Objective To investigate the effect of artorvastatin on macrophage accumulation in tubulointerstitium of unilateral ureteral obstructive (UUO) nephropathy and its possible mechanism.Methods Twenty-one rats were randomly divided into three groups: sham-operatipn, UUO, UUO+ artorvastatin. Immunohistochemistry staining of CD68 and M-CSF was used to define the macrophage accumulation and expression of interstitial M-CSF. Lipid profile in these groups was also determined. Results CD68 + cells and M-CSF expression were significantly increased at day 10 after UUO operation, this kind of CD68 + cell accumulation and M-CSF expression up-regulation were ameliorated by artorvastatin treatment. In UUO and atorvastatin treated groups, the number of macrophage was positively correlated with tubulointerstitial M-CSF expression. There was no significant difference about serum lipid among the three groups. Conclusion Atorvastatin can reduce interstitial macrophage accumulation in UUO nephropathy. This therapeutic effect might relate to down-regulation of tubulointerstitial M-CSF expression.

Craniocervical unstability may cause severe motor and respiratory compromise due to recurrent upper spinal cord and/or brain stem impingement.In recent years,by improving internal fixation materials and surgical techniques,the methods of surgical treatment of craniocervical unstability has made great progress.With the appearance of these new surgery and internal fixation methods,the successful rate and safety of the operation obviously increased and the complications was reduced greatly.We reviewed the surgery methods for craniocervical unstability in this article.

Objective To investigate the effect of positive ventilation pressure on the radiotherapy of primary cancer of stage Ⅲ.Methods 19 patients diagnosed as of primary,cancer of stage Ⅲ were randomly divided into two groups:the combining therapy group and the simple radiotherapy group.The patients of combining therapy group were treated with positive pressure ventilation using BIPAP respirator and radiotherapy.The recently therapy results and the radiotherapy associated side effects were observed between these two groups.Results(1)The combination of radiotherapy and BI- PAP provides significant superiority of local effects over radiotherapy.P

Objective To investigate the influence of fasudil on the epithelialmesenchymal transdifferentiation of renal tubular epithelial cells in diabetic rats and to explore the mechanism. Methods Wistar mts were randomly divided into three groups:control,diabetes and fasudil-treatment.All the rots were sacrificed after three months of feeding with or without fasudil.Pathological changes of the glomeruli and renal interstitium were studied by periodic acidSchiff'S staining and Masson staining,respectively.Expression of ROCKI,α-SMA,E-cadherin and the distribution of β-catenin was examined by immunohistochemistry.Changes in the MYPT1 phosphorylation profile and α-SMA,E-cadherin and membrane β-catenin expression were detected bv Western blot.Changes in the levels of ROCKI,E-cadherin and total β-eatenin mRNA expression were analyzed by real-time PCR. Results Fasudil treatment notably attenuated renal interstitial fibrosis in diabetic rats.Compared to the control rats.diabetic rats showed an elevated phosphorylation of MYFF1(P<0.01),increased expression of α-SMA(P<0.01),decreased expression of E-cadherin and membrane β-catenin(P<0.01,respectively)and increased expression of ROCKI,total β-catenin mRNA(P<0.01,respectively),decreased expression of E-cadherin mRNA(P<0.01 ). Fasudil treatment for diabetic rats attenuated MYPT1 phosphorylation (P<0.01), decreased α-SMA expression (P<0.01), increased E-cadherin and membrane (β-catenin expression (P<0.01, respectively), and reduced ROCKI, total β-catenin mRNA expression (P <0.01, respectively), increased expression of E-cadherin mRNA (P<0.01). Conclusions Fasudil may reduce the epithelial-mesenchymal transdifferentiation and renal interstitial fibrosis in diabetic rats through the inhibition of ROCK activity. Such effect further facilitates the recovery of the cell-cell adhesion among renal tubular epithelial cells and the formation of adhesion complex.

Objective To investigate the renoprotective effects of KB-R7943 on renal injury induced bycontrast media. Method Tubular epithelial cells were trested with varions cencentration of KB-B7943 (10-5,10-6 mol/L) for 12 hours before contrast media was used. After cells we, re incubated with contrast media (CM)(110 mgI/L) for 1 hour, cells injury was assessed by using LDH, and cell morphologic changes and cells apopto-sis were evaluated with inverted microscope and flow cytometry, respoelively. Intracellular Ca2+ and reactive oxy-gen species (ROS) were analyzed by using confocal microscope. The expression of Na+/Ca2+exchanger mRNAwas evaluated by RT-PCR. Mannitol with same osmolarity (20% mannitol, 770 mOsm/L) of CM was used as con-trol. One-way analysis of variance and q-test were used for comparison between groups. The simple linear correla-tion was employed to analyze the correlation. P < 0.05 was considered significant. Results Contrast media sig-nificantly induced tubular cells damage significantly and apoptosis at 1 hour after incubation, meanwhile, intracel-lular Ca2+ and ROS were inoreased progressively in CM group. KB-R7943 significantly attenuated cells damage andapoptosis in dose-dependent in association with decreased intracellular Ca2+ and ROS. Expression of Na+/Ca2+exchanger mRNA was not changed. Conclusions KB-R7943 has renoprotective effects on the contrast-media-in-duced renal tubular cyotoxicity

