大鼠肾缺血再灌注损伤中ICAM-1表达的变化

目的:观察细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)在大鼠肾缺血再灌注(ischemia/reperfusion,I/R)不同时间点表达的变化并与肾功能恶化程度做相关性分析,从而探讨ICAM-1在肾I/R损伤中所起的作用.方法:应用苦味酸法和二乙酰一肟反应法测定大鼠肾I/R不同时间点血肌酐和尿素氮值, HE染色光镜下观察石蜡包埋切片肾组织损伤的形态学改变,免疫组化法分析ICAM-1在肾I/R不同时间点表达的变化.结果:肾功能检测发现, 再灌注1 h后血肌酐和尿素氮值开始增高和正常对照组比较有统计学差异(P＜0.05),12 h达峰值.HE染色光镜下观察肾组织细胞以近端肾小管变性、坏死为主,I/R各时间点肾组织病理损伤变化与肾功能变化规律相一致.再灌注后早期ICAM-1表达以内皮细胞为主,后期肾脏各部均可表达,小管上皮尤甚.肾脏表达的ICAM-1与肾功能恶化程度存在明显的正相关(P＜0.01).结论:I/R早期肾脏即有ICAM-1表达,其表达量与肾功能恶化程度呈正相关,提示ICAM-1在肾I/R损伤发病机制中起促进作用.     

丹参及血栓通注射液对缺血再灌注大鼠肾脏的影响

丹参及血栓通注射液对缺血再灌注大鼠肾脏的影响徐幼筠，杜学海，邹万忠ＴＨＥＥＦＦＥＣＴＯＦＳＡＬＶＩＡＥＭＩＬＴＩＯＲＲＨＩＺＡＥ（ＳＭ）ＡＮＤＡＲＡＳＡＰＯＮＩＮ（ＡＲ）ＯＮＩＳＣＨＥＭＩＡ－ＲＥＰＥＲＦＵＳＩＯＮＲＡＴＫＩＤＮＥＹＸｕＹｏｕｊｕｎ；...     

缺血预处理对大鼠急性缺血-再灌注肾细胞凋亡的影响

目的:探讨缺血预处理对急性肾缺血-再灌注细胞凋亡的影响。方法:采用8 min缺血加5 min再灌注预处理在体肾缺血-再灌注模型(I45 min I-R 6h),将实验动物随机分为正常(A组)、假手术(S组)、单纯缺血(B组)、缺血再灌注(C组)、预处理(D组)五组,采用透射电镜、流式细胞仪检测肾细胞凋亡和细胞增殖周期,利用光学显微镜进行组织学观察,同时测定血清中尿素氮(BUN)、肌酐(Cr)及MDA含量。结果:与A、S组相比,C组细胞凋亡率显著增高(P<0.01);与C组相比,D组细胞凋亡率和细胞增殖指数均降低(P<0.01),G0/G1时段增加(P<0.01),肾组织损伤病理评分显著降低(P<0.05),同时肾超微结构破坏较轻。结论:缺血预处理对急性肾缺血-再灌注有保护作用,可以减轻急性肾缺血-再灌注引起的细胞凋亡,其作用机制可能与调节细胞增殖周期有关。     

缺血后处理对大鼠肾缺血再灌注损伤的影响

目的探讨缺血后处理对大鼠肾缺血再灌注损伤的影响。方法SD大鼠32只,雌雄不拘,随机分为4组（n=8）,假手术组（Ⅰ组）;对照组（Ⅱ组）建立肾缺血再灌注（I/R）模型;不同时间缺血后处理组（Ⅲ组和Ⅳ组）,建立I/R模型,Ⅲ组于缺血后再灌注10s,停灌10s,反复3次;Ⅳ组缺血后再灌注2min,停灌2min,反复3次。测定再灌注24h时血清尿素氮（BUN）、肌酐（Cr）浓度、超氧化物岐化酶（SOD）活性和丙二醛（MDA）浓度,光镜下进行肾组织病理形态学观察,采用免疫组化法测定肾组织血红素氧合酶-1（HO-1）表达。结果再灌注24h时,与Ⅰ组比较,其余3组血清Cr、BUN和MDA浓度升高,SOD活性和HO-1表达降低（P〈0.01）;与Ⅱ组比较,Ⅲ组和Ⅳ组血清Cr、BUN、MDA浓度和HO-1表达降低,SOD活性升高（P〈0.05或0.01）;Ⅲ组和Ⅳ组各指标差异无统计学意义（P〉0.05）。Ⅲ组和Ⅳ组病理改变明显轻于Ⅱ组。结论缺血后处理可减轻大鼠肾缺血再灌注损伤,其机制与上调HO-1的表达和清除氧自由基有关。     

