辛伐他汀对糖尿病大鼠肾脏氧化应激的抑制作用

目的：研究辛伐他汀对糖尿病大鼠肾脏氧化应激反应和肾脏功能的影响。 方法： 链脲佐菌素诱导的糖尿病大鼠，给予辛伐他汀治疗8周后，检测辛伐他汀对糖尿病大鼠肾脏氧化应激水平和肾功能的影响。 结果： 糖尿病组大鼠血清和肾皮质超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性显著低于正常对照组，丙二醛(MDA)含量明显高于正常对照组，同时血尿素氮（BUN）、血肌酐（Scr）、尿白蛋白排泄率（UAER）、尿白蛋白/肌酐、肾重及肾肥大指数（肾重/体重）均高于对照组。辛伐他汀治疗组SOD活性与糖尿病组无明显差异，其余异常均明显轻于糖尿病组。 结论： 辛伐他汀能有效抑制糖尿病大鼠肾脏氧化应激反应，改善肾脏功能。     

伊贝沙坦联合舒洛地特对糖尿病大鼠肾脏协同保护作用的研究

目的： 探讨伊贝沙坦联合舒洛地特对大鼠糖尿病肾脏协同保护作用及其机制。 方法：将雄性SD大鼠随机分为5组:正常对照组（C）、糖尿病模型组(D)、伊贝沙坦组(I)、舒洛地特组（S）及伊贝沙坦与舒洛地特联合给药组（I+S）,糖尿病大鼠模型用STZ诱导。 12周后观察尿白蛋白的排泄率(UAER),做肾组织病理检查,测定肾组织中MDA含量与SOD、CAT、GSH-PX的活性变化。RT-PCR法检测肾组织中ICAM-1 mRNA的表达。EMSA 检测NF-κB的活性。结果：各给药组均可抑制糖尿病大鼠UAER的增加及肾组织病理结构损害,联合组优于单独给药组。对肾组织MDA含量增加及抗氧化应激的SOD、CAT、GSH-PX活性降低的改善作用,联合组优于单给药组。各给药组均可抑制肾组织NF-κB活性,以联合组最明显;糖尿病大鼠肾组织ICAM-1 mRNA表达明显高于对照组,各给药组肾组织ICAM-1 mRNA表达明显低于模型组,其中以联合组最明显。 结论：伊贝沙坦与舒洛地特联合用药对糖尿病肾脏保护作用优于任一单种用药,其机制可能部分是通过对糖尿病肾组织氧化应激、NF-κB 活性及 ICAM-1 mRNA表达协同抑制而实现的。     

锌指转录因子Snail 1在糖尿病大鼠肾组织中的表达

目的： 观察锌指转录因子Snail 1在糖尿病大鼠肾组织中的表达并探讨其与糖尿病肾病（DN）发生、发展的关系。方法: 链脲佐菌素（STZ）诱发大鼠糖尿病（DM），分为2、4、8、12、16、20、24周以及16周A、20周A和24周A组，其中A组动物从第13周起用胰岛素控制血糖至正常水平，每个时点均设鼠龄匹配的正常对照组。测定各组血糖、24 h尿蛋白、血肌酐（Scr）、肾脏指数。PAS染色光镜观察肾脏病理改变。免疫组化、RT-PCR方法检测肾皮质Snail 1和纤连蛋白（FN）的蛋白及mRNA水平，Western blotting检测Snail 1蛋白表达。结果: DM各组大鼠的血糖、24 h尿蛋白、血肌酐、肾脏指数明显高于正常对照组（P<0.05,P<0.01），A组上述指标均明显低于DM组（P<0.05,P<0.01）。Snail 1免疫组化阳性染色见于各组DM大鼠肾小管，正常对照组未见阳性表达，A组见弱阳性表达，并随治疗时间延长而减少。DM组肾皮质Snail 1、FN蛋白和mRNA的表达水平高于正常对照组（P<0.01），而A组显著低于DM组（P<0.01）。Snail 1与FN mRNA的表达水平呈显著正相关（P<0.01），Snail 1蛋白表达水平与血糖、尿蛋白、血肌酐、肾脏指数亦呈正相关（ P<0.01）。结论: Snail 1基因和蛋白在DM大鼠肾组织过度表达，提示Snail 1可能参与了DN的发生、发展机制。     

