Objective To study the effect of recombinant human erythropoietin (rHuEPO) on in aged patients undergoing maintenance hemodialysis. Methods Blood pressure and its mechanism 52 elderly patients undergoing maintenance hemodialysis divided into two groups, HBP group (23 cases with hypertension) and NBP group(29 cases without hypertension). The plasma vasoactive substances were measured by radioimmunological methods. Fifteen cases in NBP group as EPO group were given a bolus of venous injection of rHuEPO (3 000 IU), others in NBP group (14 cases) were injected 0.9% saline as control group. The plasma vasoactive substances were assayed before and 1, 3, 6, 9, 12, 18, 24, 30, 44 hours after therapy with or without rHuEPO. Results (1) The plasma dopamine (DA) in HBP group were significantly higher than that of NBP group. (2) Endothelin levels increased transiently but DA levels increased steadily in EPO group. Conclusions The study suggests that the effect of rHuEPO induced on hypertension in the elderly patients undergoing maintenance hemodialysis is associated with the increasing plasma DA.

Objective To investigate effective dosage of ACEI in renoprotective effect in primary glomerular dieases.Method In 154 patients with primary glomerular diseases,we performed a 4 month therapy,including 40 cases with high or low doses of captopril and 51 cases with high or low doses of cilazapril and 45 cases with high low doses of enalapril,and 18 cases with amlodipine as control.Mean arterial pressure (MAP),uninary protein,urinary albumin excretion rate and renal function were measured at basis and after 1,2,3,4 month of therapy,and ACE gene polymorphism was determined in these patients.Result 1.There were no difference on ACE gene polymorphism and diet protein and diet salt among control group and different ACEIs group;2.The antiproteinuria and the effect on renal function were same between patients with high and low dose of different ACEIs.Conclusion The low dose of ACEI has the same renoprotective effect as general dose in primary glomerular diseases.

Objective To screen out useful monitors of heparin therapy in glomerular diseases.Methods In 40 diabetic nephropathy (DN) patients and 39 chronic glomerulonephritis (CGN) patients,we implemented a bolus venous injection of heparin 1500 U,and measured the parameters of coagulation and fibrinolysis by ELISA at basis and 30 minutes,2 hours after injection.Result After injection with heparin,the levels of prothrombin fragment 1+2 (PF1+2),thrombi-antithrombin Ⅲ (TAT),fibrinopeptide A (FPA) and coagulative factor X (FX) activity significantly decreased,but the activated partial thromboplastin time (APTT) and the other parameters of coagulation-fibrinolysis didn't change in either the DN patients or the CGN patients.Conclusion The level of PF1+2,TAT,FPA and XF activity are valuable monitors in heparin therapy.

Objective To evaluate the effect of isoflurane on the expression of phosphorylated glycogen synthase kinase-3 beta (p-GSK-3β) and β-catenin in neural stem cells (NSCs) in the hippocampus of developing rats.Methods Twenty-four 7-day-old Sprague-Dawley rats,weighing 15-20 g,were divided into 2 groups (n =12 each) using a random number table:control group (group C) and 2％ isoflurane group (group Ⅰ).Group C inhaled 30％ oxygen for 4 h.Group Ⅰ inhaled 2％ isoflurane in 30％ oxygen for 4 h.Six rats were randomly selected from each group,and 5-bromodeoxyuridine (BrdU) 200 mg/kg was intraperitoneally injected immediately before anesthesia to assess the proliferation of NSCs in the hippocampal dentate gyrus.The rats were sacrificed at 6 h after the end of anesthesia,and hippocampi were isolated for determination of the number of BrdU positive cells in the dentate gyrus (by immunohistochemistry) and expression of p-GSK-3β and β-catenin in hippocampal tissues (by Western blot analysis).Results Compared with group C,the number of BrdU positive cells was significantly decreased,and the expression of p-GSK-3β and β-catenin was down-regulated in group Ⅰ (P＜0.05).Conclusion Isoflurane can inhibit the proliferation of NSCs in the hippocampal dentate gyrus of developing rats,and the mechanism may be related to down-regulation of the expression of p-GSK-3β and β-catenin.

Objective To evaluate the effect of isoflurane anesthesia on Wnt3a expression in the hippocampus of developing rats.Methods Twenty-four 7-day-old male Sprague-Dawley rats,weighing 125-155 g,were randomly divided into 3 groups (n=8 each) using a random number table:control group (group C),4 h inhalation of 2％ isoflurane group (group I4),and 6 h inhalation of 2％ isoflurane group (group I6).The rats were sacrificed at 6 h after the end of treatment in each group,and the hippocampi were removed for determination of Wnt3a mRNA expression (by real-time reverse transcriptase polymerase chain reaction) and Wnt3a expression (by Western blot).Results Compared with group C,the expression of Wnt3a and Wnt3a mRNA in hippocampi was significantly up-regulated in I4 and I6 groups (P＜0.05).Compared with group I4,the expression of Wnt3a in hippocampi was significantly up-regulated (P＜0.05),and no significant change was found in the expression of Wnt3a mRNA in hippocampi in group I6 (P＞0.05).Conclusion The mechanism of isoflurane-induced neurotoxicity is probably related to upregulation of Wnt3a expression in the hippocampal tissues of developing rats.

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Objective:To study the mechanism of immune tolerance induce by protal venous injection of donor spleen cells on the dog model of renal transplantation.Methods:The donor spleen cells were injected through the protal vein during operation,one week later,renal transplantation was performed.IL-2 and IL-6 were studied by method of ELISA.Results:Level of IL-2 and IL-6 in protal venous group and cyclosporin group was higher than that of control group.There were no difference between protal venous group and cyclosporin group.Conclusion:Immune tolerance could be produced by protal venous injection of donor spleen cells.