缺血后处理对大鼠肾缺血再灌注损伤的影响

目的探讨缺血后处理对大鼠肾缺血再灌注（I／R）损伤的影响及其机制。方法18只雄性SD大鼠随机分为3组（n=6）：假手术组（S组）、缺血再灌注组（I／R组）和缺血后处理组（IPo组）。采用夹闭双侧肾蒂45min-再灌注6h制备肾脏缺血再灌注损伤模型。IPo组在夹闭双侧肾蒂45min后，再灌注10s，缺血10s，重复3次后，完全恢复肾血流。再灌注6h时开胸，取心脏血后处死大鼠，取肾组织。测定血清肌酐（Cr）、尿素氮（BUN）和尿酸（UA）浓度，肾组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性；光镜下观察肾组织病理学改变；采用原位末端脱氧核苷酸转移酶标记（TUNEL）法检测肾组织中凋亡细胞，光镜下计数凋亡细胞，并计算肾小管上皮细胞凋亡指数（AI）。结果与S组比较，I／R组和IPo组Cr和BUN浓度升高（P〈0．05），UA浓度差异无统计学意义（P〉0．05），肾组织SOD活性降低，MDA含量升高，肾小管上皮细胞凋亡指数增加（P〈0．05），病理损伤明显。与I／R组比较，IPo组Cr和BUN浓度降低（P〈0．05），UA浓度差异无统计学意义（P〉0．05），SOD活性升高，MDA含量降低，肾小管上皮细胞凋亡指数减少（P〈0．05），病理损伤减轻。结论缺血后处理能减轻大鼠肾缺血再灌注损伤，其机制与增强肾脏抗氧化能力和抑制肾组织细胞凋亡有关。     

臭氧氧化预处理对大鼠肾缺血再灌注损伤的热休克蛋白表达的影响

目的 探讨臭氧氧化预处理通过诱导热休克蛋白70(HSP70)的合成,保护大鼠肾脏缺血再灌注损伤的作用与机制.方法 建立原位大鼠单侧肾缺血再灌注动物模型,I/R前15 d经直肠吹入氧气和臭氧的混合气体5.0～5.5 ml(臭氧浓度50 mg/L,1 mg/kg体蕈,每日 1次).全自动生化分析仪检测尿素氮(BUN)、肌酐(Cr),比色法测定血清的脂质过氧化产物丙二醛(MDA)、超氧化物歧化酶(SOD).Western blot检测HSP70蛋白的含量;逆转录聚合酶链反应(RT-PCR)方法检测HSP70的表达.结果 肾缺血再灌注24 h后,血清中BUN、Cr、MDA明显增高,肾组织内HSPT0表达明显增强(P<0.05),经臭氧氧化预处理后,血清中的BUN、Cr、MDA均降低,SOD升高;HSP70表达升高更加明显(P<0.05).结论 臭氧氧化预处理可以诱导大鼠肾缺血再灌注组织中HSP70表达,减轻大鼠肾脏缺血再灌注损伤.     

α2肾上腺素受体在大鼠肾缺血再灌注损伤中的作用

采用放射受体结合分析法研究大白鼠肾缺血６０分钟时肾α２肾上腺受体的改变，发现大白鼠肾α２受体具有高、低亲和力两个位点。肾缺血６０分钟时，肾α２受体高亲和力位点亲和力增加，位点数量减少；低亲和力位点亲和力降低，位点数量增多。提高肾缺血６０分钟时肾α２受体呈超敏状态，表明肾α２受体在肾缺血及再灌注损伤中可能起重要作用。     