吡咯烷二硫代氨基甲酸酯对2型糖尿病大鼠心肌的保护作用

目的: 探讨吡咯烷二硫代氨基甲酸酯(PDTC)的降糖作用及对糖尿病大鼠心肌的保护作用。方法: 37只雄性Wistar大鼠,随机分为正常对照组(NC)和高脂饮食组(HFD)。喂养8周后,高脂饮食组大鼠腹腔注射单剂量链脲佐菌素(STZ)27 mg/kg复制2型糖尿病大鼠模型。造模成功后再随机分为模型组和PDTC治疗组。PDTC治疗组大鼠每天腹腔注射PDTC(50 mg/kg)1次,模型组和正常对照组每天注射相同剂量的生理盐水,连续注射1周后,检测血糖及各种生化指标,处死大鼠。检测心肌组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性;用透射电镜观察心肌组织的超微结构;用免疫组化观察心肌组织中诱导型一氧化氮合酶(iNOS)和硝基酪氨酸(NT)的表达。结果: 糖尿病模型组与正常对照组大鼠相比,血糖和MDA水平显著升高,SOD和GSH-Px活性明显下降(P<0.01);PDTC治疗后,血糖和MDA水平明显降低,SOD和GSH-Px活性明显升高(P＜0.01)。糖尿病组心肌变性坏死、线粒体损伤及炎症细胞浸润;PDTC治疗后线粒体损伤明显减轻。糖尿病组较正常对照组心肌中iNOS和NT的表达均明显增加;PDTC治疗后iNOS和NT的表达均明显减少。结论: 高血糖可引起氧化应激,使心肌组织中iNOS和NT生成过多,损伤了心肌细胞的结构和功能。PDTC不仅具有降糖作用,而且还可以通过减少iNOS和NT的产生,进而阻止或延缓糖尿病心肌病的发生。     

α-硫辛酸减轻高尿酸血症大鼠氧化应激损伤

目的观察α-硫辛酸对高尿酸血症大鼠氧化应激和血管内皮细胞形态的影响。方法建立高尿酸血症大鼠模型3周后,每天给予10、30和90 mg/kg不同剂量的α-硫辛酸,灌胃2周,另设对照组,分析大鼠血清尿酸、SOD、GSH-Px、CAT和MDA水平,取胸主动脉,Westernblot法检测SOD和CAT蛋白表达,同时光镜和电镜观察胸主动脉血管内皮形态和超微结构。结果模型组大鼠血清尿酸、SOD、GSH-Px、CAT酶活力均低于对照组,MDA含量高于对照组,胸主动脉SOD及CAT蛋白表达低于对照组(P0.05);α-硫辛酸干预后,大鼠血清尿酸和MDA水平明显降低,中、高剂量组SOD酶活力和胸主动脉SOD及CAT蛋白表达均升高(P0.05);电镜显示高尿酸血症大鼠胸主动脉内皮细胞水肿、脱落,内膜凸起,线粒体增多,经α-硫辛酸干预后,中、高剂量组胸主动脉内皮水肿、凸起数量减少,线粒体数量一过性增加。结论α-硫辛酸可增加高尿酸血症大鼠抗氧化酶活性和蛋白表达,缓解氧化应激,保护血管内皮细胞。     

