糖尿病肾病的发病机制及治疗进展

糖尿病肾病是糖尿病严重的微血管并发症之一，是终末期肾病的主要原因。近年来的研究发现糖尿病肾病的发病机制涉及多方面因素，其中对炎症、免疫因素及细胞因子等的研究越来越多，同时也为治疗糖尿病肾病提供了新的方向。

LOW MOLECULAR WEIGHT HEPARIN DECREASES THE ALBUMINURIA AND RENAL PATHOLOGICAL CHANGES IN DIABETIC NEPHROPATHY RATS

Objective To investigate the renoprotection effect of low molecular weight heparin(LMWH)in diabetic rats.Methods Diabetic rats were induced by injection of steptozotocin(STZ).Rats were randomly divided into three groups:control group,diabetic model group,and LMWH treatment group.The levels of total cholesterol(TC),triglyceride(TG),prothrombin time(PT),kaolin partial thromboplastin time(KPTT),24-hour urinary albumin excretion rate(UAER),and serum soluble P-selectin were determined after 8 weeks.Glomerular morphology was observed by light microscopy.Results The levels of TG,UAER,and P-selectin in LWMH treatment group were lower than those in model group(all P<0.01).The levels of PT and KPTT in LWMH treatment group were shorter than those in model group.And LWMH improved the histological changes of diabetic rats.Conclusion LMWH has some renal protective effects in diabetic rats,partly through down-regulating the expression of P-selectin.

Effect of short-term acumagnetotherapy on diabetic kidney disease in patients with type Ⅱ diabetes and study on the molecular mechanism

Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eight patients with type Ⅱ diabetes（T2D） were undergone pulsed electromagnetic fields（PEMF） stimulation at the acupoints of Píshū（脾俞 BL 20）, Zúsānl（足三里 ST 36）, Shènshū（肾俞 BL 23） and Yíshū（胰俞, EX-B3） for a period of 4 weeks. Urinary micro-albumin（U-m Alb） excretion, plasma methane dicarboxylic aldehyde（MDA and lipopolysaccharide（LPS） of the patients were used for evaluating therapeutic efficacies. Results After the acumagnetotherapy, U-m Alb excretion in the participated patients was markedly reduced（27.21±3.51 vs 8.51±0.95, P0.001） accompanied with decreased MDA（16.46±1.17 vs 12.40±1.86, P0.05） and LPS（37.41±3.84 vs 21.63±3.61, P0.05） levels in plasma while the metabolic control of these patients was not significantly altered. Acumagnetotherapy increased IκBα content（0.69±1.17 vs 1.30±0.29, P0.01）, an inhibitory protein of inflammatory response, and correspondingly reduced the protein levels of inflammatory activating proteins, NF-κB p65（0.98±0.42 vs 0.43±0.28, P0.05） and NF-κB p50（1.19±0.40 vs 0.76±0.30, P0.05）. The acumagnetotherapy also inhibited the oxidantproducing enzyme, Nox4 protein expression（1.32±0.40 vs 0.37±0.23, P0.05） in patient ＇s blood lymphocytes. Conclusion Short-term intervention of acumagnetotherapy in patients with T2 D mitigates DKD progress potentially by its anti-oxidative and anti-inflammatory effects.

Identification and function of glucose transporter 1 in human mesangial cells

Objective To evaluate the role of glucose transporter 1 (GLUT1) in the glucose uptake of glomerular mesangial cells.Methods Cultured human glomerular mesangial cells were used. The expressions of glucose transporter 1 mRNA and protein were detected with reverse transcription-polymerase chain reaction (RT-PCR), flow cytometry and immunofluorescence staining. Glucose uptake was determined with 2-deoxy-［3H］-D-glucose uptake assay.Results The expressions of GLUT1 mRNA and proteins were detected in human mesangial cells. Glucose uptake and its kinetics assay showed that GLUT1 is a functional glucose transporter in cultured human mesangial cells, and that its function could be inhibited by the specific inhibitor, Phloretin. Conclusion GLUT1 is the predominant glucose transporter in human mesangial cells, which has the kinetic characteristics of high affinity and low capacity for D-glucose. This suggests that in order for mesangial cells to take up excessive quantities of glucose, as in diabetes, changes in glucose transporter expression, translocation or activity may be required.