维生素E对糖尿病大鼠肾脏的保护作用

目的探讨维生素E对糖尿病大鼠肾脏保护作用及其可能机制。方法实验动物分为正常对照组、链脲佐菌素诱导的糖尿病未治疗组、糖尿病给予维生素E（20mg.kg-1.d-1）治疗组,共观察8周。测定尿白蛋白排泄量(UAE),内生肌酐清除率（Ccr）、血浆及肾脏组织一氧化氮（NO）、一氧化氮合成酶（NOS）、内皮素（ET）和肾小球蛋白激酶C（PKC）。结果2周时糖尿病未治疗组Ccr［(6.47±1.51)ml·min-1·kg-1］、尿白蛋白排泄量［(15.60±1.64)μg/24h］、NO［(37.30±3.77)μmol/L］、NOS［(34.89±3.83)U/L］及肾小球细胞膜PKC［(86.85±11.37)pmol·min-1·mgprotein-1］明显高于对照组,ET低于对照组。8周时糖尿病大鼠肾小球细胞膜PKC［(84.18±12.14)pmol·min-1·mgprotein-1］仍明显高于对照组,但NO［(22.75±2.89)μmol/L］及NOS［(21.34±1.92)U/L］低于对照组,ET高于对照组。给予维生素E治疗组8周时,Ccr［(4.46±0.49)ml·min-1·kg-1］及尿白蛋白量［(16.31±1.12)μg/24h］显著低于未治疗组,8周时肾小球细胞膜PKC［(65.19±8.83)pmol·min-1·mgprotein-1］,2周时NO［(33.13±3.77)μmol/L］及NOS［(30.16±2.89)U/L］明显低于未治疗组,维生素E治疗组2周时与8周时的NO及NOS下降幅度明显小于未治疗组。结论维生素E通过抑制蛋白激酶C可以纠正糖尿病早期的肾脏高滤过、高灌注,并与抑制肾脏NO合成有关,抑制蛋白激酶C活性对糖尿病肾病防治尤为重要。     

老年糖尿病患者自由基与微血管并发症关系的探讨

目的　探讨老年糖尿病患者自由基和抗氧化能力的变化及其与微血管并发症的关系。　方法　测定 6 5例老年糖尿病患者和 6 5例健康老年对照者血浆或红细胞中脂质过氧化物 (LPO)、超氧化物岐化酶 (SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GSH PX)、维生素C(VC)、维生素E(VE)、β 胡萝卜素 (β CAR)、谷胱甘肽 (GSH) ,同时测定患者的空腹血糖、餐后 2h血糖、糖化血红蛋白(HbA1c)、空腹和餐后 2hC肽、血脂、尿微量白蛋白排泄率、肌电图。　结果　老年糖尿病患者LPO(42 97± 6 99)nmol/g高于健康老年组 (31 5 9± 7 4 4 )nmol/g ,SOD(1712 4 4± 15 7 0 4 )U/L、CAT(2 17 0 1± 2 9 36 ) μg/g、GSH PX(2 1 0 1± 3 38)× 10 -10 U/RBC、VC(40 98± 10 5 1) μmol/L、VE(16 4 4± 2 4 5 ) μmol/L、β CAR(1 19± 0 2 3) μmol/L、GSH(0 98± 0 16 )nmol/L低于健康老年组〔分别为 (192 8 38± 14 3 4 4 )U/L、(2 6 4 4 0± 6 3 5 5 ) μg/g、(2 5 16± 6 4 1)× 10 -10 U/RBC、(5 2 2 3± 10 5 1) μmol/L、(2 3 0 4± 5 38) μmol/L、(1 6 3± 0 4 0 ) μmol/L、(1 2 5± 0 2 0 )nmol/L〕 ,合并糖尿病微血管并发症者变化更加明显 ,LPO和年龄呈正相关 (r=0 310 ,P <0 0 5 ) ,SOD、C     

