,the Mel concentration in urine of Group B and C were drug exposure time dependent.In Group A,the urine protein,urine creatinine clearance,serum creatinine,and renal/weight ratio were 6.45 ± 1.45 mg/24 h,28.0 ± 7.4mmol/l,0.56 ±0.03 ml · min-1 · 100g-1,2.29 ±0.89 mg/g,while in Group B and C,the urinary protein urine,serum creatinine,creatinine clearance,kidney/weight ratio were 14.56 ± 7.69,56.8 ± 5.2,0.29 ±0.05,4.16 ±0.27 and 16.44 ±6.29,55.8 ±7.4,0.30 ±0.07,4.40 ±0.56,respectively.Compared with group A,in Group B and C,the urinary protein increased significantly,urine creatinine clearance reduced,serum creatinine reduced,and renal/weight ratio increased.Compared with Group B,the improvement of renal function in Group C was not significant,and the decrease of serum creatinine and urinary protein were not obvious (P ＞ 0.05).In Group B and C,the urine H2O2,8-IP and mitochondrial oxidatie detection reagent SOD,GSH-PX numerical were 28.5 ± 5.2 mmol/1,3.26 ± 1.6 pg/ml,21.1 ± 7.8 U/mg prot,19.0 ±2.5 energy unit and 26.7 ±4.8 mmol/l,2.99 ±8.5 pg/ml,20.3 ±6.9 U/mg prot,17.9 ±4.8 energy unit,respectively.The difference between Group B and C was not statistically significant (P ＞0.05).Pathological analysis showed Mel was mainly concentrated in crystal tubular lumen (Group B and C),kidney interstitial damage was apparent,and kidney inflammation and fibrosis progressive developed with the increase of the drug exposure time. Conclusions Mel can induce kidney damage and stone formation in rats,and stone was mainly in tubular location in inner medullary zone.It is not the oxidative stress way that Mel leads to kidney damage.

Objective To investigate the protective effect of taurine on HK-2 cells exposed to oxalate (Ox) and calcium oxalate monohydrate crystal (COM) in vivo.Methods HK-2 cells,a proximal tubular epithelial cell line,were cultured.Five groups were divided in this study:control group (only HK-2 cells) ; Ox and COM group (HK-2 cells + Ox + COM) ; Taurine group (HK-2 cells + Ox + COM + Taurine) ; Apocynin group (HK-2 cells + Ox + COM + Apocynin) ; Catalase group (HK-2 cells + Ox + COM +Catalase).After 6 hrs,the cultures medias from each group were tested for LDH,H2O2,8-isoprostane,and MCP-1 protein.Cellular expression of MCP-1 mRNA and P47phox mRNA were determined by reverse transcriptase-polymerase chain reaction.After 24 hrs,cells livability was investigated by MTT.Results Compared with the control,cells livability was reduced when exposed to Ox and COM (P ＜ 0.05),Treatment with Taurine,Apocynin and Catalase significantly increased the cells livability (P ＜ 0.05).Compared with the control,the expression of LDH,H2O2,8-isoprostane,and cellular expression of MCP-1 mRNA and P47phox mRNA were increased following exposure to Ox and COM (P＜0.01,P＜0.01,P＜0.01,P＜0.01,P ＜0.05).Treatment with Taurine,Apocynin and Catalase significantly reduced the expression of LDH,H2O2,8-isoprostane,as well as the cellular expression of MCP-1 mRNA.Expression of P47phox mRNA in Taurine group was not reduced significantly (P ＞ 0.05).Conclusions This study showed that Taurine protected the HK-2 cells from oxidative injury exposed to Ox and COM by the pathway that may not be in relation to the inhibition of P47phox mRNA expression.

AIM: To investigate the protective effect of taurine on kidney in a rat model of calcium oxalate nephrolithiasis.METHODS: Animal model of calcium oxalate nephrolithiasis was established by administration of 2.5% ethylene glycol+2.5% ammonium chloride 2 mL two doses daily to adult male Sprague-Dawley rats in company with restriction of drinking water intake for 4 weeks.Four groups of 8 rats each were studied: group A,untreated control animals;group B,nephrolithiasis without treatment;group C,nephrolithiasis with taurine(2.0% mixed with the chow);group D,only taurine(2.0% mixed with the chow).Intake of drinking water in each group for each rat was limited to 20 mL/d.Indexes of oxidative stress(OS) and renal injury in urine and kidney,and the enzymatic activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) in mitochondria of homogenized kidney samples were assessed at the day when the rats were sacrificed.Crystals deposited in kidney were scored under light microscopy.Renal tubular ultrastruture changes were analyzed by transmission electron microscopy.Expression of macrophage cell marker CD68 in kidney was evaluated by immunohistochemistry.RESULTS: Compared to the control group,oxidative stress and renal injury were developed after induction of nephrolithiasis,in accordance with increase in expression of CD68 in kidney.The enzymatic activities of SOD and GSH-Px in mitochondria were decreased significantly.Administration of taurine significantly reduced OS and renal injury,as well as the crystals deposited in kidney.Expression of CD68 in kidney was also reduced,while the enzymatic activities of SOD and GSH-Px in mitochondria were improved significantly.CONCLUSION: Attributed to its antioxidant capacity,taurine showed renal protective action in this rat model of calcium oxalate nephrolithiasis.