褪黑素对急性肾缺血再灌注损伤的预防作用

褪黑素 (Ｍｅｌ)是松果体合成分泌的神经内分泌激素 ,有多种生物学功能。近十年的研究证实它是迄今已知的最强的自由基清除剂 ,国内尚未见相关的研究报道。我们用钳夹大鼠双侧肾蒂造成急性肾缺血再灌注损伤 (ＡＲＩＩ)动物模型 ,探讨褪黑素对ＡＲＩＩ的预防保护作用。一、材料与方法1.动物分组与模型 :36只健康成年ＳＤ大鼠 ,雄性 ,随机分为 6组 (ｎ =6 ) :(1)假手术对照组 ;(2 )手术对照组 :缺血前 30分钟腹腔注射生理盐水 0 3ｍｌ作为阴性对照 ;(3)手术 维生素Ｃ组 :按15 0ｍｇ/ｋｇ计算 ,于缺血前 30分钟腹腔注射作为阳性对照 ;(4)～ (…     

大鼠肾冷缺血再灌注损伤模型的建立

目的 建立大鼠肾冷缺血再灌注损伤(IRI)的模型.方法 封闭群SD大鼠24只,随机分为2组(n=12):A组(对照组),B组(实验组).A组切除右肾并游离左肾蒂,60 min后关闭腹腔切口.B组采用冷缺血再灌注模型,主要步骤:(1)冷灌注:右肾动脉插管对左肾原位灌注.通过右肾静脉插管将灌注液引流出体外,完成冷灌注后切除右肾,阻断左肾蒂.(2)冷缺血保存:将已充分游离的左肾牵至腹腔外,在自制保存袋中冷保存.(3)再灌注:60min后,去除保存袋,开放血流,再灌注左肾,左肾复位,缝合切口;2组大鼠均在术后24 h再次手术切除左.肾.肾组织进行光镜、电镜形态学检查,检测肾组织匀浆中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量,术前与术后24 h取血标本进行测定血尿素氮(BUN)、肌酐(Cr)评估肾功能.结果 (1)形态学检查(光镜与电镜超微结构):A组肾脏组织形态结构正常,B组损伤表现明显;(2)A组手术前后比较血浆BUN、Cr测定值差异均无统计学意义(P＞0.05).IR后的B组均高于术前,差异有统计学意义(P＜0.05);(3)IRI后A组肾组织匀浆SOD活力高于B组(P＜0.05),A组肾组织匀浆MDA含量测定值低于B组,差异有统计学意义(P＜0.05).结论 建立的模型要求条件简单、易行,可用于肾移植冷缺血再灌注损伤相关的研究;

Abstract：

Objective In this study,for studying IRI in kidney transplantation. ,we established the models of cold ischemia and reperfusion injury in rats. Methods Twenty four SD rats were randomly assigned to two groups:control (A) ,and experimental (B) group. Group A was only removed the right kidney. Cold ischemia reperfusion was performed as the follow-listed model in Group B. The main process of the model: ( 1) Perfusing left kidney: after resected the right kidney of the rat, one pipe was put in the remainder right renal artery to perfuse the left kidney. The perfusion flowed out through another pipe in the right renal vein. The blood vessels of left kidney were clipped after cold perfusion. (2) Cold ischemic conservancy : the operation table was leant to left side, and the left kidney was taken out of abdominal cavity then stored in a cold bag which was full of ice and water,but the vessels of that were intact. (3) Reperfusing left kidney: after 60 minutes, the clip was removed. Left kidneys of all rats in two groups were removed to be detected. Structure of the kidney was evaluated by light microscopy and electronic microscopy. Superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content in the renal tissues was examined,and the renal function was also assessed by determining the levels of blood urea nitrogen ( BUN) and serum creatinine (CR) before and 24 hours after operation. Results (1) Morphologic change (hematoxylin-eosin staining) :A normal morphology was observed by light microscopy and electon microscopy in group A.Significant injury was detected in group B. (2 ) In group A, there was not significant difference about BUN and CR between before and after operation (P ＞0. 05) ,but in Group B,those increased significantly at 24 hour after operation (P ＜0. 05). (3) Activity of SOD in renal tissues in group A was higher than those in group B (P ＜ 0. 05 ) , meanwhile, Content of MDA in group A was lower than those in group B ( P ＜0. 05 ).Conclusion The rat renal cold ischemia reperfusion model we established is feasible regardless of experimental conditions, and can be studied as the events following IRI in kidney transplantation.     

