Objective To investigate the change of erythrocyte immune function and T lymphocyte subsets in patients with uremia and the effect of hemodialysis on them. Methods Flow cytometry and immune adherence rosette method were used to measure the activity of RBC-CR1and the changes of T lymphocyte subsets in 23 uremic patients without hemodialysis, 22 uremic patients before and after sigle hemodialysis and 21 healthy subjects as the control group. Results The activity of RBC-CR1, the number of T lymphocyte subsets significantly changed in patients with uremia, and hemodialysis could partially improve this condition. There was obvious correlation between erythrocyte immune function and T lymphocyte subsets. Serum creatinine was positively relative to the value of RBC-C 3b RR(P

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 explore the expression and significance of nestin in renal tubular epithelial cells in hypercholesterolemic rats. Methods Dietary-induced hyperlipidemia were induced in female SD rats by given 4% cholesterol and 1% cholic acid diet for 16 weeks. Changes of serum lipid, urinary albumin, serum creatinine and renal interstitial pathological changes were assessed. The expression of nestin and a-smooth muscle actin (α-SMA) were detected by immunohistochemical stain. Results The serum levels of total cholesterol, low density lipoprotein, urinary albumin and serum creatinine were significantly increased in hyperlipidemia group, accompanied with renal interstitial injury and fibrosis. As time extended, the expression of nestin and a-SMA in renal tubular epithelial cells were increased significantly. There was positive correlation among the expression of nestin and total cholesterol, low density lipoprotein, urinary albumin and serum creatinine( r =0.963,0.830,0.944,0.706, P <0.01). Nestin also had a positive correlation with tubular-interstitial index ( r = 0. 974, P < 0. 01) and α-SMA ( r = 0. 804, P < 0. 01). Conclusion The increased expression of nestin may be associated with renal tubular-interstitial fibrosis and tubular epithelial myofibroblast transdifferentiation in hypercholesterolemic rats.

Objective To evaluate the proteetive effect of Valerian oil on lipid-induced nephropathy in Hypercholosterolemic rats and study its possible mechanisms.Methods SD rats were randomly divided into control group,hyperlipidemia group,low-dose[12.5mg/(kg·d)]valerian oil group,middle-dose[25mg/(kg·d)]valerian oil group,high-dose[(50me/(kg·d)]valerian 0il group and simvastatin group[5ms/(kg·d)for lavage].Dietary-induced hyperlipidemia were by given 4％cholosteml and 1％cholic acid diet for 16 weeks.Changes of serum lipid,urinary albumin,renal function and renal pathobiology index were assessed.The expression of integrin α3β1in glomeruli was detected by immunohistochemical stain,the expression of integrin ot3～l and TGF-β1 mRNA were detected by RT-PCR at the same time.Results The serum levels of total cholesterol,low density lipopmtein and seruln creatinine in Valerian group and simvastatin group were decreased more than that in hypedipidemia group.Urinary albumin excretion Was significantly reduced。in Valerian group after treatment for 8 weeks,and significantly reduced in simvaatatin group after 16 weeks.The morphological analysis revealed that the pathobiology index in Valerian group were significantly decreased than that in simvastatin group after 16 weeks.At the sanle time,the expression of integrin α3β1 mRNA and protein in Valerian group were significantly increased than that in hyperlipidemia group and simvastatin group,and the expression of TGF-β1mRNA were markedly decreased in Valerian group.The treatment effect in Valerian group Wag better than that insimvaatatin group.Conclusion Valerian oil has the protective effects on lipid-induced nephropathy by decreasing serum lipid,increasing the expression of integrin α3β1 and inhibiting the expression of TGF-β1.The protective effects of Valerian oil ale better than simvastatin.