阿魏酸钠对糖尿病大鼠肾脏非酶糖基化和氧化的影响

目的:探讨阿魏酸钠(SF)对糖尿病(DM)大鼠肾脏非酶糖基化和氧化的影响。方法:对链脲佐菌素(STZ)诱导的DM大鼠灌胃给予SF 110 mg·kg^-1·d^-1,治疗8周,测定各组大鼠肾重／体重、肌酐清除率(Ccr)、24 h尿蛋白定量、血清和肾皮质果糖胺(FMN)、血清和肾皮质丙二醛(MDA)含量及抗氧化酶活性,并分别测定肾皮质糖基化终产物(AGEs)含量,观察肾脏病理改变。结果:糖尿病对照组(DM组)大鼠肾重／体重、Ccr、24 h尿蛋白定量、血清FMN、肾皮质FMN和AGEs显著高于正常对照组(N组);SF治疗组(SF组)肾重／体重、Ccr、24 h尿蛋白定量、血清FMN和肾皮质AGEs显著低于DM组;DM组大鼠肾皮质和血清超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性显著低于N组,MDA含量显著高于N组,SF治疗组大鼠肾皮质和血清SOD、CAT活性显著高于DM组,MDA含量显著低于DM组:DM组大鼠肾脏病理改变异常显著,SF组的肾脏病理学改变轻于DM组大鼠。结论: SF通过保护肾脏抗氧化酶,减轻氧化应激,抑制AGEs在肾脏的沉积对DM大鼠肾脏产生保护作用。     

过氧化物酶Ⅰ、过氧化氢酶、超氧化物歧化酶在大鼠肝缺血再灌注损伤小肠内的表达变化

目的:观察过氧化物酶Ⅰ(PrxI)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)在大鼠肝缺血再灌注损伤模型小肠内的表达变化以及小肠内氧化应激的水平,探讨肝缺血再灌注损伤对小肠的影响及PrxI、CAT、SOD的抗氧化作用。方法:制备大鼠70%肝缺血再灌注损伤模型。肝缺血再灌注6h后取血、肝和小肠。采用全自动生化分析仪测定血清丙氨酸氨基转移酶(ALT)活性;钼酸比色法和硫代巴比妥酸比色法测定血清、小肠中H_2O_2和丙二醛(MDA)的含量;H-E染色法观察肝、小肠的形态学改变;RT-PCR测定小肠组织PrxI、CAT、SOD mRNA水平的表达,免疫印迹测定其蛋白水平的表达。结果:与对照组相比,肝缺血再灌注损伤组大鼠血清ALT活性、MDA和H_2O_2的含量明显升高;H-E染色结果显示模型组大鼠肝组织形态结构受损明显;小肠组织内MDA和H_2O_2的含量明显高于对照组,PrxI、CAT、SOD的mRNA和蛋白表达水平与对照组相比也升高明显。结论:PrxI、CAT和SOD在小肠组织处于高度氧化应激状态过程中可能发挥了抗氧化应激作用。     

银杏叶提取物对2型糖尿病大鼠肾脏结构和功能的影响

目的：研究银杏叶提取物（GBE）对2型糖尿病（T2DM）大鼠肾脏结构和功能的影响。方法：SD大鼠随机分为正常对照组、高脂组、糖尿病组（高脂饮食+STZ造模）及糖尿病GBE治疗组（GBE 8 mg·kg-1·d-1），8周后处死大鼠,检测体重、肾重、尿量、24 h尿蛋白和N-乙酰-β-氨基葡萄糖苷酶(NAG)水平；电镜观察肾脏超微结构；RT-PCR法测定基质金属蛋白酶-9（MMP-9）、基质金属蛋白酶组织抑制因子-1（TIMP-1）、Ⅳ型胶原的基因表达水平。结果：糖尿病组大鼠肾皮质TIMP-1、Ⅳ型胶原mRNA表达高于正常对照组，MMP-9 mRNA表达低于正常对照组，肾重指数、尿量、24 h 尿蛋白、NAG均高于对照组。电镜下见肾小球基底膜增厚，厚薄不均匀，足细胞突起肿胀，变短，并可见足突融合，球囊壁层细胞内线粒体扩张，肾小球内胶原纤维增多。而糖尿病GBE治疗组肾小球基底膜及足细胞病变明显较轻，肾皮质MMP-9表达高于糖尿病组，Ⅳ型胶原mRNA表达低于糖尿病组，尿量、24 h尿蛋白、NAG均低于糖尿病组。TIMP-1 mRNA表达无明显差异。结论：GBE可改善2型糖尿病大鼠肾脏的结构和功能，其作用机制与降低TIMP-1、Ⅳ型胶原mRNA表达，升高MMP-9 mRNA表达，阻止ECM的堆积有关。     

