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.

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

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 renoprotective effect of erythropoietin(EPO) in streptozotocin-induced diabetic rats and to explore the possible mechanism.Methods The SD rats were randomly divided into there groups: normal control rats, diabetic, diabetic treated with EPO(NC, DM, DE groups).The rats were sacrificed after 8 weeks treatment.Renal morphology was observed by light microscopy.The expression of erythropoietin receptor(EPOR) in kidney was detected by immunofluorescence and Western blotting.The expression of p47phox, transforming growthfactor (TGF)β1andfibronectin (FN)proteininkidneywasdetectedby immunohistochemistry and Western blotting.The activity of antioxidants including total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the level of malondialdehyde(MDA) in kidney were also measured.Results EPO treatment notably attenuated renal pathologic and functional changes.The expression of EPOR was found in kidney,but there was no difference among groups(P＞0.05).Compared with normal rats, diabetic rats showed an elevated expression of p47phox, TGF-β1, FN proteins and MDA levels in kidney as well as reduced activities of SOD, GSH-Px and T-AOC (all P＜0.01).Compared with diabetic rats, EPO could decrease the protein expression of p47phox,TGF-β1and FN in kidney (all P＜0.05).Meanwhile, elevated MDA level in the kidney was decreased as well as decreased SOD, GSH-Px,T-AOC activities were significantly remitted in DE group(all P＜0.01).Conclusion EPO can amelioraterenaldamagevia theinhibition of oxidativestressandTGF-β1andFNprotein expression in streptozotocin-induced diabetic rats.

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 observe the release of inflammation-related factors after angiotensin Ⅱ (Ang Ⅱ ) stimulation in rat tubular epithelial cells (NRK-52E), to analyze whether these effects were mediated by TLR4-MyD88 pathway, and to reveal the novel mechanism of injury by Ang Ⅱ on NRK-52E cells. Methods After synchronization, cells incubated with AngⅡ (10-7 mmol/L) were used as the stimulation group, cells without stimulation were as normal control. To determine the role of TLR4 and the adaptor MyD88, equal number of NRK-52E cells was added with 10-5 mmol/L candesartan or 20 mg/L TLR4 blocking peptide for 1 h and then incubated with Ang Ⅱ (10-7 mmol/L) respectively. RT-PCR was used to analyze TLR4 mRNA and MyD88 mRNA expression. Immunofluorescence and confocal microscopy were used to observe TLR4 protein expression. ELISA was used to detect the concentration of tumor necrosis factor-alpha (TNF-α) and heat shock protein 47(HSP47) in cell supernatant respectively. Results TLR4 and MyD88 were highly expressed in Ang Ⅱ-induced NRK-52E cells (P＜0.01), and the TNF-α and HSP47 levels were also increased markedly compared with control group (P＜0.01). In NRK-52E cells that were pre-incubated with candesartan, TLR4 and MyD88 expression were obviously inhibited,subsequently, HSP47 and TNF-α production decreased remarkably compared with Ang Ⅱ group (P＜0.01). TLR4 blocking peptide had the similar effect in a dose-dependent manner, in which its effect was dependent on inhibiting TLR4-MyD88 expression. Conclusion The mechanism of Ang Ⅱ -induced injury effect on NRK-52E cells is related to the increase of TLR4-MyD88 activity,which is followed by the enhance of TNF-α and HSP47 expression. This process is inhibited by candesartan via modulation of innate immune pathway.

Objective To investigate whether erythropoietin (EPO) can inhibit the proapoptotic effect of high glucose on rat proximal tubular epithelial cells, and the possible mechanisms in which EPO exerts its anti-apoptotic role. Methods Rat proximal tubular epithelial cells (NRK-52E) were divided into 5 groups: normal control group, osmolarity control group, high glucose group, high glucose with EPO (50 U/ml) group and high glucose with EPO (100 U/ml) group. The expression of EPO receptor (EPOR) in NRK-52E cells was examined by immunocytochemistry. The effect of high glucose on the expression of EPOR was detected by Western blotting. The rate of apoptosis was evaluated by flow cytometry Annexin V-FITC/PI double stains. The intracellular ROS was detected using fluorescent probe CM-H2DCFDA. The expression of bcl-2, bax and caspase-3 mRNA were examined by RT-PCR. Results The expression of EPOR was demonstrated in NRK-52E cells, and high glucose could up-regulate the expression of EPOR. High glucose could induce oxidative stress in NRK-52E cells, and up-regulate the mRNA expression of bax and caspase-3, down-regulate the mRNA expression of bcl-2. These effects of high glucose on NRK-52E cells could be reversed by EPO. Conclusion EPO inhibits NRK-52E cells apoptosis induced by high glucose through attenuating oxidative stress,up-regulating theexpression of bcl-2 mRNA and down-regulating the expression of bax and caspase-3 mRNA, which may be mediated by EPOR.

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