黄芪对肾缺血再灌注损伤的保护作用

目的 探讨黄芪注射液对肾脏缺血再灌注损伤的影响。方法 观察黄芪注射液对肾缺血再灌注损伤大鼠血浆超氧化物歧化酶（ＳＯＤ）,脂质过氧化产物丙二醇（ＭＤＡ）,内以素－１（ＥＴ－１）,一氧化氮（ＮＯ）变化及肾组织病理改变。结果 黄芪治疗组血浆ＥＴ０－１,ＭＤＡ水平较缺血再灌注组显著下降,ＳＯＤ显著升高,且病理改变较轻。结论 黄芪对肾脏缺血再灌注损伤具有保护作用。．     

银杏达莫联合厄贝沙坦治疗糖尿病肾病的临床疗效

目的总结银杏达莫注射液联合厄贝沙坦治疗糖尿病肾病的疗效。方法将68例Ⅲ期糖尿病患者分成治疗组和对照组各34例,对照组在糖尿病原治疗方案上加用厄贝沙坦片,治疗组加用厄贝沙坦片和银杏达莫注射液,疗程3周。观察患者24hUAER、β2-MG改变。结果治疗组治疗后的UAER、β2-MG明显下降,差异有统计学意义（P〈0.05）;与对照组治疗后比较,差异均有统计学意义（P〈0.05）。结论银杏达莫注射液联合厄贝沙坦治疗能有效降低糖尿病肾病患者尿微量白蛋白和β2-MG的排泄,对肾功能有保护作用。对糖尿病肾病的病程进展有一定防治作用。     

辛伐他汀对大鼠肾缺血再灌注损伤中Wnt/JNK影响的研究

目的:探讨辛伐他汀(simvastatin SIM)对大鼠肾缺血再灌注损伤中Wnt/JNK的影响。方法:雄性wistar大鼠36只随机分为:假手术组、手术组、SIM干预组,每组12只,再将每组按取材时间不同分为6 h、48 h两个时相组。手术方法:假手术组开腹分离双侧肾动脉,但不夹闭,后关闭腹腔;手术组游离双侧肾动脉,动脉夹夹闭45 min后恢复灌注建立肾IRI模型;SIM干预组术前1周给大鼠灌胃SIM 20 mg.kg-1.d-1,其余处理同手术组。肾IRI后6 h、48 h,检测血清Scr值,肾组织行病理学观察及免疫组织化学法测定Wnt4、JNK1及其信号通路下游炎症因子TNFα的表达,并采用real time PCR法测定肾组织Wnt4 mRNA、JNK1 mRNA的表达。结果:肾组织病理学观察:假手术组肾组织形态结构基本正常;手术组肾小管上皮细胞有不同程度的肿胀、坏死和脱落、排列紊乱,管腔扩张,肾间质水肿、炎细胞浸润明显,以IRI后6 h为著;SIM干预组肾组织损伤程度较手术组明显减轻。Scr值测定:手术组Scr值较假手术组明显升高(P<0.01);SIM干预组Scr值较手术组有所下降(P<0.01);以IRI后6 h,Scr值较高(P<0.01)。免疫组化检测:假手术组肾小管上皮细胞Wnt4、JNK1、TNFα表达较弱;手术组IRI后肾小管上皮细胞胞浆内Wnt4、JNK1、TNFα表达均比假手术组增强(P<0.01),以6 h时为著(P<0.01)。SIM干预组Wnt4、JNK1、TNFα表达水平较手术组减弱(P<0.05)。real time PCR检测:假手术组肾小管上皮细胞Wnt4 mRNA、JNK1 mRNA表达较弱;手术组肾小管上皮细胞Wnt4 mRNA、JNK1 mRNA表达均较假手术组增强(P<0.01),以6 h为著(P<0.01);SIM干预组Wnt4 mRNA、JNK1 mRNA表达比手术组均有所下降(P<0.01)。相关性分析:JNK1与Wnt4、TNFα均成正相关(rs=0.94,rs=0.95);Wnt4 mRNA、JNK1 mRNA成正相关(rs=0.75);且均与Scr成正相关(rs分别为rs=0.93,rs=0.96,rs=0.94,rs=0.70,rs=0.35)。结论:辛伐他汀预处理可能通过抑制Wnt/JNK信号通路的表达,从而减轻肾IRI程度。     

Posttreatment with Aminoguanidine Attenuates Renal Ischemia/Reperfusion Injury in Rats