吸氧对慢性缺氧高二氧化碳大鼠肺血管L-精氨酸转运的影响

目的　探讨慢性缺氧 (O2 )高二氧化碳 (CO2 )对大鼠肺动脉L 精氨酸 (L Arg)转运的影响与吸氧的作用。方法　将 4 0只大鼠以随机区组设计法分成 4组 ,用 0 2mmol/L和 5 0mmol/L [3 H] Arg将肺动脉孵育 ,测定其对 [3 H] L Arg的摄取率、一氧化氮合酶 (NOS)活性与一氧化氮 (NO2 /NO3)含量。每组 1 0只。正常对照组 (A组 )、慢性缺O2 4周后伴高CO2 4周组 (B组 )、慢性缺O2 4周伴高CO24周后吸空气 4周组 (C组 )及慢性缺O2 4周伴高CO2 4周后吸O2 4周组 (D组 )。结果　 (1 )肺动脉平均压 (mPAP)、右心室 (RV)和左心室 +室间隔 (LV +S)重量比值 (RV/LV +S) :B组 (33% )与A组(35 % )比较差异有显著性 (P均 <0 0 1 ) ;D组 (2 4 % )与C组 (2 4 % )比较 ,差异也有显著性 (P均 <0 0 5 )。 (2 )离体孵育的肺动脉摄取低浓度 (0 2mmol/L)和高浓度 (5 0mmol/L) [3 H] L Arg比较 :B组分别为 [(3 0 4± 0 1 6 ) μmol·g-1 min-1 ]、[(8 1 2± 0 1 4 ) μmol·g-1 ·min-1 ],A组分别为 [(4 6 2± 0 5 5 )μmol·g-1 ·min-1 ]、[(1 1 2 4± 1 0 2 ) μmol·g-1 ·min-1 ],A、B两组比较差异有显著性 (P均 <0 0 1 ) ;而D组分别为 [(4 30± 0 1 8) μmol·g-1 ·min-1 ]、[(1 2 31± 0 6 5 ) μmol·g-1 ·m     

糖尿病大鼠一氧化氮与骨代谢变化的研究

目的　研究糖尿病 (DM )大鼠血清一氧化氮 (NO)与早期骨代谢改变的关系。方法2 0只SD大鼠分为 2组 ,一组以链脲佐菌素诱导建立糖尿病 (STZ DM )大鼠模型 ,另一为正常对照组 ,测定 2组大鼠的空腹血糖 (FBG)、HbA1c、血清胰岛素、全身、股骨和腰椎骨密度 (BMD)、骨代谢相关指标〔血清钙、骨钙素、降钙素、甲状旁腺素 (PTH)、维生素D3 及尿吡啶酚 /肌酐比〕和血清NO水平。结果　STZ DM大鼠与正常对照组相比 ,血清NO水平显著升高〔(5 1.3± 11.9vs 38.1± 12 .0 )μmol/L ,P <0 .0 1〕 ;全身、股骨和腰椎的BMD显著降低〔(0 .15± 0 .0 7vs 0 .2 1± 0 .0 2 ) g/cm2 ,P<0 .0 1;(0 .16± 0 .0 2vs 0 .19± 0 .0 3) g/cm2 ,P <0 .0 5 ;(0 .12± 0 .0 4vs 0 .18± 0 .0 6 ) g/cm2 ,P <0 .0 5〕 ;血清钙浓度显著升高〔(135 .9± 11.3vs 117.2± 6 .5 )mg/L ,P <0 .0 0 1〕 ,骨钙素水平显著升高〔(0 .0 7± 0 .0 4vs 0 .0 5± 0 .0 1) μg/L ,P <0 .0 5〕 ,维生素D3 水平显著降低〔(7.6± 1.9vs 11.6± 4 .1)μg/L ,P <0 .0 5〕 ,尿吡啶酚 /肌酐显著降低〔(4.8± 0 .8vs 75 .8± 6 0 .7)nmol/mmolCr,P <0 .0 1〕 ;而降钙素和PTH水平改变无统计学意义。相关性分析显示 ,血清NO与尿吡啶酚排泄呈负相关 (r= - 0 .74 ,     

