血管紧张素Ⅱ-1型受体拮抗剂对阿霉素肾病大鼠干预效果的实验研究

目的 探讨血管紧张素Ⅱ-1受体拮抗剂(AT1RA)缬沙坦对大鼠肾病综合征病理及相关临床指标的干预作用及可能机制。方法 采用阿霉素肾病(AN)模型，将大鼠分为阿霉素肾病组和缬沙坦及苯拉普利治疗组，检测大鼠24h尿蛋白排泄量、血肌酐、尿素氮及其他生化指标，并取肾脏进行光镜及电镜检查，放射免疫分析法测定血浆及肾组织血管紧张素Ⅱ含量，并没正常对照组。结果 缬沙坦及苯拉普利可降低阿霉素肾病大鼠的蛋白尿排泄，改善生化指标。结论 缬沙坦对阿霉素肾病大鼠的肾脏具有保护效应，减轻肾损伤，降低蛋白尿。     

肾茶对阿霉素肾病大鼠血清NF-KB、IL-8水平的干预研究

目的:观察肾茶对阿霉素肾病大鼠外周血中核因子-KB(Nuclear factor-KB,NF-KB)、白细胞介素-8(Interleukin-8,IL-8)表达的影响,探讨肾茶治疗肾病综合征(Nephrotic Syndrome,NS)的可能机制。方法:40只Wistar雄性大鼠随机分为两组:正常组(n=10)注射生理盐水0.5mL,肾病组(n=30)尾静脉单次注射阿霉素5mg/kg(用生理盐水溶解至0.5mL)制备NS模型。注射后第7天检测所有大鼠24h蛋白尿,尿蛋白>30mg/24h者为NS模型成功。将模型成功的肾病组再随机分为两组:肾病组(n=10)、肾茶组(n=10)。肾茶组在造模成功后第7天开始灌胃给药5mL/kg,正常组和肾病组给予等量生理盐水灌胃。第7、21、42天测各组大鼠24h尿蛋白定量(免疫比浊法)及外周血单个核细胞提取物NF-KB(酶联免疫吸附法)及其上清液IL-8(酶联免疫吸附双抗体夹心法)的变化。结果:①肾病组24h尿蛋白定量、NF-KB及IL-8含量均高于正常组和肾茶组,有显著性差异(P<0.01)。②肾茶组24h尿蛋白定量、NF-KB及IL-8含量均比肾病组明显下降,有显著性差异(P<0.01)。③肾病组和肾茶组的24h尿蛋白、NF-KB、IL-8两两之间呈直线相关性(P<0.01)。结论:肾茶可能直接或间接抑制NF-KB,降低IL-8水平,减轻尿蛋白,从而延缓疾病进展。     

霉酚酸酯对糖尿病大鼠肾组织Nephrin与Podocin表达的影响及机制

目的探讨霉酚酸酯(Mycophenolate mofetil,MMF)对糖尿病大鼠肾组织Nephrin与Podocin蛋白表达的影响及机制。方法建立链脲佐菌素诱导的单侧肾切除大鼠糖尿病模型,将模型大鼠随机分成糖尿病组(DM组)与MMF给药组(DM+MMF组,10mg·kg-1.d-1灌胃给药),另设对照组(C组)。8wk末检测血糖、24h尿白蛋白排泄率(AER)变化,通过免疫组化方法检测肾组织ED-1表达,Westernblot方法检测肾组织Nephrin、Podocin、白细胞介素-1(IL-1)与肿瘤坏死因子-α(TNF-α)蛋白表达。结果DM组大鼠尿AER明显高于C组(P<0.01),DM+MMF组大鼠尿AER明显低于DM组(P<0.05)。DM组大鼠肾小球ED-1阳性细胞数明显高于C组(P<0.01),DM+MMF组肾小球巨噬细胞浸润明显低于DM组(P<0.05)。DM组肾组织Nephrin与Podocin表达较C组分别下降80.2%与65.1%,MMF可明显恢复肾组织Nephrin与Podocin表达(P<0.01)。DM组肾组织IL-1与TNF-α表达较C组分别增加2.8倍与3.8倍,MMF可明显降低肾组织IL-1与TNF-α表达(P<0.01)。结论MMF可能通过恢复糖尿病大鼠肾组织Nephrin与Podocin蛋白表达减少尿白蛋白排泄。     