Acute renal failure secondary to ischemia/reperfusion (I/R) injury is associated with significant mortality and morbidity. Aminoguanidine (AG), an inducible nitric oxide synthase inhibitor with antioxidant properties, has been reported beneficial in renal I/R injury. The aim of the present study was to investigate the effect of AG on renal I/R injury and compare the effectiveness of different AG treatment modalities. Sprague-Dawley rats were randomly assigned to one of four groups. The control group (n?=?6) received sham operation. The I/R group (n?=?6), AG-I group (n?=?8), and AG-II group (n?=?8) received bilateral renal ischemia for 45 min followed by 24 hours of reperfusion. The AG-I group received AG (50 mg/kg) intraperitoneally four hours and 10 minutes before the induction of ischemia. The AG-II group received AG (50 mg/kg) intraperitoneally four hours and 10 minutes after the initiation of reperfusion. Serum urea and creatinine levels increased significantly in the I/R and AG-I groups compared to the control group. Kidney samples from rats in the I/R and AG-I groups revealed severe tubular damage at histopathological examination. Posttreatment with AG significantly reduced serum urea and creatinine levels and improved histopathological lesions compared with the I/R group. Although pretreatment with AG failed to protect kidneys against I/R injury in this experimental model, posttreatment with AG attenuated renal dysfunction and histopathological changes after I/R injury.     

银杏达莫注射液治疗不稳定型心绞痛56例疗效观察

目的 观察银杏达莫注射液治疗不稳定型心绞痛的作用.方法 112例患者随机分为治疗组56例使用银杏达莫注射液治疗,对照组56例常规给予硝酸甘油制剂等治疗,疗程为2周.观察两组患者治疗前后心绞痛的缓解情况、心电图及临床症状的变化和不良反应情况.结果治疗组、对照组的心绞痛改善总有效率分别为94.6%、83.9%,两组比较差异有统计学意义（P＜0.05）,两组患者心电图的总有效率分别为91.1%、82.1%,差异有统计学意义（P＜0.05）.结论 银杏达莫注射液治疗冠心病不稳定型心绞痛疗效显著.     

Remote Renal Injury Following Partial Hepatic Ischemia/Reperfusion Injury in Rats

Liver ischemia/reperfusion has been shown to result in injury of remote organs such as the heart and lungs. Whether or not acute liver injury also results in kidney injury has so far not been adequately addressed. In anesthetized Wistar rats, partial (70%) normothermic hepatic ischemia was applied for 75 min. After 24 h of reperfusion, renal injury was assessed by histology, creatinine and blood urea nitrogen (BUN) serum concentrations, renal expression of proinflammatory genes [quantitative real-time polymerase chain reaction (qRT-PCR)], caspase-3 activation (Western blot), and neutrophil accumulation (myeloperoxidase assay). Twenty-four hours after hepatic ischemia, creatinine (0.57 ± 0.06 vs. 0.32 ± 0.04 mg/dL) and BUN (40.7 ± 15.3 vs. 14.3 ± 2.0 mg/dL) were increased when compared to sham. qRT-PCR revealed higher renal intercellular adhesion molecule-1 gene expression following hepatic ischemia (166 ± 45% when compared to sham) but no differences in renal monocyte chemoattractant protein-1, macrophage inflammatory protein-2, and inducible NO synthase expression. In both groups, kidneys showed no morphological damage and no increase in caspase-3 and myeloperoxidase activity. Severe hepatic ischemia results in a moderate impairment of renal function in rats but does not trigger an inflammatory response in the kidney and does not result in morphological damage of the kidney. A part of this study has been presented as a poster presentation at the 2006 Congress of the American Hepato-Pancreato-Biliary Association in Miami Beach, FL, March 9–12.     