Objective:To observe the theraputic effect and changes of glomerular extracellular matrix components(ECM) and PAI-1 and their relationships after cure with methyl-prednisone on immune complexes nephritis rats.Methods:Immune complexes nephritis rats model were induced with C-BSA.Levels of FN,LN in different treatment groups were analyzed by ELISA, level of PAI-1 in rats renal tissue was determined by color developing substrate,was theraputic effect of methyl-prednisone with 24 hours volumes of urine protein.Results:The levels of PAI-1,FN and LN of model groups were significantly higher than those of normal and control groups,and PAI-1 was significantly correlated with LN and FN,Glomerular mesangial matrix proliferated slightly and moderately;The levels of FN,LN and PAI-1 decreased signifcantly and glomerular mesangial matrix proliferation lessen differently after cure of methyl-prednisone for 1 and 2 weeks,but not reaching the level of normal groups;24 hours volumes of urine protein decrease significantly in treatment groups.Conclusion:The ECM accumulation correlate with PAI-1 increase in immune complexes rats,methyl-prednisone may affect ECM accumulation by interfering with PA/PAI-1 system to reach a treatment purpose.

Objective To observe the changes of STAT3 signaling transduction pathway and autophagy activity in human glomerular mesangial cells cultured in high glucose, as well as the effect of STAT3 on autophagy, exploring whether SAT3 further influence extracellular matrix proteins type IV collagen secretion through the regulation of autophagy. Methods Culture human renal mesangial cells under different conditions, STAT3 pathway was inhibited with specific blocking agent S3I?201 and siRNA respectively. The experiment was divided into: (1) Control group: normal glucose concentration; (2) High glucose group: divided into 12 h, 24 h, 48 h, 72 h incubation group. (3) High glucose+S3I?201 group: pretreated cells with 30 μmol/L S3I?201 (Selleck S1155) for 1 h, then incubation with high glucose for another 24 hours. (4) High glucose+STAT3?siRNA group: siRNA transfection firstly, then incubation with high glucose for 24 hours. (5) High glucose+S3I?201+3?MA group: pretreated cells with 2 mmol/L 3?MA (Selleck S2767) and 30 μmol/L S3I?201 for 1 h, then incubation with high glucose for another 24 hours. Western blot was employed to detect the protein of STAT3, p?STAT3 and autophagy related protein LC3, p62 expressions. The changes of autophagosome quantity was observed with transmission electron microscope. The extracellular matrix protein collagen IV expression was measured with ELISA. Results Compared with the control group, glomerular mesangial cells cultured with high glucose for 24h, the expressions of STAT3 and p?STAT3 increased (P<0.01), while the expression of autophagy related proteins LC3II/LC3I decreased. The expression of p62 increased and the number of autophagosome reduced under transmission electron microscope, which all indicated the decrease of autophagy activity (P<0.05). Blocking STAT3 signaling pathway with S3I?201 and STAT3?siRNA respectively, compared with high glucose group, LC3II/LC3I was up?regulated and p62 was down?regulated, and the number of autophagosome was increased significantly, which all indicated the increase of autophagy activity (P<0.05). Extracellular matrix proteins collagen IV expression of cells cultured with high glucose was higher than the control group (P<0.05), and the application of S3I?201 blocking STAT3 pathway caused type IV collagen expression to decrease (P<0.05). The application of the autophagy inhibitor 3?MA could convert the result and lead to an increase of type IV collagen expression (P<0.01). Conclusions High glucose could active STAT3 signaling pathway of human renal mesangial cell and increase STAT3, p?STAT3 expression. High glucose could inhibit autophagy activity of human renal mesangial cells. Inhibition of STAT3 pathway activation may reduce the inhibitory effect of high glucose on autophagy of human renal mesangial cells. High glucose leads to an increase of type IV collagen secretion of human glomerular mesangial cells. The activation of STAT3 pathway may increase type IV collagen secretion through negative regulation of autophagy, which eventually leads to diabetic nephropathy.

Objective To determine the role of extracellular signal-regulated kinases (ERK1/2) in aldosterone-induced rat mesangial cells (RMCs) proliferation. Methods RMCs were obtained from intact glomeruli of 4- to 6-week-old Sprague-Dawley rats and characterized according to published methods. RMCs between passages 5 and passages 10 were used. Protein levels of mineralocorticoid receptor (MR) in RMCs were analyzed by Western blotting. The cells were divided into the following groups: control group, PD98059 (10 (μmol/L) group, eplerenone (1 μmol/L) group, aldosterone (100 nmol/L) group, aldosterone (100 nmol/L) +PD98059 (10 μmol/L) group, aldosterone (100 nmol/L)+eplerenone (1 μmol/L) group. ERK1/2 activity was measured by Western blotting. Cell proliferation of RMCs was evaluated by [3H]-thymidine uptake measurements.Results MR protein expression in RMCs was confirmed by Western blotting. Aldosterone activated ERK1/2, and the maximal ERK1/2 activation induced by aldosterone was at a concentration of 100 nmol/L. Aldosterone (100 nmol/L)-induced activation of ERK1/2 peaked at 10 minutes (P＜0.05).Pretreatment with a selective MR antagonist eplerenone (1 μmol/L) significantly attenuated aldosterone-induced ERK1/2 phosphorylation. Aldosterone (100 nmol/L) treatment for 30 hours increased [3H]-thymidine incorporation of RMCs (135% ±8% of controls, P ＜0.05). Cellular proliferation induced by aldosterone could be prevented by pretreatment with eplerenone or an ERK (MEK) inhibitor PD988059. Conclusion Aldosterone induces RMCs proliferation through MR and ERK1/2 activation, which may contribute to the pathogenesis of glomerular mesangial injury.