血管内皮生长因子在肾病大鼠中的表达及意义

目的:探讨血管内皮生长因子(VEGF)在阿霉素肾病大鼠中的表达及意义。方法:雄性Wistar大鼠62只,随机分为正常对照组、肾病综合征组(NS)。于7d、14d、28d检测血、尿、肾组织VEGF的含量。结果:N S组VEGF在血、尿、肾组织中的含量均显著高于正常对照组(P<0.01),且均与24h尿蛋白量呈正相关(r=0.775;0.807;0.629;P<0.01)。结论:阿霉素肾病大鼠血、尿、肾组织VEGF的表达与24h尿蛋白量呈正相关,提示VEGF参与了阿霉素肾病大鼠蛋白尿的发生。     

核因子-κB对原发性肾病综合征患儿IL-8调控及黄芪的干预作用

目的 观察NF-kB对原发性肾病综合征患儿IL-8调控及黄芪干预作用.方法 在原发性肾病综合征患儿和正常儿童外周血单个核细胞中,分别加NF-kB的刺激剂、抑制剂及黄芪,测IL-8浓度和NF-kB活性.结果 肾病患儿NF-kB活性及IL-8含量增高,2者呈正相关;IL-1β刺激后,黄芪降低肾病患儿NF-kB活性及IL-8含量、降低正常儿童NF-kB活性而不影响IL-8含量;用对甲苯磺酰-L-苯丙氨酸氯甲基甲酮(TPCK)抑制后,黄芪可提高肾病患儿NF-kB活性及IL-8含量、提高正常儿童NF-kB活性;而不影响IL-8含量.结论 原发性肾病综合征患儿NF-kB活性上调及IL-8水平增高,黄芪通过抑制NF-kB过度活化从而下调IL-8过高表达继而发挥效应;黄芪对NF-kB活性有双向调节作用.     

阿托伐他汀对慢性肾病大鼠血清及肾组织microRNA-92a表达的影响

目的明确阿托伐他汀对慢性肾病的保护作用部分是通过其对microRNA-92a/KLF2通路的影响实现的。方法 24只健康SD大鼠随机分为正常对照组、肾病组和治疗组。肾病组与治疗组均行5/6肾脏切除制备动物模型,治疗组给予阿托伐他汀6 mg/kg·d进行干预治疗,肾病组和正常对照组每天给予等量的生理盐水灌胃,大鼠自由进食、饮水。末次术后8周处死大鼠。测定血生化,使用ELISA方法测血清中hs-CRP及IL-1β含量;采用RT-PCR方法测定血清及肾组织中miR-92a的含量;用RT-PCR和Western Blot方法测定肾组织中KLF2及其mRNA的表达。结果 5/6肾脏切除术后8周,血尿素氮(BUN)、肌酐(SCr)明显增高(P<0.01),肾功能异常,miR-92a表达增加,KLF2表达减少,炎症指标hs-CRP及IL-1β明显增加。阿托伐他汀治疗后血清及肾组织miR-92a均显著下降,KLF2表达较肾病组增加,hs-CRP及IL-1β表达较肾病组明显下降。结论阿托伐他汀除纠正脂代谢紊乱外,还可以有效降低血清及肾组织miR-92a表达,使KLF2表达增加,抑制CKD炎症反应,延缓肾功能不全进展。     

青藤碱对实验性多柔比星肾病大鼠尿蛋白、IL-6影响的研究

目的：观察白细胞介素-6（IL-6）在多柔比星肾病大鼠肾组织及尿中的表达及青藤碱对其表达的影响。方法：雄性Wistar大鼠50只。随机分为正常组（10只）,肾病组（40只）。肾病组大鼠一次性尾静脉注射多柔比星5mg/kg,制备MCNS模型。注射后第7天检测所有大鼠24h尿蛋白定量,尿蛋白〉30mg/24h者为MCNS模型成功。采用酶联免疫吸附法检测各组大鼠肾组织及不同时期尿液中IL-6的表达。结果：①肾病组大鼠尿蛋白排泄量逐渐增加,各时期与正常组比较,均有显著性差异（P〈0.01）;②肾病组大鼠肾组织及尿中IL-6表达较正常组明显增加,治疗组IL-6的表达也增高,但较肾病组为低;3肾病组在不同时期尿及肾组织中IL-6的变化与24 h尿蛋白的排泄量呈正相关（P〈0.01）;4肾组织与尿中IL-6呈正相关（P〈0.01）。结论：①IL-6在MCNS尿及肾脏组织中存在异常表达,青藤碱可减少蛋白尿减轻肾损害;②IL-6可能是蛋白尿发生的原因之一。     