高压氧对模型大鼠颅脑损伤CAT、SOD、GSH-Px和Nrf2影响的研究

目的:研究高压氧对模型大鼠颅脑损伤过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和核因子E2相关因子2(Nrf2)的影响。方法:健康SD大鼠30只,体重250~300 g,4~5月龄,随机分为3组:假手术组、模型组和高压氧组,每组10只,参照Feeney自由落体冲击造模法建立颅脑损伤大鼠模型。假手术组只给予手术,不造成颅脑损伤;模型组和高压氧组给予颅脑损伤处理;高压氧组用高压氧治疗,1次/d,10 d。用ELISA法检测脑组织CAT、SOD、GSH-Px和Nrf2含量,采用实时荧光定量PCR检测脑组织CAT、SOD、GSH-Px和Nrf2 mRNA相对表达量,用Western Blot测定脑组织Nrf2胞质蛋白和Nrf2核蛋白。结果:假手术组、模型组、高压氧组之间的CAT、SOD、GSH-Px、Nrf2 mRNA水平均有差异(P0.05)。模型组脑组织CAT、SOD、GSHPx、Nrf2 mRNA水平低于假手术组(P0.05),而高压氧组则高于模型组(P0.05)。假手术组、模型组、高压氧组之间的脑组织CAT、SOD、GSH-Px和Nrf2核蛋白水平存在差异(P0.05),模型组低于假手术组(P0.05),高压氧组高于模型组(P0.05)。Western Blot检测显示:与假手术组比较,模型组和高压氧组脑组织细胞质(核)中Nrf2蛋白表达量有明显升高(P0.05),高压氧组升高更明显(P0.05)。结论:高压氧对模型大鼠颅脑损伤CAT、SOD、GSH-Px和Nrf2表达具有调节作用,通过这些调节改善机体氧化性损伤。     

PTEN、FOXO3a和氧化应激相关蛋白在胃癌组织中的表达

目的:探讨PTEN、FOXO3a和氧化应激相关蛋白在胃癌中的表达及它们之间的相互关系。方法:采用紫外分光光度法测定胃腺癌患者(n=45)和健康自愿者(n=30)血浆中过氧化氢酶(CAT)、超氧化物歧化酶(SOD)及丙二醛(MDA)的表达水平;采用荧光定量RT-PCR法检测胃腺癌组织(n=84)和正常组织(n=48)中PTEN mRNA和FOXO3a mRNA的表达水平。PTEN和FOXO3a的表达与氧化应激的关系采用Spearman方法进行相关性分析。结果:胃癌组血浆中CAT、SOD表达低于对照组,MDA表达高于对照组;胃癌组织中PTEN mRNA和FOXO3a mRNA表达低于正常组织;PTENmRNA表达与SOD、CAT的含量呈正相关,与MDA的含量呈反相关。结论:胃腺癌患者体内存在过高的氧化应激水平及过低的抗氧化水平,机体抗氧化能力的降低有可能降低抑癌基因PTEN mRNA和FOXO3a mRNA的表达。     

Oxidative stress and gene expression of antioxidant enzymes in the streptozotocin-induced diabetic rats under hyperbaric oxygen exposure

