Protective effects of astragaloside in rats with adriamycin nephropathy and underlying mechanism

The present study was designed to determine the mechanism underlying the treatment of nephrotic syndrome using astragaloside by observing the effects of astragaloside on the expression of nephrin and podocin proteins and genes in kidneys of rats with adriamycin nephropathy. The rats were injected with adriamycin and, after successful model establishment, randomly divided into a model group, a Methylprednisolone(MP) group, and an astragaloside group. The 24-h complete urine samples were collected. Biochemical indicators were monitored, and kidney tissues were collected for pathological analysis using light microscopy and electron microscopy. The m RNA expression of nephrin and podocin was measured in the kidney tissues using the real-time q PCR, and the protein expression levels of nephrin and podocin were detected using Western blot analysis. At the end of 12 weeks of drug intervention, the urinary protein level was lower in the MP and astragaloside groups than that in the model group(P = 0.008 and P = 0.01, respectively). Serum albumin was higher in the MP and astragaloside groups than in the model group(P < 0.001 and P = 0.012, respectively). Podocytes in the MP group were nearly normal, and fusion of podocytes in the astragaloside group was significantly less than that in the control group. The nephrin and podocin m RNA and protein expression levels in the intervention groups were higher(P < 0.05) than that in the model group. Due to the increased expression of podocyte-related nephrin and podocin proteins, astragaloside maintained slit diaphragm integrity and decreased the level of proteinuria in rats with adriamycin nephropathy.

Glycated albumin may be a choice, but not an alternative marker of glycated hemoglobin for glycemic control assessment in diabetic patients undergoing maintenance hemodialysis

Background It has been suggested that glycated hemoglobin （HbAlc） underestimate the actual glycemic control levels in maintenance hemodialysis （MHD） patients, because of anemia and the using of erythropoietin （EPO）; it was recommended that glycated albumin （GA） should be an alternative marker. Therefore, the assessment performances of glycemic control were compared between GA and HbAlc in this research by referring to mean plasma glucose （MPG） in diabetes mellitus （DM） patients undergoing MHD or not. Methods MPG was calculated according to the data registered at enrollment and follow-up 2 months later and corresponding HbAlc, albumin （ALB）, GA, etc. were measured in 280 cases. A case-control study for comparing GA and HbAlc was done among the groups of MHD patients with DM （n=88） and without DM （NDM; n=90）, and non-MHD ones with DM （n=102） using MPG for an actual glycemic control standard. Results In these 3 groups, only for DM patients＇ （whether undergoing MHD or not）, GA and HbAlc correlated with MPG significantly （P 〈0.01）. Through linear regression analysis, it could be found that the regression curves of GA almost coincided in MHD and non-MHD patients with DM, because the intercepts （2.418 vs. 2.329） and slopes （0.053 vs. 0.057） were very close to each other. On the contrary, regression curves of HbAlc did not coincide in the two groups, because variance of the slopes （0.036 vs. 0.052） were relatively large. Through comparing receiver operating characteristic （ROC） areas under the curve （AUC）, it could be understood that the assessment performances of GA and HbAlc in MHD patients were lower than those in non-MHD ones, and assessment performance of HbAlc in MHD patients was better than GA （P 〈0.05）. In addition, the effects of Hb and EPO dose on HbAlc, or that of ALB on GA were unobvious in our study. Conclusions Actual glycemic control level in MHD patients with DM may be underestimated by HbAlc, and it could be avoided by GA; however, glycemic evaluating performance of HbAlc may be still better than that of GA. Therefore, HbAlc should not be replaced completely although GA can be used as a choice to monitor glycemic level.

Protective Effects and Mechanisms of Shenhua Tablet(肾华片)on Toll-Like Receptors in Rat Model of Renal Ischemia-Reperfusion Injury

Objective: To investigate the protective effects and potential mechanisms of Shenhua Tablet(肾华片, SHT) on the toll-like receptors(TLRs)-mediated signaling pathways in a rat model of kidney ischemia-reperfusion injury(IRI). Methods: Sixty male Wistar rats were randomly divided into 5 groups: sham surgery, model control, astragaloside(150 mg·kg^(-1)·d^(-1)), low-and high-dose SHT(1.5 and 3.0 g·kg^(-1)·d^(-1), repectively) groups. One week after drug treatment, rats underwent surgery to establish the IRI models. At 24 h and 72 h after the modeling, serum creatinine(Scr) and blood urea nitrogen(BUN) were analyzed; pathological damage were scored after periodic acid-Schiff staining. TLR2, TLR4 and myeloid differentiation factor 88(My D88) protein and m RNA expressions were detected by inmmunohistochemistry, Western blot and qPCR. Tumor necrosis factor α(TNF-α) and interleukin-6(IL-6) protein expressions were detected by enzyme linked immunosorbent assay. Results: Compared with the sham group, the model group exhibited severe change in renal function(Scr: 189.42±21.50, P<0.05), pathological damage(damage score: 4.50±0.55, P<0.05), and the expression levels of TLR2, TLR4, MyD88, TNF-α, IL-6 were significantly higher than other groups. Meanwhile, the levels of TLRs in model group showed upward tendency from 24 to 72 h, unparalleled with pathological and functional changes. The aforementioned parameters were alleviated to a certain extent, and, in addition to TLRs, presented the obvious downward trending from the 24 to 72 h after the intervention in the SHT and astragaloside groups relative to the model(P<0.05); in particular, the most significant mitigation of these changes was observed in the SHT-H group(P<0.05). Conclusions: TLRs may be an important spot to treat and research in acute kidney injury. SHT could effectively mitigate renal injuries and promote recovery of IRI injuries through suppression of degeneration induced by up-regulation of TLR2 and TLR4 expression levels in the My D88-dependent signaling pathway and exhibit some dose dependence.