洛汀新对大鼠阿霉素肾病的保护作用

为探讨洛汀新对大鼠阿霉素肾病（AN）的保护作用及其机理，观察洛汀新对AN大鼠尿蛋白、血清蛋白、血清胆固醇及肾脏病理变化的影响，并用放射免疫分析法检测血浆及肾组织血管紧张素Ⅱ（ATⅡ）含量。结果显示：AN大鼠血浆及肾组织ATⅡ含量明显升高，洛汀新可降低AN大鼠尿蛋白及血清胆固醇，减轻肾小球损害，降低血浆及肾组织ATⅡ含量。洛汀新对大鼠AN有一定保护作用，其机理与降低ATⅡ（特别是局部ATⅡ）含量有关。     

原发性肾病综合征患儿肾组织中IL-17、IL-6TGF-β1表达水平与临床病理分析

迄今,儿童原发性肾病综合征(PNS)发病机制尚未完全明了。近年来,国内外研究[1]一致认为,细胞免疫功能的失衡以及相关细胞因子分泌异常在PNS的发生、发展过程中发挥了重要的作用。本研究检测了我院35例PNS患儿肾组织中白介素-17(IL-17)、白介素-6(IL-6)及转化生长因子β1(TGF-β1)表达水平,分析了其与不同肾组织病理改变和临床蛋白尿的相关性,现报告如下。1资料与方法     

细胞间黏附分子-1在多柔比星肾病大鼠中的表达及意义

目的:观察细胞间黏附分子-1( intercellular adhesion molecule-1,ICAM-1)在多柔比星肾病大鼠肾组织中的表达,探讨 ICAM-1在微小病变肾病综合征(MCNS)尤其是蛋白尿中的作用机制.方法:雄性Wistar大鼠85只随机分为正常组(40只)、肾病组(45只).肾病组单次尾静脉注射多柔比星5mg/kg,建立MCNS模型,正常组注射等量生理盐水.于造模后第7d、14d、28d、42d测定各组大鼠24 h尿蛋白、血清白蛋白、胆固醇、甘油三酯、肌酐及尿素氮含量,同时采用免疫组织化学染色检测肾组织中ICAM-1的表达.结果:①肾病组大鼠尿蛋白排泄量逐渐增加,且各时期与正常组比较明显升高,均有显著性差异(P＜0.01) ;②肾病组大鼠肾组织中ICAM-1表达较正常组明显增加,有显著性差异(P＜0.01);③肾病组肾组织中ICAM-1的表达与24h尿蛋白的排泄量呈正相关(r=0.919,P<0.01).结论:ICAM-1在MCNS肾组织中表达明显增多,它的异常表达与蛋白尿的发生密切相关.     

灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响

目的探讨灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响。方法建立STZ诱导的单侧肾切除糖尿病模型,随机分:对照组、模型组、灯盏花素给药组与MMF给药组。8wk末检测尿白蛋白排泄率(AER)、肾组织蛋白激酶C(PKC)活性,应用免疫组化方法检测肾组织ED1及单核细胞趋化蛋白1(MCP1)与细胞间黏附因子1(ICAM1)表达。结果灯盏花素或MMF给药组大鼠肾重、肾重/体重、AER明显低于模型组(P<0.05)。模型组肾组织细胞浆、细胞膜及细胞总PKC活性明显高于对照组(P<0.01),灯盏花素给药组肾组织PKC活性明显低于模型组(P<0.05),MMF给药组肾组织PKC活性与模型组相比无差异。模型组肾小球ED1阳性细胞数及MCP1、ICAM1表达明显高于对照组(P<0.01),灯盏花素或MMF给药可明显缓解这些变化(P<0.05)。结论灯盏花素对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织巨噬细胞浸润有关。     