Diabetes mellitus (DM) causes not only hyperglycemia but oxidative stress, resulting mainly enhanced production of mitochondrial reactive oxygen species (ROS). Hyperbaric oxygen (HBO) treatments are applied various diseases including diabetic patients with unhealing foot ulcers, however, and also increases the formation of ROS. Recently, it has been reported that oxidative stress worsens many pathological conditions including DM and obesity suggesting possible changes in regulation of genes associated with the oxidative stress, however, effects of HBO which could induce ROS on the gene expressions of oxidative stress parameters in DM animals are unknown. The purpose of this study is to investigate the effect of HBO exposure on the gene expression of three important antioxidant enzymes, cytosolic superoxide dismutase (Cu-Zn SOD), cytosolic glutathione peroxidase (GPx-1), and catalase (CAT) in DM rats, respectively. We used streptozotocin-induced DM model rats and examined both mRNA expressions and the activities of these antioxidant enzymes in the liver, skeletal muscle, and pancreas. The mRNA expressions of Cu-Zn SOD and CAT decreased significantly (p < 0.001), and GPx increased significantly (p < 0.001) in all the studied organs of DM rats under HBO exposure compared to those from DM-induced rats not exposed to HBO. Similarly, activities of these three enzymes changed in accordance with the mRNA levels. These results suggested that DM induction and HBO exposure might synergistically affect antioxidant enzymes, resulting increase of oxidative stress state. Thus, HBO exposure seems to be an excellent model system for investigating oxidative stress.     

姜黄素类似物L6H4对2型糖尿病大鼠膈肌的保护作用

目的:探讨姜黄素类似物L6H4对2型糖尿病大鼠膈肌的保护作用及机制。方法:40只SPF级雄性SD大鼠,随机均分成5组:正常对照(NC)组、高脂(HF)组、高脂治疗(FT)组、糖尿病(DM)组和糖尿病治疗(DT)组。后4组采用高脂饲料喂养,4周后DM组及DT组腹腔注射链脲佐菌素诱导2型糖尿病模型,造模成功后FT组和DT组用L6H4灌胃治疗8周。生化法检测空腹血糖及血脂水平;放射免疫法检测空腹血清胰岛素(FINS)水平并计算胰岛素抵抗指数(HOMA-IR);ELISA法检测血清脂联素(APN)水平;光镜和电镜观察大鼠膈肌形态改变;酶组织化学染色观察膈肌内脂质沉积及琥珀酸脱氢酶(SDH)和还原型辅酶Ⅰ四氮唑还原酶(NADH-TR)活性;硫代巴比妥酸法和羟胺法分别检测膈肌丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性;免疫组化和Western blot检测膈肌脂联素受体1(AdipoR1)蛋白的表达。结果:HF组和DM组大鼠的血糖、血脂、FINS和HOMA-IR较NC组均有升高(P0.01),L6H4治疗后均下降(P0.01);HF组与DM组大鼠血清APN水平较NC组下降,L6H4治疗后升高(P0.01)。HF组及DM组大鼠膈肌纤维萎缩,肌纤维内脂肪颗粒堆积,线粒体轻微肿胀;DM组大鼠膈肌纤维化,L6H4治疗后,大鼠膈肌的形态学损害减轻。HF组和DM组大鼠膈肌MDA含量及SDH和NADH-TR活性较NC组升高,L6H4治疗后下降(P0.05);HF组和DM组大鼠膈肌SOD活性和AdipoR1蛋白表达较NC组下降,L6H4治疗后升高(P0.05)。结论:姜黄素类似物L6H4对2型糖尿病大鼠的膈肌具有保护作用;膈肌AdipoR1蛋白表达增强、血清APN浓度增加及抗脂质过氧化可能参与其中。     

苦参素降低大鼠肾脏缺血-再灌注损伤

目的观察苦参素的抗大鼠肾缺血再灌注损伤的作用并从抗氧化方面探讨其机制。方法用双肾肾蒂夹闭45 min建立IRI模型,将SD大鼠随机分为假手术组(sham);缺血再灌注组(I/R);苦参素治疗组(oxymatrine+I/R)。苦参素治疗组又分为高、中和低3个剂量组,在缺血再灌注前,连续7 d经腹腔注射。用自动生化仪测定血清肌酐(Scr)和尿素氮(BUN)水平,观察苦参素对肾缺血再灌注的保护作用及确定最优剂量;以最优剂量干预用分光分析法测定肾组织丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)水平。结果不同剂量组均能明显减轻肾脏IRI的病理形态学改变,改善肾功能。与I/R组相比,再灌注72 h后,MDA水平,血清肌酐(Scr)和尿素氮(BUN)水平明显降低(P<0.05);苦参素治疗组的CAT、T-SOD、GSH-Px活性改善明显(P<0.05)。苦参素无体外抗氧化作用。结论苦参素对大鼠肾缺血再灌注损伤具有保护作用,作用机制可能与调控机体的抗氧化系统有关。     