阿魏酸钠对单侧输尿管梗阻大鼠肾脏损害的改善作用

目的观察阿魏酸钠(SF)对单侧输尿管梗阻(UUO)大鼠肾脏损害的改善作用。方法将W istar大鼠48只随机分为假手术组、UUO组、苯那普利治疗组及阿魏酸钠治疗组,于给药2和4 w后分别检测各组大鼠肾脏指数、左右肾重比、尿NAG酶活性、尿液尿素氮、尿肌酐、血尿素氮、血肌酐及24 h尿蛋白排泄量等指标。结果给药2 w后,与模型组比较,阿魏酸钠组大鼠肾脏指数(0.64±0.10)、尿NAG酶活性〔(18.0±5.43)U/L〕、血尿素氮〔(7.3±1.1)mmol/L〕、血肌酐〔(35.2±8.4)μmol/L〕及24 h尿蛋白排泄量〔(9.8±4.4)mg/24 h〕均明显降低(P<0.05),苯那普利组与阿魏酸钠组结果相似;给药4 w后,阿魏酸钠组大鼠肾脏指数(0.57±0.23)、尿肌酐〔(551±196)μmol/L〕和血尿素氮〔(11.1±1.8)mmol/L〕均较模型组明显减低(P<0.05)。结论阿魏酸钠对UUO引起的大鼠肾损害具有明显改善作用。     

糖尿病肾病患者血清和尿IV型胶原的变化

目前有关糖尿病肾病的发生发展机制中非肾小球损伤如间质纤维化促进糖尿病肾病进展[1] 的报道甚少。我们检测 3 9例糖尿病和糖尿病肾病患者血清和尿ＩＶ型胶原 (ＣＩＶ )。现分析如下。对象与方法1.对象 :糖尿病患者 3 9例 ,男性 17例 ,女性 2 2例。按肾脏受累程度分为 3组 :(1)无肾受累组 ,平均年龄 (62± 10 )岁 ,尿白蛋白排泄率 <2 0 μｇ/ｍｉｎ ;(2 )肾受累组 ,平均年龄 (61± 9)岁 ,尿白蛋白排泄率≥ 2 0 μｇ/ｍｉｎ ,内生肌酐清除率≥ 80ｍｌ/ｍｉｎ ;(3 )肾功能不全组 ,平均年龄 (62± 7)岁 ,内生肌酐清除率 <70ｍｌ/ｍｉｎ。对照…     

桑叶提取液对实验性糖尿病大鼠血糖、LPO含量及SOD水平的影响

目的　观察桑叶提取液对实验性糖尿病大鼠血糖、LPO含量及 SOD活性的影响。方法　以 2 0 0 mg/ kg四氧嘧啶皮下注射造成糖尿病大鼠模型 ,以拜糖平为阳性药物对照 ,用桑叶提取液 (0 .4g/ ml)灌胃 4w,测定各组血糖、L PO、SOD水平。结果　与对照组比较 ,桑叶提取液、拜糖平均有明显降血糖作用 (P<0 .0 5)。桑叶提取液组血糖由 1 8.95± 4.2 8降至 1 0 .82± 3.2 2 (mmol/ L,P<0 .0 1 ) ,L PO含量由 1 0 .2 0± 2 .50降至 5.56± 2 .38(nmol/ L,P<0 .0 5) ,SOD水平由 5.61± 2 .0 3升至 7.45± 2 .1 4 (u/ ml,P>0 .0 5)。拜糖平组血糖由 1 8.90± 2 .42降至 1 1 .85± 3.82 (mmol/ L,P<0 .0 5) ,LPO含量由 9.57± 2 .41降至 4.82± 2 .32 (nmol/ L,P<0 .0 5) ,SOD水平由 6.57± 2 .45升至 7.1 4± 3.1 6(u/ ml,P>0 .0 5)。结论　蚕桑叶水提取液能降低四氧嘧啶糖尿病大鼠血糖及 LPO含量 ,同时能升高 SOD水平。     