霉酚酸酯对糖尿病大鼠肾小管-间质损伤的保护作用

目的观察免疫抑制剂霉酚酸酯(MMF)对糖尿病大鼠肾小管-间质单核细胞趋化蛋白-1(MCP-1)及CD68表达的影响,探讨MMF对糖尿病大鼠肾小管间质损伤的保护作用及机制。方法Wistar大鼠行右肾切除术2wk后,随机分为右肾切除对照组(NC)、糖尿病组(DM),霉酚酸酯治疗组(DM+MMF,MMF15mg·kg-1.d-1灌胃)。腹腔注射链脲佐菌素(STZ,65mg·kg-1)诱发糖尿病模型。检测各组8wk末的左肾重/体重比值、24h尿蛋白(Upro)、血糖(BG)、血肌酐(Scr),观察肾小管-间质形态学变化,免疫组化检测肾组织中MCP-1及CD68表达,RT-PCR测定肾组织中MCP-1 mRNA表达。结果与NC组相比,DM组大鼠血糖、Upro及左肾重/体重比值均上升(P<0.01);肾间质纤维化面积扩大(P<0.01);肾组织内MCP-1蛋白、CD68表达及MCP-1 mRNA的表达均上调(P<0.01)。DM+MMF组上述指标除BG和Scr外均被抑制(P<0.05或P<0.01)。结论MMF对糖尿病大鼠肾小管-间质损害具有明显的保护作用,可能与抑制MCP-1基因及蛋白表达有关。     

Prevention of early renal injury by mycophenolate mofetil and its mechanism in experimental diabetes

Previously it was shown that treatment with mycophenolate mofetil (MMF) attenuated renal inflammation and glomerular injury in a model of diabetes. However, the mechanism involved in the renoprotective effects of MMF in experimental diabetes has not been clearly delineated. Diabetes was induced by injection of streptozotocin (STZ) after uninephrectomy. Diabetic animals received no treatment or treatment with MMF (10 mg/kg once daily by gastric gavage) for 8 weeks, non-diabetic rats served as controls. Level of malondialdehyde (MDA) in renal tissue and urine as well as the activity of antioxidant enzymes (AOE) in renal tissue was determined. Renal injury was evaluated. Immunohistochemistry for ED-1 macrophages marker, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) was performed. Expression of transforming growth factor (TGF)-beta1 protein was determined by Western blotting analysis. Treatment with MMF had no effect on blood glucose level, but did prevent increased urinary albumin excretion and glomerular damage in diabetic rats. Oxidative stress was reduced by MMF treatment, as indicated by a reduction in MDA level in renal tissue and urine. Activity of AOE such as glutathione peroxidase (GSH-PX) was markedly elevated while superoxide dismutase (SOD) and catalase (CAT) were not changed by MMF treatment. In diabetic animals receiving no treatment, there were increases in ED-1-positive cells, ICAM-1 expression and MCP-1 expression in glomeruli and tubulointerstitium, which were effectively suppressed by MMF treatment. Western blotting analysis showed that the expression of TGF-beta1 protein was increased by 1.92-fold in renal tissue in diabetic rats, and MMF treatment significantly reduced the increased expression of TGF-beta1 protein by 45%. Our data suggest that MMF treatment ameliorates early renal injury via the inhibition of oxidative stress and overexpression of ICAM-1, MCP-1 and TGF-beta1 in renal tissue in diabetic rats.     

霉酚酸酯对大鼠糖尿病肾病及CD2相关蛋白表达的影响

目的研究霉酚酸酯（MMF）对大鼠糖尿病肾病（DN）及CD2相关蛋白（CD2AP）表达的影响。方法纯种雄性SD大鼠24只,分正常对照（A）组、DN模型（B）组和MMF干预DN（C）组。饲养8周后行有关血尿生化指标和光镜组织学、透射电镜、逆转录聚合酶链反应（RT-PCR）CD2AP mRNA表达检测。结果MMF明显减少DN大鼠24h尿蛋白的排泄,预防血肌酐的升高。组织学显示C组大鼠肾小球面积明显减少,系膜增宽及细胞外基质积聚明显改善。电镜下B组大鼠足细胞足突增宽,部分融合,肾小球毛细血管袢基膜增厚,系膜区增宽,系膜基质增多,C组大鼠以上病变都明显减轻。CD2AP mRNA表达在B组显著高于A组和C组。结论MMF具有治疗SD大鼠DN的作用,并且在转录水平逆转肾皮质CD2AP表达上调。     

Comparison of the effects of tacrolimus and cyclosporine on the pharmacokinetics of mycophenolic acid