Catechin protects against oxidative stress and inflammatory-mediated cardiotoxicity in adriamycin-treated rats

Catechin has anti-inflammatory and antioxidative effects. Cardiotoxicity, which results from intense cardiac oxidative stress and inflammation, is the main limiting factor of the adriamycin use in the treatment of malignant tumors. Thus, the present study aimed to assess the antioxidant and anti-inflammatory effects of catechin on adriamycin-induced cardiotoxicity in rats. Forty-five rats were allocated to three groups: control group, adriamycin group and adriamycin?+?catechin group. We performed the following measurements: lipid peroxidation (MDA), catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities as well as, the expression of inflammatory cytokines genes namely nuclear factor kappa-B, tumor necrosis factor and inducible nitric oxide synthase. Catechin administration significantly decreased MDA level and significantly increased CAT, GSH-Px and SOD activities. Also, catechin significantly decreased the expression levels of inflammatory cytokines. Catechin provided cardioprotection on adriamycin-induced cardiotoxicity through their antioxidant and anti-inflammatory properties.     

Brief communication: omega-3 essential fatty acid supplementation and erythrocyte oxidant/antioxidant status in rats

Fish oil contains large amounts of essential omega-3 fatty acids, such as eicosapentaenoic and docosahexaneoic acids, which are building structures of cell membranes. The goal of this study was to elucidate the effects of dietary omega-3 fatty acid supplementation on the oxidant/antioxidant status of erythrocytes in rats. The malondialdehyde (MDA) and nitric oxide (NO) levels and the catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) activities were assayed in erythrocytes of male Wistar albino rats after 30 days of dietary supplementation with fish oil (0.4 g/kg/day). Erythrocyte CAT activity in the treated group was increased in comparison with the control group. Erythrocyte MDA and NO levels were lower in the treated group than the controls. Erythrocyte GSH-Px and SOD activities did not differ significantly in the 2 groups. Negative correlations were found between SOD and CAT activities, and between SOD and GSH-Px activities in the treated group. In conclusion, omega-3 fatty acid supplementation helps to prevent lipid peroxidation and to safeguard erythrocytes from oxidative injury. Dietary supplementation with omega-3 fatty acids might possibly protect tissues from oxygen free radical injury in the various diseases in which the oxidant/antioxidant defense mechanisms are disturbed.     

牛磺酸治疗糖尿病大鼠骨骼肌病变的实验研究

目的：研究牛磺酸对糖尿病大鼠骨骼肌酶的影响。方法：SD大鼠24只，随机分为对照（NC）组、糖尿病（DM）组、牛磺酸（Tau）组，每组8只：DM组和Tau组腹腔注射链脲菌素（STZ）50mg／kg复制DM大鼠模型。NC组和DM组给予自来水、Tau组给予牛磺酸（1％饮水）4周后，测量腓肠肌组织中的乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）、肌酸激酶（CK）的活性及丙二醛（MDA）含量的变化；光镜下观察肌纤维病理改变。结果：与NC组相比，DM组组织中SOD、CK活性显著降低（P〈0．01），LDH活性、MDA含量显著增加（P〈0．01）；光镜下，肌纤维发生明显紊乱。变细，甚至断裂。给予牛磺酸后可抑制上述现象。结论：牛磺酸对糖尿病大鼠骨骼肌病变有保护作用。     

Effects of poly (ADP-ribose) polymerase inhibitor on early peripheral neuropathy in streptozotocin-diabetic rat