苯那普利对糖尿病肾病UALB、TGF-β1、CⅣ和LAM影响

目的 评价苯那普利对糖尿病肾病(DN)的临床疗效,并探讨相应作用机制.方法 采用随机对照研究,观察苯那普利治疗前后DN患者24 h平均尿微量白蛋白排泄量以及尿转化生长因子β1(TGF-β1)、层黏连蛋白(LAM)和Ⅳ型胶原(CⅣ)的变化.结果 苯那普利治疗6月后,患者24 h尿微量白蛋白平均排泄量为(0.044±0.034) g,尿TGF-β1为(1.48±0.59) μg/L,LAM为(22.74±23.26 )μg/L量,CⅣ浓度为(13.47±10.94) μg/L量,均较治疗前有显著降低(P＜0.05),而对照组则较基线值明显升高(P＜0.05).结论 苯那普利可以有效降低血压、抑制肾脏TGF-β1、LAM及CⅣ的表达、显著减少DN患者尿蛋白的排出,从而发挥其肾脏保护作用.     

洛沙坦降低糖尿病大鼠肾组织膜3型基质金属蛋白酶mRNA的表达

目的　研究洛沙坦对糖尿病大鼠肾组织膜 3型基质金属蛋白酶 (MT3 MMP)mRNA表达的影响。方法　雄性Wistar大鼠分为 3组 ,A组 (11只 )为正常对照组 ,B组 (11只 )为糖尿病未干预组 ,C组 (9只 )为糖尿病大鼠洛沙坦 (血管紧张素Ⅱ 1型受体阻断剂 )干预组。以链脲佐菌素 (STZ)制备糖尿病大鼠模型。大鼠饲养 18周后取出肾脏检测MT3 MMPmRNA表达、电镜检测大鼠肾小球基底膜厚度及系膜基质密度 (系膜基质面积 /系膜面积 ) ;收集 2 4h尿测定尿白蛋白排泄量 (UAE)。mRNA表达采用RT PCR ,以 β actin作为内对照。UAE测定采用大鼠白蛋白特异的酶免疫分析试剂盒。结果　肾组织MT3 MMPmRNA表达在B组大鼠 (1.37± 0 .96 )显著高于A组 (0 .75± 0 .34,P <0 .0 5 )和C组 (0 .75± 0 .30 ,P <0 .0 5 ) ,而后两组比较差异无显著性。UAE、肾小球基底膜厚度及系膜基质密度在B组大鼠均显著高于A组和C组 (P <0 .0 5 )。结论　STZ糖尿病大鼠肾组织MT3 MMPmRNA表达明显增加 ,洛沙坦处理能延缓糖尿病肾病的发生 ,与此同时降低MT3 MMPmRNA表达。提示MT3 MMP与糖尿病肾病发病可能有一定关系。     

青年夜尿游离皮质醇与原发性高血压的关系

目的 :研究青年夜尿游离皮质醇的排泄量与原发性高血压的关系。方法 :对 188名青年进行血压及相关因素、夜 8小时尿游离皮质醇的测定。结果 :青年男性原发性高血压者夜 8小时尿游离皮质醇的排泄量显著高于血压正常者 ( 2 1 5 7± 6 2 8μg/8h对 10 5 4± 5 46μg/8h ,P <0 0 5 ) ;高血压家族史阳性者显著高于高血压家族史阴性者 ,在男、女性中分别为 16 90± 6 5 0 μg/8h对 9 44± 4 95 μg/8h(P <0 0 5 ) ,10 5 4± 5 46μg/8h对 6 2 2± 3 18μg/8h(P <0 0 5 ) ;男性明显高于女性 ,12 73± 5 85μg/8h对 7 80± 4 15 μg/8h(P <0 0 5 )。结论 :青年男性高血压者夜 8小时尿游离皮质醇的排泄量明显高于血压正常者 ,夜尿游离皮质醇的排泄量与高血压的家族史相关联 ,且存在明显的性别差异。提示青年高血压患者及其易感者中已存在皮质醇代谢的异常 ,糖皮质激素可能参与高血压的发病过程。     