Mycophenolate mofetil (MMF) is almost completely absorbed from the gut and is rapidly de-esterified into its active drug, mycophenolic acid (MPA). The main metabolite is glucuronidated MPA (MPAG), which is excreted into bile and undergoes enterohepatic recirculation. Studies in healthy volunteers treated with cholestyramine show that interruption of the enterohepatic recirculation decreases MPA exposure by approximately 40%. Published data show a difference in mycophenolic acid plasma concentrations between kidney transplant recipients treated with MMF plus cyclosporine (CsA) and those treated with MMF plus tacrolimus (TRL). However, the interpretation of these data is complicated by interpatient differences in variables that may influence MMF pharmacokinetics (e.g., underlying disease, co-medication, and time since transplantation). To understand the influence of TRL and CsA on MMF pharmacokinetics (PK) more completely, the authors eliminated confounding variables in clinical studies by performing drug interaction studies in inbred rats. To achieve a steady state, 3 groups of Lewis rats (n = 8 per group) were treated once daily with oral CsA (8 mg/kg), TRL (4 mg/kg), or placebo on days 0-6 before all rats began once-daily oral treatment with MMF (20 mg/kg) on day 7. Combined treatment with either MMF + CsA, MMF + TRL, or MMF + placebo was continued for 1 week (days 8-14). Thereafter, CsA and TRL treatments were stopped but MMF treatment was continued on days 14-21. Blood was sampled during the 24 hours subsequent to dosing on day 7 (after the first MMF dose), on day 14 (after multiple MMF doses) and on day 21 (after CsA/TRL washout). Rats in the MMF + TRL group and in the MMF + placebo group showed a second peak in the MPA-PK profiles consistent with enterohepatic recirculation of MPA. The MPA-PK profiles for the MMF + CsA-treated animals did not show a second MPA peak. On Day 14, the mean plasma MPA-AUC(0-24 hours) for the CsA-treated animals was significantly less than MPA exposures for rats in the MMF + TRL- and the MMF + placebo-treated groups. Furthermore, in contrast to results from other investigators, co-administration of CsA and MMF significantly increased MPAG-AUC(0-24 hours). Serum creatinines did not differ among rats in the three groups. CsA but not TRL decreased MPA plasma levels and increased MPAG-AUC(0-24 hours). These data suggest that CsA inhibits MPAG excretion into bile and offer an explanation for the well-known increased MPA exposure in organ transplant patients caused by conversion from CsA- to TRL-based immunosuppression.     

卡介菌多糖核酸对肾病大鼠血清IL-4和IL-12的影响

目的：通过肾病综合征大鼠血清IL-4、IL-12的动态变化,探讨微小病变型肾病综合征（MCNS）的免疫学发病机制,揭示卡介菌多糖核酸（BCG-PNS）防治肾病可能途径。方法：本研究将40只大鼠随机分为正常组、肾病组、治疗组和预防组,每组10只。阿霉素5mg/kg制MCNS模型,BCG-PNS进行防治。观察大鼠一般情况,1、2、4周测24小时尿蛋白,2、4周取血生化仪测定血清白蛋白和总胆固醇水平,ELISA方法检测血清IL-4、IL-12的水平。实验结束时观察大鼠肾脏形态学改变。结果：1与正常组比较,肾病组出现大量的蛋白尿,低白蛋白血症,高胆固醇血症和明显的水肿,血清IL-4升高,IL-12降低,且均呈持续性加重。阿霉素注射4周,治疗组和预防组除IL-12与正常组无显著差异外,其它均有显著性差异。2与肾病组比较,治疗组在阿霉素注射4周,各指标均有显著性改善。预防组在阿霉素注射后2周与同期肾病组比较各指标均存在显著性差异。结论：1MCNS存在TH1/TH2功能紊乱,IL-4、IL-12参与了MCNS的免疫机制。2BCG-PNS可能通过诱导TH1型反应,促进IL-12的分泌,抑制TH2型反应,使IL-4分泌减少,而调整TH1/TH2的平衡,为MCNS防治提供实验依据。     