Objective To develop a rat model of type 2 diabetes, and to investigate the effect of AT1 receptor antagonist-irbesartan on activation of renal NF-?B in type 2 diabetic rat. Methods The rats of model groups were intraperitoneally given low-dose streptozotocin (STZ, 30 mg/kg) after having the sucrose-and fat-enriched diets(20% sucrose, 10% pig fat, 2. 5% cholesterol) for one month. Immuohistochemistry and computer image-pattern analysis system were used to analyze activation of NF-?B and expression of monocyte/macrophage (ED-1) in renal tissues. Results (1) Insulin resistance was induced by feeding diets enriched in sucrose and fat, and hyperglycemia was induced with a dose of STZ that did not cause diabetes in chow-fed rats. After 6 weeks, rats of model group presented itself early changes of diabetic nephropathy (DN). (2) Compared to normal group, the activation of NF-?B and expression of ED-1 increased in glomeruli of experimental type 2 diabetic rat. Irbesartan inhibited significantly the activation of NF-?B, ameliorated monocyte/macrophage infiltration, partly improved the renal function and matrix accumulation. Conclusions (1) A rat model of type 2 diabetes mellitus is developed successfully by combination of dietary-induced insulin resistance and low-dose STZ-induced hyperglycemia. (2) Renal NF-?B activation is greatly increased in experimental type 2 diabetic rat. The protection of irbesartan against kidney is associated, at least in part, with down-regulating NF-?B activation and monocyte/macrophage recruitment in renal tissue.

Objective To observe the renal expression of cyclooxygenase-2 (COX-2) in rats with type 2 diabetes, and explore the effect of selective COX-2 inhibitor Mobic on the expression of renal COX-2, matrix metalloproteinase-9(MMP-9), tissue inhibitor of matrix metalloproteinase-1(TIMP-1), TXB 2 and 6-Ket-PGF1?, as well as renal structure and function. Methods All rats were divided into control group, diabetes mellitus group and treatment group. Type 2 diabetic rats were treated with Mobic and vehicle respectively. Immunohistochemistry was used to detect the expression of COX-2,MMP-9 and TIMP-1 in renal tissues. The urinary TXB 2 and 6-Ket-PGF1? concentration was determined by radioimmunoassay at 6th week. Results There were an increasing expression of COX-2, TIMP-1 and decreasing MMP-9 expression in the renal tissue of type 2 diabetic rats. Mobic could increase MMP-9 expression and depress TIMP-1 expression througth inhibiting the expression of COX-2 in the renal tissues of type 2 diabetic rats. Conclusion COX-2 was involved in the pathogenesis of type 2 diabetic nephropathy. Selective COX-2 inhibitor Mobic might exert its renoprotective effects through inhibiting COX-2 activity, decreasing prostagladins systhesis, and modulating MMP-9 and TIMP-1 expression.

Objective To investigate the renoprotective effect of irbesartan on tubulointerstitial fibrosis in rats with adriamycin-induced nephropathy and its possible mechanism. Methods Rats received twice-intravenous injections of adriamycin(ADR) after the right kidney was removed. Those rats were randomly assigned to irbesartan treatment group and nephropathy group. Treatment group received 50 mg? kg-1 ? d-1 irbesartan for 4 weeks. Rats with sham operation served as normal control. Proteinuria and serum creatinine of were measured after 4 weeks. Renal histopathological changes were evaluated as well. Immunohistochemistry was used to examine the protein expression of TGF-?1, MMP-9 and TIMP-1. The mRNA levels of MMP-9 and TIMP-1 were detected by in situ hybridization. Results Proteinuria of treatment group decreased significantly as compared to nephropathy group. TGF-?1, TIMP-1 and MMP-9 were significantly lower than that of nephropathy group in tubulointerstitium and consistently associated with tubular degeneration and interstitial fibrosis progressed. Conclusion Irbesartan has a renoprotective effect on tubulointerstitial fibrosis by modulating the ECM degradation.

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 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.

AIM: To evaluate the protective effects of mycophenolate mofetil on the kidneys of type 2 diabetic rats and discover their mechanisms. METHODS: Wistar rats were divided into three groups, such as normal control rats, diabetic rats, and diabetic rats in the treatment with mycophenolate mofetil (MMF, 15 mg?kg -1 ?d -1 ). Thirteen weeks later, urinary albumin excretory rate (UAE), creatine clearance (Ccr), blood glucose, blood insulin and blood lipid were measured, and kidney pathology was observed. Inmmunohistochemistry was used to analyze the expression of CTGF, ColI and ColⅢ. RESULTS: Mycophenolate mofetil decreased UAE, Ccr and reduced glomerular volume. The expression of CTGF and deposition of ECM decreased after diabetic rats received mycophenolate mofetil. CONCLUSION: Mycophenolate mofetil can protect the kidney of diabetic rats. Its mechanism may be related to the decrease of CTGF expression and extracellular matrix deposition in renal tissue.