Objective: To explore the effects and mechanisms of poly (ADP-ribose) polymerase (PARP) inhibitor 3-aminobenzamide on nerve lesions in streptozotocin-diabetic rats. Methods: Experimental rats were divided into normal control group(NC group), diabetic control group (DC group)and diabetic group treated with 3-aminobenzamide (DT group ) .Nerve conduction velocity (NCV),serum superoxide dismutase (SOD) activity and serum malondialdehyde (MDA) concentration,phosphocreatine (Pcr),creatine (Cr) concentration in sciatic nerves were evaluated after 4 weeks. Results: SOD, Pcr activity, and NCV were higher (P ＜ 0.05)and MDA concentration were significantly lower in DT group, compared with DC group (P ＜ 0.01). Meanwhile, ATP and Cr in sciatic nerves were similar in DT group, compare d with DC group (P ＞ 0.05). Conclusion: 3-aminobenzamide could alleviate the established functional and metabolic abnormalities of early DPN in the streptozotocin-induced diabetic rat models,which provided a novel approach for prevention and treatment of diabetic neuropathy.     

Protective role of aminoguanidine on gentamicin-induced acute renal failure in rats

The toxicity of aminoglycosides including gentamicin (GEN), the most widely used drug in this category, is believed to be related to the generation of reactive oxygen species (ROS) in the kidney. Aminoguanidine (AG) is known as an effective antioxidant and its free radical scavenger effects may protect GEN-induced acute renal failure (ARF). Therefore, this study was focused on investigating the possible protective effect of AG against GEN-induced nephrotoxicity in an in vivo rat model. We investigated the effects of AG on GEN-induced changes in renal tissue malondialdehyde (MDA) levels; nitric oxide (NO) generation; glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities; glutathione (GSH) content; serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined using light microscopy. GEN administration to control group rats increased renal MDA and NO levels but decreased GSH-Px, SOD, CAT activities and GSH content. AG administration with GEN injection resulted in significantly decreased MDA, NO generation and increased GSH-Px, SOD, CAT activities and GSH content when compared with GEN alone. Serum levels of Cr and BUN significantly increased as a result of nephrotoxicity. Also, AG significantly decreased Cr and BUN levels. Morphological changes in the kidney, including tubular necrosis, intracellular edema, glomerular and basement membrane alterations were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of AG reduced the GEN-induced kidney damage. We propose that AG acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level.     

阿魏酸钠抑制糖尿病大鼠心肌非酶糖基化的形成

目的探讨阿魏酸钠(SF)对糖尿病(DM)大鼠心肌非酶糖基化的影响。方法对链脲佐菌素(STZ)诱导的DM大鼠灌胃给予SF110mg/(kg.d)治疗8周,测定各组大鼠血清超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及血清果糖胺(FMN)、丙二醛(MDA)水平,并用酶免法测定心肌糖基化终产物(AGEs)含量。结果DM大鼠心肌AGEs及血清FMN、MDA显著高于对照组,血清SOD、CAT活性降低,SF治疗显著改善上述指标的变化。结论SF可显著抑制DM大鼠心肌AGEs的形成,机制与其保护抗氧化酶有关。     

Alterations in the erythrocyte antioxidant system of blood stored in blood bags

In the present study, we measured the concentrations of reduced glutathione (GSH) and malonyldialdehyde (MDA) and the activities of glutathione peroxidase (GSH-Px), glutathione S-transferase (GSH-S-T), superoxide dismutase (SOD), catalase (CAT) and glucose-6-phosphate dehydrogenase (G-6-PD) in erythrocytes obtained freshly from adult male donors which was preserved with CPDA-1 anticoagulant (citrate,phosphate, dextrose, adenine) on different days of storage. At the end of the study, storage-associated alterations in antioxidant activities were noted and discussed. GSH, GSH-Px, GSH-S-T, SOD, CAT and G-6-PD activities decreased, but erythrocyte MDA levels, as anindex of lipid peroxidation, increased during the storage period. According to our results, glutathione-dependent antioxidant systems in erythrocytes might be depleted during long storage in blood bags.