血管紧张素转换酶抑制剂对糖尿病大鼠肾皮质细胞膜胰岛素受体的调节

目的研究血管紧张素转换酶抑制剂（ＡＣＥＩ）对糖尿病大鼠肾皮质细胞膜胰岛素受体表达的调节。方法实验大鼠随机分三组：单侧肾切除组（Ｃ组,６例）;糖尿病组（Ｄ组,７例）及糖尿病苯那普利治疗组（ＤＢ组,７例）。观察四周后各组血糖、血胰岛素及血肌酐水平和体重、肾重及肾重／体重之比的变化,测定血浆、肾皮质及髓质血管紧张素转换酶（ＡＣＥ）活性,采用Ｗｅｓｔｅｒｎ杂交分析肾皮质细胞膜胰岛素受体蛋白表达。结果苯那普利治疗四周后能够改善糖尿病大鼠血糖、血胰岛素及血肌酐水平的异常,对糖尿病肾脏肥大有显著抑制作用,对血浆、肾皮质及髓质ＡＣＥ活性抑制分别达９２．００％,８８．７７％与７３．４０％。肾皮质细胞膜胰岛素受体蛋白表达比对照组增加约２．１０倍,苯那普利治疗四周后对此有明显的下调作用。结论苯那普利可下调糖尿病状态下肾皮质细胞膜胰岛素受体蛋白高表达,这可能是其对糖尿病肾脏保护作用的重要机制之一。     

Longitudinal evaluation of the renal clearance of glycated albumin in the diabetic rat

This study has examined glycation of serum albumin and its role in evolving diabetic proteinuria. Renal clearances of endogenous glycated and nonglycated albumin were studied in groups of normal and streptozotocin-induced diabetic Wistar-Kyoto rats over a 32 week period. Concentrations of glycated and nonglycated albumin in serum and urine were measured by rat albumin radioimmunoassay following separation on m-aminophenylboronate affinity columns. Levels of glycated serum albumin in diabetic rats were significantly higher than in normal rats (5.9 +/- 0.7% vs 4.4 +/- 0.3%, P less than 0.05). Median total urinary albumin excretion increased from 120 micrograms/24 h at baseline to 879 micrograms/24 h (P less than 0.05) 28-32 weeks after induction of diabetes. The renal clearance of glycated albumin was approximately twice as great as that of nonglycated albumin in both normal (P less than 0.01) and diabetic (P less than 0.01) rats. However, the glycated albumin/nonglycated albumin clearance ratio in diabetic rats did not correlate with duration of diabetes or with the level of albuminuria. These results indicate that glycation of albumin does not contribute disproportionately to the development of proteinuria in the diabetic rat, during which median renal albumin clearance increased 7-fold. Other factors, such as glycation of the glomerular filtration surface, may have a more important role in the pathogenesis of proteinuria in experimental diabetes.     

