Objective To discuss whether mild hyperuricemia can lead to kidney damage and the protection of decreased uric acid,through observing that hyperuricemia did damage to glomerulus endothelial function and cell proliferation of vascular smooth muscle in rats. Methods Fifty-four male SD rats were divided into four groups,the control group,model group (Oxonate),allopurinol group and Oxonate+allopurinol group.Rats were administered on a low sodium diet and their systolic blood pressure (SBP) were measured each 10 days.ELISA was used to detect rat plasma markers of endothelial function damage [nitric oxide (NO),type-1 plasminogen activator inhibitor (PAI-1),endothelin 1 (ET-1)] and cell proliferation of vascular smooth muscle[plateletderived growth factor (PDGF),cycloxygenase 2 (COX2),monocyte chemotactic protein-1 (MCP-1)],and the markers of inflammatory reaction[interleukin-18 (IL-18),tumor necrosis factor α(TNF-α)].PDGF and nitric oxide synthase (NOS) levels of rats were detected by immunohistochemical method.Renal tissue pathology of rats was observed. Results Compared to the control group,the plasmic concentration of COX2,ET-1,IL-18,PAI-1,PDGF,TNF-o,MCP-1 increased,and NO decreased significantly in rats of model group (all P＜0.05),expression of NOS significantly reduced and PDGF increased (all P＜0.05).Under light microscope,vascular wall thickening,intimal proliferation and lumen slight stricture without uric acid crystals in renal tissue were found in model group,which were obviously improved by using allopurinol. Conclusion Mild hyperuricemia can do damage to endothelial function of glomerulus and lead to vascular cell proliferation,which can be improved through decreasing uric acid.

Objective To investigate the effectiveness of bone marrow mesenchymal stem cell (MSC) and different transplantation methods of MSC on adriamycin (ADR) model of nephropathy in rats. Methods The ADR model of nephrop-athy was induced by left nephrectomy plus injection of ADR (2.5 mg/kg) in Sprague-Dawley (SD) rats, once a week for two weeks. The model rats with nephropathy were randomly divided into three groups: adriamycin nephropathic model control group (ADR, n=12), MSCs transplantation through right renal artery group (M-A, n=12) and MSCs transplantation through peripheral veins group (M-V, n=12). Another 12 SD rats were served as normal controls (N, n=12). MSCs were cultured, transplanted via right renal artery (2×106/mL) to rats in M-A group, and were transplanted via peripheral veins 2×106/mL) to rats in M-V group. The same procedure was repeated in two weeks. The blood urea nitrogen, serum creatinine, 24 h urine protein and 24 h uromicroprotein were detected before transplantation and in one and two weeks after the second transplanta-tion. The renal morphology and labeled cells were examined in the kidney one week after the second transplantation. Results The values of blood urea nitrogen, serum creatinine, 24 h urine protein and 24 h uromicroprotein were significant-ly higher in M-A group, M-V group and ADR group than those of N group (P<0.01). The level of 24 h uromicroprotein was significantly lower before the second transplantation in M-A group than that of ADR group (P<0.01). The serum level of cre-atinine was significantly decreased in M-A group than that of ADR group and M-V group (P<0.01). The levels of 24 h urine protein and 24 h uromicroprotein were significantly lower after one week transplantation in M-A group than those of M-V group (P<0.01). The serum level of creatinine was significantly lower two weeks after the second transplantation in M-A group than that of ADR group and M-V group (P<0.01), but no significant differences in the levels of urine protein and uro-microprotein between M-A group and M-V group. Conclusion Transplantation of MSCs can alleviate renal damage of chronic ADR-induced nephropathy, which is more effective in rats with MSCs transplantation via renal artery than that in rats with MSCs transplantation via peripheral vein.

Objective To investigate the effects of uric acid (UA) and UA under oxidative stress on cultured human umbillical vein endothelial cells (HUVEC).Methocds HUVECs were incubated with different concentration UA (0,4,8,16 mg/dL),H2O2 (500 mmol/l) and UA+H2O2 (500 mmol/l) for 24,48 and 72 hours.Then we observed the morphology of HUVECs and evaluated the proliferation of HUVECs by MTT assay.NO and ET-1 in supernatant medium was detected by ELISA.Results For the viability of HUVECs,there was no statistically significant difference between 4 mg/dL UA group and control group after incubation for 24,48 and 72 hours (P＞0.05) and between UA groups(8 mg/dL and 12 mg/dL) and control group after incubation for 24,48 and 72 hours (P＞0.05).After incubation with 12 mg/dL of UA for 48 hours or 8 mg/dL of UA for 72 hours,the viability of HUVECs decreased significantly (P ＜0.05) The viability of HUVECs in H2O2 group decreased significantly (P＜0.05).The viability of HUVECs in UA+H2O2 groups after incubation for 24 h was significantly better than H2O2 group.There was no signifiant difference in the cell viability between (8 mg/dL or 12 mg/dL) UA+H2O2 group and H2O2 group.Compared with the control group,the NO levels were decreased and the ET-1 levels were increased in the supernatants of HUVECs in 12 mg/dL UA group for 72 hours (P＜0.05).Compared with H2O2 group,the NO levels were increased and the ET-1 levels were decreased in the supematants of HUVECs in (8 mg/dL or 12 mg/dL) UA +H2O2 groups for 24 hours (P＜0.05),while for (12 mg/dL) UA +H2O2 group for 72 hours,the results were just the contary.Conclusion The effects of UA on HUVECs are related with both concentration and action rime.Acutely increased UA may protect HUVECs form injury,while long action of UA may injure HUVECs,especially under oxidative stress.