Objective To investigate the effect of surfactant protein A (SP-A) on the production of MIP-2 and binding activity of NF-?B in rat tubular epithelial cells, and evaluate its possible role in renal inflammation. Methods Confluent cultures of NRK-52E cells (a renal tubular epithelial cell line of rat origin) were pretreated with various concentrations of SP-A(0 to 80 ?g/ml) and stimulated by lipopolysaccharide (LPS) (10 ?g/ml) with 2% serum. MIP-2 expression was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The effect of SP-A on NF-?B binding activity was assessed by electrophoretic mobility shift assay (EMSA). Results MIP-2 mRNA and protein was expressed and up-regulated in NRK-52E cells stimulated by LPS. The expression of MIP-2 was down-regulated by SP-A. NF-?B binding activity was inhibited by SP-A in a concentration-dependent manner. Conclusion SP-A binding activity and down-regulates the expression of MIP-2 in renal tubular epithelial cells, which may play an important role in the modulation of renal tissue inflammation.

Objective To study the role of connective tissue growth factor(CTGF) and vascular endothelial growth factor(VEGF) in the early stage of compensatory renal growth,and to explore the mechanisms of renal compensatory hypertrophy on rat kidney following unilateral nephrectomy.Methods The 48 Sprague Dawley rats were randomly divided into 2 groups with 24 rats in each.The rats in the operation group were underwent right nephrectomy operation and those of the control group were without any treatment.Six rats of each group were sacrificed on the 1st,4th,8th and 16th day of the experiment,respectively.The immunohistochemical method was used to investigate the expressions of CTGF and VEGF in the remnant left kidney of rats in each group.Results In the operation group,the weight of left kidney was increased obviously and the left kidney on the 16th day was obviously heavier than that on the 1st day of the experiment(P

AIM: To investigate the relationship between change of inducible nitric oxide synthase (iNOS) and rat renal damage in dietary hypercholesterolemia. METHODS: High cholesterol (HC) group was fed with diet supplemented with 4% cholesterol and 1% cholic acid for 8 weeks. Another group was fed with normal diet. Expression of iNOS at protein level was evaluated by immunohistochemical staining and iNOS mRNA levels in renal cortex by reverse transcription-polymerase chain reaction (RT-PCR). The apoptotic cells in renal tissue at 8th week were evaluated by TUNEL method. RESULTS: Total serum cholesterol and LDL-cholesterol levels in HC group were higher than that in control group ( P

Objective To investigate the effects of fluvastatin on the tubulointerstitium damage in progressive diabetic kidney disease. Methods A rat model of type 2 diabetic nephropathy (DN) was developed successfully by combination of dietary induced insulin resistance and low dose STZ induced hyperglycemia after unilateral nephrectomy. Female SD rats were randomly divided into three groups: control rats, type 2 diabetic rats and type 2 diabetic rats treated with fluvastatin (2mg/kg/d). After 6 weeks, blood glucose, serum insulin, serum triglyceride and cholesterol, serum creatinine, and urinary protein were measured respectively. The protein expressions of c Jun and tansforming growth factor (TGF) ? 1 were studied by immunohistochemistry. TGF ? 1 gene expression was studied with a RT PCR technique. Results Fluvastatin at lower doses, which did not influence blood glucose and blood lipid level, significantly inhibited expression of c Jun protein(0 2536?0 0180 vs 0 5855?0 0314, P

Objective To investigate whether the effect of contrast media on renal tubular cell apoptosis is mediated via mitogen activated protein kinase(MAPK) activation. Methods NRK 52E cells were incubated in cell culture media[+1%fatel calf serum (FCS)] containing buffer (control) or increasing concentrations of diatrizoate or iohexol for various time periods. In separate experiments, NRK 52E cells were incubated with diatrizoate in the presence of 10 or 20 ?mol/L SB203580, an inhibitor of p38 MAPK, for 4 h. Cell membrane integrity was assessed by trypan blue exclusion experiment. Apoptosis was assessed by flow cytometric DNA analysis, FITC Annexin Ⅴbinding/PI staining and electron microscopy. MAPK activity and phosphorylation was evaluated by immunoprecipitation and Western blot analysis. Results Diatrizoate, a kind of hyperosmolal contrast media, induced apoptosis in cultured NRK 52E cells in an osmotic pressure and duration dependent manner. Iohexol, another kind of less hyperosmolal contrast media, could not induce NRK 52E cells apoptosis. In NRK 52E cells incubated with diatrizoate, the level of p38 MAPK phosphorylation and activity increased after 15 min, and remained elevated even at 1 h. In contrast, the level of total p38 protein was not changed in whole experimental period. SB203580 significantly inhibited apoptosis in NRK 52E cells incubated with diatrizoate. The level of p44/p42 MAPK phosphorylation was not changed in whole experimental period. Conclusions Contrast media induces apoptosis in cultured NRK 52E cells in an osmotic pressure and duration dependent manner, which is related to the hypertonicity of contrast media. Contrast media induces apoptosis in NRK 52E cells via activation of p38 MAPK.