银杏叶提取物对实验性糖尿病大鼠肾组织HGF/c-met表达的影响

目的：研究银杏叶提取物（ginkgo biloba extract,EGb）对实验性糖尿病大鼠肾脏保护作用及其可能机制。方法：SD大鼠随机分为糖尿病对照组（DC）、银杏叶提取物（金纳多）治疗组（DG）和正常对照组（NC）,观察各组大鼠肾脏病理改变;应用免疫组化监测HGF、TGF-β1表达量,运用RT-PCR监测HGF、c-met的mRNA表达情况。结果：免疫组化显示：HGF在NC组微量表达于肾小球系膜区,DC组第2周表达明显增加,与NC组相比差异有统计学意义（P〈0.01）,第6周表达较前明显下降;DG组第2周表达明显增加,第6周表达较前有所下降,与NC组同期相比差异有统计学意义（P〈0.01）,与DC组相比差异有统计学意义（P〈0.05）;TGF-β1在NC组中无阳性表达,DC组表达明显升高,与NC组同期相比差异有统计学意义（P〈0.01）,DG组表达升高,但低于DC组（P〈0.01）,与NC组同期相比差异有统计学意义（P〈0.01）;RT-PCR结果显示：HGF/c-metmRNA在NC组中有一定量表达,第2周与第6周之间差异无统计学意义（P〉0.05）;DC组与NC组相比,在第2周表达量升高（P〈0.01）,第6周表达量较前明显下降;DG组与DC组平行相比表达量显著升高（P〈0.01）。结论：HGF在DN的病程进展中发挥着重要作用,EGb可以抑制ACE,下调TGF-β1的表达,上调HGF/c-met的表达,减轻肾小球系膜区增生,改善肾功能。     

Nebivolol Reduces Experimentally Induced Warm Renal Ischemia Reperfusion Injury in Rats

Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. The objective of the present study was to examine the role of nebivolol in modulating peroxynitrite species-induced inflammation and apoptosis after renal warm ischemia/reperfusion injury in rats. The present study was designed to investigate the effects of nebivolol on the renal warm ischemia/reperfusion injury in rats treated with the nitric oxide synthase inhibitor, N^ω-nitro-L-arginine methyl ester. After right nephrectomy, nebivolol was administered for 15 days. On the 16^th day, ischemia was induced in contra lateral kidney for 45 min, followed by reperfusion for 24 hr. Renal function, inflammation, and apoptosis were estimated at the end of 24 hr reperfusion. Nebivolol improved the renal dysfunction and reduced inflammation and apoptosis after renal ischemia/reperfusion injury. In conclusion, nebivolol shows potent anti-apoptotic and anti-inflammatory properties due to its NO-releasing property. These findings may have major implications in the treatment of human ischemic acute renal failure.     

大黄灵脾颗粒对缺血再灌注急性肾损伤大鼠肾纤维化的干预作用

目的:探讨大黄灵脾颗粒对缺血再灌注急性肾损伤模型大鼠肾纤维化的影响。方法:30只雄性SD大鼠随机分为正常组、模型组、大黄灵脾颗粒(中药)组,每组10只,通过夹闭肾蒂45 min后恢复肾脏血流再灌注建立模型,建模成功后次日各组大鼠开始灌胃治疗,正常组和模型组灌服生理盐水,中药组给予大黄灵脾颗粒灌胃。术后12周检测各组大鼠Scr、BUN、24 h尿蛋白等生化指标;HE染色观察肾组织病理;Masson染色观察肾纤维化情况;免疫组化法检测肾组织TGF-β1和α-SMA蛋白的表达水平。结果:各组大鼠Scr、BUN差异无统计学意义(P>0.05);与模型组比较,HE染色显示中药组肾组织损伤轻于模型组,且中药组24 h尿蛋白显著低于模型组(P<0.05);Masson染色显示中药组纤维化程度较模型组明显减轻,中药组肾组织TGF-β1和α-SMA蛋白的表达水平也显著低于模型组(P<0.05)。结论:大黄灵脾颗粒可改善AKI大鼠肾脏病理,降低尿蛋白水平,抑制TGF-β1和α-SMA的表达,并减轻AKI后肾纤维化的发生。     

银杏叶注射液对糖尿病肾病尿蛋白的影响

目的:探讨银杏叶注射液对糖尿病肾病尿蛋白排泄率的影响.方法:选择糖尿病肾病患者 68 例,将病人分为两个组.A组为微量白蛋白尿组,B组为大量白蛋白尿组.两组均给与银杏叶注射液 15ml,每日一次静脉滴注,4周为一疗程,同时维持原降糖药物治疗,比较两组在治疗前后尿蛋白的变化情况.结果:两组比较,A组尿蛋白排泄率显著降低 ( P<0.01).结论:银杏叶注射液能够明显降低尿微量白蛋白,对糖尿病肾病患者的早期治疗具有治疗作用.