转化生长因子βI型受体在糖尿病大鼠肾皮质中的表达及苯那普利对其 …

目的 研究转化生长因子βⅠ型受体（ＴＧＦβＲⅠ）在糖尿病大鼠肾皮质中的表达及血管紧张素转换酶抑制剂苯那利普利对其调节作用。方法 纯种雄性成年Ｗｉｓｔａｒ大鼠随机分单侧肾切除组（Ｃ组）,糖尿病组（Ｄ组）和糖尿病苯那普利治疗组（ＤＢ组）,给药４周末观察各组血清、血肌酐水平、体重、肾重和肾组织蛋白含量及血浆、肾皮质、髓质血管紧张素转换酶（ＡＣＥ）活性的变化;分别采用逆转录聚合酶链反应（ＲＴ－ＰＣＲ）、Ｎ     

氨氯地平和苯那普利联合治疗对高血压患者肾功能的影响

目的探讨氨氯地平、苯那普利单独治疗和联合治疗对高血压病患者肾功能的影响。方法66例高血压病患者随机分为3组:氨氯地平组(5mg,qd,22例);苯那普利组(10mg,qd,22例);氨氯地平和苯那普利联合治疗组(氨氯地平5mg,qd,苯那普利10mg,qd,22例)。疗程24周。治疗前、后观察肾功能指标变化。结果①氨氯地平、苯那普利及联合治疗组高血压病患者治疗后均能显著降低血压(P<0.01)及尿蛋白的排泄量。但联合治疗组降低尿蛋白排泄的幅度比氨氯地平组、苯那普利组明显高,而氨氯地平组和苯那普利组之间差异无统计学意义(P>0.05)。②治疗后,肾小球滤过率在联合治疗及苯那普利组明显增高,而氨氯地平组无明显变化。③三组治疗后尿白蛋白下降幅度与血压下降幅度均无显著相关。结论氨氯地平、苯那普利长期单独治疗均可减少蛋白尿,保护肾功能,两药联合治疗对减少蛋白尿、保护肾功能有一定相加作用。     

苯那普利对糖尿病肾小球细胞外基质增生的抑制作用及机制

目的 :了解血管转换酶抑制剂苯那普利对单侧肾切除糖尿病大鼠肾脏结构和功能改变的保护作用及机制。　 方法 :应用生物化学分析 ,RT- PCR方法检测苯那普利治疗对糖尿病大鼠血尿素氮、肌肝、血脂、肾小球细胞外基质 (ECM)以及肾皮质内金属蛋白酶 - 3(MMP- 3)的m RNA表达的影响。　 结果 :糖尿病大鼠的尿素氮、肌酐及甘油三酯、胆固醇水平均较非糖尿病大鼠明显增加 ,PAS染色发现肾小球系膜区 ECM明显积聚。苯那普利治疗后肾功能指标、甘油三酯水平明显下降 ,升高的胆固醇也有下降趋势 ,ECM积聚显著被抑制 ,苯那普利治疗组大鼠肾皮质内金属蛋白酶 3m RNA表达明显增加。　 结论 :单侧肾切除加重了糖尿病大鼠的肾脏病变 ,苯那普利治疗可通过多种途径发挥显著的防治作用 ;其中对组织学改变的保护作用可能与其上调金属蛋白酶的表达 ,促进 ECM降解密切相关。     

Protective effect of Gui Qi mixture on the progression of diabetic nephropathy in rats.

Huang Qi (root of Astragalus membranaceus) and Dang Gui ( Angelica sinensis), two of the most widely used herbs in traditional Chinese medicine, have been proven to be effective in the treatment of diabetes mellitus (DM) although the underlying molecular mechanisms are not fully elucidated. This study was designed to investigate the protective effect of Dang Gui and Huang Qi mixture (GQM) on the development of diabetic nephropathy in rats with streptozotocin (STZ)-induced DM and the possible underlying molecular mechanism. The diabetic animal model was made by a single intraperitoneal injection of STZ and then treated with GQM or benazepril. Blood glucose, triglyceride (TG), cholesterol (CHO), high density lipoprotein (HDL), serum creatinine (Scr), creatinine clearance rate (Ccr), blood urea nitrogen (BUN), urine beta (2)-microglobin (beta (2)-MG), kidney/body weight (K/B) ratio, glomerular area (GA), renal transforming growth factor-beta (1) (TGF-beta (1)) mRNA expression and blood and renal angiotensin II (AngII) expression were determined 8 weeks after the treatment. The blood glucose, CHO and TG levels, BUN, SCr, Ccr. K/B ratio, GA, the excretion of beta (2)-MG, renal TGF-beta (1) mRNA expression and blood and renal AngII expression were significantly increased while the HDL level was decreased 8 week after STZ injection. The changes in blood glucose, TG, CHO and HDL were reversed by GQM, not by benazepril, whereas the changes in other variables were reversed by both GQM and benazepril. Our results suggest that GQM alleviates the disorder in blood glucose and lipids, protects against the progression of renal nephropathy in diabetic rats, probably by inhibiting the expression of AngII and TGF-beta (1) mRNA.     