吗替麦考酚酯治疗难治性肾病综合征的疗效观察

目的：探讨吗替麦考酚酯（MMF）治疗激素抵抗肾病综合征的疗效。方法：选择本院确诊为肾病综合征患者24例,经强的松1mg·kg^-1·d^-1 8周以上疗效不佳或复发的患者,其中个别患者还经过环磷酰胺或环孢霉素A治疗。所有患者均采用MMF联合小剂量激素治疗,MMF起始剂量为1．0～1．5g／d,至少3个月后开始减量,维持量在0．5～1．0g／d,强的松剂量5—20mg／d,随访时间≥6个月,主要观察治疗前后尿蛋白、血清白蛋白、肝功能、肾功能等的变化。结果：患者治疗后尿蛋白由治疗前（3．4±1．7）g／d降至（0．9±0．2）g／d,血清白蛋白由治疗前（19．6±5．4）g／L增至（36．1±7．7）g／L,血肌酐由治疗前（105．7±6．4）umol／L降至（90．1±5．8）umol／L。20例（83．3％）患者病情缓解,其中完全缓解15例（65．2％）,部分缓解5例（20．8％）,无反应4例（16．6％）。副作用：胃肠适症状8例（33．3％）,细菌性肺炎4例（16．6％）,带状疱疹1例（4．1％）,轻度肝酶升高3例（12．5％）。结论：MMF联合小剂量激素治疗激素抵抗肾病综合征是有效和安全的,可成为难治性肾病综合征（refractory nephrotic syndrome,RNS）的治疗选择。     

Alpha-lipoic acid protects against renal ischaemia-reperfusion injury in rats

1. Oxygen free radicals are important components involved in the pathophysiological processes observed during ischaemia-reperfusion (I/R). The present study was designed to assess the possible protective effect of alpha-lipoic acid (ALA) on renal I/R injury. 2. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min renal pedicle occlusion followed by 24 h reperfusion. Saline or ALA (100 mg/kg, i.p.) was administered 15 min prior to ischaemia and immediately before the reperfusion period. At the end of 24 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) activity were measured in serum samples, whereas tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, 8-hydroxydeoxyguanosine (8-OHdG) and total anti-oxidant capacity (AOC) were assayed in plasma samples. 3. Kidney samples were taken for the determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as Na(+)/K(+)-ATPase and myeloperoxidase (MPO) activity. The formation of reactive oxygen species in renal tissue samples was monitored using a chemiluminescence (CL) technique with luminol and lucigenin probes. Oxidant-induced tissue fibrosis was determined by tissue collagen content and the extent of tissue injury was analysed microscopically. 4. Ischaemia-reperfusion caused a significant increases in blood creatinine, BUN, LDH, IL-1beta, IL-6, TNF-alpha and 8-OHdG, whereas AOC was decreased. In kidney samples from the I/R group, MDA, MPO, collagen and CL levels were found to be increased significantly; however, glutathione levels and Na(+)/K(+)-ATPase activity were decreased. Conversely, ALA treatment reversed all these biochemical indices, as well as histopathological alterations induced by I/R. 5. In conclusion, these data suggest that ALA reverses I/R-induced oxidant responses and improves microscopic damage and renal function. Thus, it seems likely that ALA protects kidney tissues by inhibiting neutrophil infiltration, balancing the oxidant-anti-oxidant status and regulating the generation of inflammatory mediators.     

大黄素对糖尿病大鼠肾组织单核细胞趋化蛋白-1表达的影响

目的探讨大黄素对糖尿病大鼠肾组织单核细胞趋化蛋白-1(MCP-1)表达的影响。方法将SD大鼠随机分为正常对照组、糖尿病对照组、糖尿病大黄素治疗组,经大黄素治疗糖尿病大鼠2,4和8周后,分别观察大鼠血肌酐及24 h尿蛋白定量,以及肾脏MCP-1表达的变化。结果与正常对照组相比,糖尿病大鼠的24 h尿蛋白以及肾组织MCP-1表达显著增加,经大黄素治疗后上述指标在一定程度上有所减轻。结论糖尿病时MCP-1表达增加,大黄素可能通过抑制糖尿病大鼠肾脏MCP-1表达而达到延缓糖尿病肾病的进展。     

氟伐他汀对糖尿病大鼠肾组织TGF-β1表达的影响

目的探讨氟伐他汀对糖尿病大鼠肾组织TGF-β1表达的影响。方法将SD大鼠随机分为正常对照组、糖尿病组、糖尿病氟伐他汀治疗组,经氟伐他汀治疗糖尿病大鼠2,4,8周后,分别观察其对大鼠血胆固醇、血肌酐及24 h尿蛋白定量和肾组织TGF-β1表达的变化。结果与正常对照组相比糖尿病大鼠的24 h尿蛋白以及肾组织TGF-β1表达显著增加,经氟伐他汀治疗后8周,糖尿病大鼠的24 h尿蛋白明显下降,肾组织TGF-β1在蛋白和基因水平表达明显减少。结论糖尿病大鼠肾组织TGF-β1表达增加,氟伐他汀可能通过抑制糖尿病大鼠肾组织TGF-β1表达而达到延缓糖尿病肾病的进展。