The renin-angiotensin system plays an important role in the progression of chronic renal diesases. At present, the main approach for treating the chronic progressive renal disease is to block the role of renin-angiotensin system. Recently, angiotensin receptor blockers have being realized in width with its few side effect and good safety. A number of experimental and clinical resultsin recent 10 years have indicated that ARB can prevent or even reverse the progression of chronic renal diseases in many ways effectively and provided great evidences for current therapy of CPRD.

Objective To study the clinical and pathological features of idiopathic membranous nephropathy(IMN),which has not been able to diagnose only by light microscopy.Methods Nine cases which has not been diagnosed as IMN only by light microscopy from January 1998 to March 2005 were selected.We analyzed their clinical manifestation and pathological findings.Results One case was 6-year old child,who had nephrotic syndrome(NS).The other 8 cases were 45~70 year old adult,their clinical diagnoses being chronic glomerulonephritis or asymptomatic hematuria and /or proteinuria.Light microscopic diagnoses were minor glomerular abnormalities and focal proliferative glomerulonephritis.Immunofluorescence demonstrated scattered granular deposits of IgG along the capillary walls.Under the electron microscopy,small high density deposits were observed along the basement membrane,mainly stage Ⅰand Ⅱ.2 cases were complicated with thin membrane disease.Conclusion Chronic glomerulonephritis or asymptomatic hematuria and /or proteinuria often mixes slightly with IMN which is difficult to be diagnosed clearly depending on simple light microscopy.Therefore,it is very important to diagnosis to perform immunofluorescence and electron microscopy further.

Antibody arrays, as a specific subset of protein arrays,are now used in a wide variety of applications. Although having evolved into indispensable tools for proteomic studies, they seems to be still at the middle point on the way to the final destination to have the antibody arrays with high sensitivity, minimized size and wide dynamic detection range to meet the needs for the detection of different samples. This article reviewed the recent development regarding how to improve the detection sensitivity of the antibody arrays.

Objective To evaluate the therapeutic effect of 89 Sr internal radiotherapy on multiple-bone metastasis of cancer. Methods Forty-nine cancer patients with multiple-bone metastasis received 89 Sr internal radiotherapy. The pain control effect, life quality improvement, change in levels of blood calcium and serum alkaline phosphatase (ALP), and side effects were analyzed respectively. Results The total effective rate of pain control was 77.6 %. The life quality was improved obviously. The levels of blood calcium and ALP were decreased. No obvious side effects were found during the treatment. Conclusion 89 Sr internal radiotherapy had a good therapeutic effect on multiple-bone metastasis of cancer.

Objective To investigate the effects of nephroblastoma over-expressed protein (CCN3) on the formation of extracellular matrix (ECM) induced by transforming growth factor-β1 (TGF-β1) in human mesangial cells (HMCs) and its underlying signal transduction mechanism related with microRNA-29(miRNA-29).Methods HMCs were pretreated with different doses of exogenous CCN3 (5 μg/L,50 μg/L and 500 μg/L) or transfected with pcDNA3.1(+)-CCN3 before exposed to TGF-β1(2 μg/L),to observe the expression of fibronectin (FN),type I collagen (COL I) and miRNA-29a,b and c.The mimics or inhibitor of the miRNA-29a were transfected into HMCs to analyze whether miRNA-29a affect CCN3.The expressions of FN mRNA,COL I mRNA and miRNA-29 family were detected by real time PCR.The protein expressions of FN and COL I were detected by Western blotting and cell immunofluorescence.Results (1) Compared with the normal control group,the expressions of FN and COL I were up-regulated in TGF-β1 group,while the expressions of miRNA-29a,b,c were down-regulated in TGF-β1 group (all P ＜ 0.05).(2) Compared with the TGF-β1 group,the expressions of FN and COL I were decreased when pretreated with the different doses of exogenous of CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P ＜ 0.05).Meanwhile,the expression of miRNA-29a was significantly increased when pretreated with 50 μg/L and 500 μg/L CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P ＜ 0.05);whereas miRNA-29b and c had no statistical difference (all P ＞ 0.05).(3) Compared with TGF-β1+CCN3 group,the expressions of FN and COL I were decreased in CCN3+TGF-β1+miRNA-29a mimics group (all P ＜ 0.05),whereas the expressions of FN and COL I in CCN3+TGF-β1+miRNA-29a inhibitors group were increased (all P ＜ 0.05).Conclusions CCN3 reduces the TGF-β1-induced production of ECM by the up-regulation of miRNA-29a.

The effect of rosiglitazone and advanced glycation end products (AGEs) on the expression of fractalkine in cultured human renal mesangial cells (HRMC) were investigated. Rosiglitazone inhibits the upregulation of fractalkine induced by AGEs in HRMC.