Discordant effects of the aldose resuctase inhibitor,sorbinil, on vascular structure and function in chronically diabetic and galactosemic rats

Effects of sorbinil, an aldose reductase inhibitor, were examined on renal glomerular structure, urinary albumin and IgG excretion, and vascular albumin permeation in eyes and aorta of 8-month diabetic, galactose-fed, and age-matched control rats. Sorbinil was added to the diet of one-half of the rats in each group at the time of induction of diabetes and galactosemia. Weight gain was impaired in diabetic and galactose-fed rats versus controls and was improved slightly in corresponding sorbinil-treated groups. Plasma glucose and glycosylated hemoglobin levels, food consumption, and 24-hr urine volume were increased in diabetic rats and were unaffected by sorbinil treatment. Food consumption and glycosylated hemoglobin levels were increased in galactose-fed rats, although the increases were smaller than in diabetic rats; glycosylated hemoglobin levels were decreased by sorbinil. Diabetes- and galactosemia-induced increases in albumin permeation in eyes and aorta were prevented by sorbinil. Urinary excretion of albumin and IgG was increased by diabetes and decreased by sorbinil, although differences between the two diabetic groups were not statistically significant for albumin. Galactosemia was associated with an increase in urinary albumin and IgG excretion that did not reach statistical significance. Glomerular capillary basement membrane width (GBMW) was increased in diabetic versus agematched control rats but was unaffected by galactose feeding. GBMW was increased in controls fed sorbinil and glomerular capillary basement membrane thickening in diabetic rats was not prevented by sorbinil. The fractional volume of the glomerulus occupied by mesangium (V_vmes) was increased in diabetic and galactose fed rats versus agematched controls, and was unaffected by sorbinil. The explanation for the discordant effects of sorbinil on generalized vascular dysfunction versus glomerular structural changes remains unclear.     

Effects of aminoguanidine and vitamin C on collagen type IV in diabetic nephropathy rats

The aim of this article is to investigate the effects of Aminoguanidine and vitamin C (VitC) on type IV collagen in diabetic nephropathy rats. Diabetic nephropathy rats were induced by intraperitoneal injection of STZ. Rats were randomly divided into five groups: normal control group (n = 10), diabetes group (n = 10), aminoguanidine group (n = 10), VitC group (n = 10), aminoguanidine and VitC group (n = 10). After 16 weeks, the general conditions, blood gloucose, glycosylated hemoglobin, blood urea nitrogen, serum creatinine, serum type IV collagen, urinary albumin excretion rate, and creatinine clearance rate were detected, type IV collagen protein was determined by immunohistochemical analysis as well as the expression of collagen type IVα1 mRNA were determined by in situ hybridization analysis in the kidneys of each group. The results were (1) diabetes mellitus and renal lesions occurred in the diabetes group, aminoguanidine group, VitC group, VitC and aminoguanidine group; (2) aminoguanidine and VitC improved the general conditions of diabetic nephropathy rats, decreased blood urea nitrogen, serum creatinine, and urinary albumin excretion rate as well as increased creatinine clearance rate. The expressions of collagen type IV were significantly down-regulated in treatment groups in contrast to the diabetes group. Aminoguanidine and VitC protect renal lesions in diabetic nephropathy, respectively, by inhibiting expression of type IV collagen, while aminoguanidine and VitC have a synergistic effect on them.     

