Study on the effect and mechanism of ascorbic acid on renal podocytes in diabetes / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effect and mechanism of ascorbic acid on podocyte, last barrier of glomerular filtration, in diabetic rats.</p><p><b>METHODS</b>Diabetic rats induced by streptozotocin injection intraperitoneally were treated by ascorbic acid for 5 weeks. The levels of blood glucose (BG), HbA1c, urinary albumin excretion rate (UAER) and superoxide diamutase (SOD), catalase (CAT) and malondialdehyde (MDA) in renal cortex were measured. The podocyte ultrastructure was observed while the expression of desmin protein, a marker of podocyte injury, was examined.</p><p><b>RESULTS</b>Compared with control group, BG and HbA1c were increased markedly in diabetic group. The activities of SOD and CAT were decreased and the concentrations of MDA were increased significantly in diabetic renal cortex. There were the increased proteinic expression of desmin, foot process effacement in podocytes and UAER markedly in diabetic rats. Compared with diabetic rats, foot process effacement and the changes of UAER were ameliorated markedly while the activities of SOD were increased, the levels of MDA and proteinic expression of desmin were decreased markedly although BG, HbA1c and the activities of CAT were no significant difference in the diabetic rats by ascorbic acid treatment.</p><p><b>CONCLUSION</b>The findings suggest that there are marked injury in podocyte, last barrier of glomerular filtration, in diabetic rats and administration of ascorbic acid can protect podocyte by increasing antioxidative capacity and ameliorating the renal oxidative stress.</p>

Preliminary clinical observation on effect of soduim ferulate in treating diabetic nephropathy / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the effect of sodium ferulate (SF) on diabetic nephropathy (DN).</p><p><b>METHODS</b>Forty-eight DN patients of early stage and 54 DN patients of clinical stage were randomly divided into two groups, the conventional treatment group and the SF treatment group. Indexes, including urinary albumin excretion rate (UAER), serum endothelin (ET), blood urea nitrogen (BUN), serum creatinine (Scr) and fasting blood glucose (FBG) were observed.</p><p><b>RESULTS</b>The levels of UAER, BUN and ET were decreased in all DN patients, either early stage or clinical stage, after treated with SF for 4 weeks (P < 0.05, P < 0.01), but changed insignificantly in those treated with conventional treatment.</p><p><b>CONCLUSION</b>SF can decrease the levels of UAER and BUN in DN patients, the mechanism may relate with the decreasing of ET production and antagonizing to the binding of ET with its receptors.</p>

Renal protective effect and its mechanism of sodium ferulate in diabetic rats / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the renal protective effect of sodium ferulate (SF) and its mechanism in rats with diabetic mellitus (DM).</p><p><b>METHODS</b>DM rats induced by streptozotocin were treated with SF 110 mg/kg per day for 8 weeks. The ratio of kidney weight/body weight (KW/BW), serum triglyceride (TG) and total cholesterol (TC), creatinine clearance rate (Ccr), urinary protein/24 hrs, levels of endothelin-1 (ET-1) and nitric oxide (NO) in renal cortex in rats were measured, the pathological change of kidney were observed and the expression of transforming growth factor-beta 1 (TGF-beta 1) and collagen IV (C-IV) in kidney were examined using immunohistochemical assay. The data obtained were compared with those obtained from untreated DM rats and normal rats respectively.</p><p><b>RESULTS</b>Compared with the normal rats, in DM rats, Ccr, urinary protein/24 hrs, ET-1, expressions of TGF-beta 1 and C-IV were significantly increased in DM model rats (all P < 0.01), and significantly abnormal pathological change in kidney was found. While in the SF treated DM rats, the above-mentioned abnormal changes were all significantly improved.</p><p><b>CONCLUSION</b>SF has effect in protecting kidney of DM rats, the mechanism might be related with its actions of reducing ET-1 production in kidney and inhibiting the expressions of TGF-beta 1 and C-IV.</p>