Objective To observe NLRP3 inflammasome expression and inflammatory cells infiltration in the BSA-overloaded rats kidney,and to investigate the potential mechanism of renal injury induced by proteinuria.Methods After unilateral right nephrectomy,eighteen healthy male Wistar rats were randomly divided into two groups:protein overload nephropathy model group (n=10),treated with intraperitoneal injections of bovine serum albumin (BSA); control group (n=8),treated with intraperitoneal injections of 0.9％ saline for 9 weeks.Body weigh were measured every week and 24 h urine were collected in 0,2,5,7,9 week.The plasma levels of blood total protein (TP),albumin (Alb),serum creatinine (Scr) and blood urea nitrogen (BUN) were determined by automatic analyzers.Renal pathological changes were evaluated by PAS and Masson stains.Immunohistochemical staining was used to detect the expression of NLRP3,caspase-1,IL-1β,and IL-18,as well as the types of inflammatory cells.The NLRP3,caspase-1,IL-1β,and IL-18 protein and mRNA levels were also analyzed by Western blot and real-time PCR in two groups.Results It was found that there was a significant increase of proteinuria and BUN in model group compare to that in control group (all P ＜ 0.05).However,there were no significant changes in body weight,TP,Alb and Scr between the two groups.Morphological study demonstrated that renal tubular epithelial cell injury,proteinaceous casts in tubular lumen,accompanying with the dominant macrophages and lymphocytes infiltration in interstitium in model group.The immunohistochemistry showed that there were more T (CD3+),B cells (CD20+) and macrophages (CD68+) in renal interstitium in model group than that in control group (P ＜ 0.05).Tubulointerstitial injury score was higher than that of the control group (P＜0.05).Immunohistochemistry,Western blot and real-time PCR all showed that the expression of NLRP3,caspase-1,IL-18 and IL-1 β were significantly increased compared to those in control group (P ＜ 0.05).Furthermore,there were significant correlations between proteinuria and IL-lβ/IL-18 expression (P ＜ 0.05).Conclusion NLRP3 inflammasome activation is involved in tubulointerstitial inflammation caused by proteinuria.

AIM: To investigate the effect of L-arginine(L-arg) on the production of collagens of human mesangial cells. METHODS: Radioimmunoassay, hydroxyproline colorimetric assay and reverse transcription polymerase chain reaction (RT-PCR) were used to determine procollagen Ⅲ, total collagen level in the supernatant and expression of collagen Ⅳ mRNA in human mesangial cells. RESULTS: L-arg significantly inhibited the production of procollagenⅢ, total collagen in the supernatants ( P

Objective To investigate the effect of tumor necrosis factor ot (TNF-α) on monocyte-renal tubular epithelial cell adhesion and to explore its associated mechanism. Methods Human renal proximal tubular epithelial cell line (HK2 cells)and monocyte cell line (U937)were used to perform cell co-culture. TNF-α (10 μg/L)was used to stimulate HK2 cells and then U937 was put into the HK2 monolayers. Three locational parts of hyaluronan around HK2 cells were extracted by different ways and the HA expression was detected by enzyme-linked binding protein assay. Monocyte adhesion was detected by florescence recording assay. Flow cytometry was applied to assess intercellular adhesion molecule-1 (ICAM-1) expression in HK2 cells. Results Stimulation of HK2 cells with TNF-α significantly increased U937 binding to HK2 cell monolayer [(2.25±0.05) folds vs control, P<0.01]. Incubation of TNF-α (10 μg/L) with HK2 cells for 24 hours did not induce the change of total HA expression surrounding the HK2 cells, whereas HA redistribution happened with conditioned medium fraction (CM-HA) increased [(1.17±0.16) fold vs control, P<0.05], the pericellular fraction (trypsin extract fraction, TE-HA) decreased (83%±11% vs control, P<0.05) and the remaining cells-associated HA (cell associated fraction, CA) did not change significantly. In addition, pre-treatment of HK2 cells with TNF-α significantly increased the ICAM-1 expression [(1.85±0.22) folds vs control, P<0.01] and ICAM-1-dependent monocytes binding. Removal of HA from the surface of confluent monolayers of HK2 cells by hyaluronidase before addition of U937 cells increased monocyte binding[ (1.35±0.06) folds vs control, P<0.05]. In contrast, the presence of either sICAM-1 (400 μg/L) or anti-CDI8 antibody (10 mg/L) led to a significant decrease in ICAM-1-dependent monocyte binding (78%±7%, P<0.05; 75%±8%, P<0.01 vs those before adding sICAM-1 or anti-CD18 antibody, respectively). Conclusion HA redistribution induced by TNF-α may facilitate ICAM-1-dependent monocyte-epithelium binding, and pericellular HA plays a protective role in monocyte-driven tissue inflammation.

Objective To investigate the influence of Cordyceps polysaceharide (Cp) on epithelial-to-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1)in proximal tubular epithelial cells (PTEC). Methods HK-2 cell proliferation was determined by MTT assay. After incubation of HK2 cells with increasing concentrations of TGF-β1 (0, 0.1, 0.5, 1, 5, 10 μg/L) at 48 h and with TGF-β1 (5 μ/L) at different time points, E-cadherin, α-SMA, FN expression at transcriptional and protein levels were detected by real-time PCR and Western blotting respectively. The cells were pretreated with 1,5, 10 g/L Cp respectively for 24 h before adding TGF-β1 (5μg/L), then the cells were incubated for additional 48 h, mRNA and proteinexpression of above 3 cytokines was examined by real-time PCR and Western blotting as well. Results CP alone (0.01, 0.1, 1,5, 10 g/L) induced HK-2 cell proliferation in a dose-dependent manner. TGF-β1 enhanced α-SMA, FN expression while inhibited E-cedherin expression at both transcriptional and" protein level in HK-2 cell. At transcriptional level, compared to single TGF-β1 (5 μg/L) stimulating group, after Cp (1,5, 10 g/L) pretreatment for 24 h, the inhibition rate of a-SMA mRNA was 37.98%, 68.08% and 84.36%, respectively; FN mRNA was 46.97%, 63.82% and 81.85%, respectively; E-cadherin was up-regulated by 0.67 fold, 2.69 folds and 5.43 folds, respectively (P＜0.05). At protein level, the inhibition rate of α-SMA was 33.40%, 47.75% and 68.50%, respectively; FN was 16.26%, 65.92% and 80.30%, respectively; E-cadherin was up-regulated by 1.33 folds, 3.19 folds and 4.29 folds, respectively (all P＜0.05). Under Light microscopy, the Cp reversed cell shape from spindle-shape induced by TGF-β1 to nearly normal shape. Conclusion Cp may exert its inhibitive effects on TGF-β1-induced EMT.