Combined therapy of rhein and benazepril on the treatment of diabetic nephropathy in db/db mice.

OBJECTIVE: Rhein and angiotensin-converting enzyme inhibitor (ACEI) have been reported to prevent the progression of diabetic nephropathy (DN). We further explore the unknown ability to induce renal-protection of rhein and ACEI combined therapy in DN compared with the therapeutic effects of single treatment of them by using db/db mouse of type 2 diabetes model. METHODS: db/db and db/m mice, 8 weeks of age, were divided into five groups according to the following treatments: (A) db/m, given saline treatment; (B) db/db, given saline treatment; (C) db/db, given rhein treatment (150 mg/kg/day); (D) db/db, given benazepril treatment (10 mg/kg/day); (E) db/db, given rhein (150 mg/kg/day) with benazepril (10 mg/kg/day). Body weight, plasma glucose, plasma lipid and 24 h urinary albumin excretion levels were measured every 4 weeks. Morphometry of renal tissue and immunohistology of transforming growth factor-beta1 (TGF-beta) and fibronectin were determined for all groups at the end of the treatment. RESULTS: It was found that after treatment urinary albumin excretion was reduced after 4 weeks treatment in group E and after 8 weeks treatment in groups C and D, when compared to group B (p<0.05). Plasma creatinine levels dropped significantly for group E, compared with the diabetic control group by the end of the treatment period. Furthermore, after the treatment body weight, plasma glucose, cholesterol, triglyceride and low density lipoprotein all decreased in groups C and E compared to group B (p<0.05). Histological morphometric analysis revealed that the whole glomerular area and extracellular matrix area was significantly reduced in groups C, D and E compared to group B, at 20 weeks of age, an effect most pronounced in group E. Using immunohistochemistry, the expression of fibronectin and TGF-beta1 in groups C, D and E was found to have decreased compared to group B, after 12 weeks treatment, again the effect being more pronounced in group E. CONCLUSIONS: There appeared to be a similar renal protective effect of rhein compared with benazepril in diabetic nephropathy. A combined therapy may offer a more beneficial complementary effect on kidney injury in db/db mice, as reflected by urinary albumin excretion, renal function and histological changes. Our findings suggest that a therapeutic approach that combines rhein with ACEI provides a more effective therapy for DN than does either agent alone.     

羟苯磺酸钙联合前列地尔治疗早期糖尿病肾病疗效及对血液流变的影响分析

目的探讨对早期糖尿病肾病患者应用羟苯磺酸钙联合前列地尔治疗的临床效果,以及对患者血液流变的影响。方法选入该院于2017年4月—2018年4月期间所收治的早期糖尿病肾病患者72例,采用随机数字表法将其平分为研究组和对照组,每组36例。对照组行前列地尔治疗,研究组在此基础上加行羟苯磺酸钙治疗,对比两组患者的治疗效果,治疗前后两组患者血液流变情况变化,两组患者的肾功能指标的变化,两组患者尿清蛋白的含量的变化。结果研究组治疗效果优于对照组,差异有统计学意义(P<0.05)。且治疗之前,两组患者的血液流变情况变化,肾功能指标的变化,尿清蛋白的含量的变化差异无统计学意义(P>0.05),治疗之后,研究组的血液流变情况变化,肾功能指标的变化,尿清蛋白的含量的变化均比对照组理想(P>0.05)。结论对于早期糖尿病肾病的患者而言,采用羟苯磺酸钙联合前列地尔治疗,能够促使治疗效果的提高,缓解患者的临床症状,血液流变的指标得到明显的改善,值得在临床上推广和应用。