苦瓜提取物对糖尿病大鼠血抗氧化酶和丙二醛含量的影响

目的：观察苦瓜提取物（MCE）对糖尿病大鼠血清SOD、CAT和MDA的影响。方法：用STZ诱导糖尿病模型,随机分为糖尿病组和MCE治疗组。治疗组灌胃给予MCE 300 mg/kg,6周。检测血清SOD、CAT和MDA含量。结果：糖尿病组大鼠血清SOD和CAT活性显著降低,MDA含量明显增加（P〈0.01）。MCE治疗组血清SOD和CAT活性明显高于糖尿病组,MDA含量明显低于糖尿病组。结论：MCE能有效改善糖尿病大鼠血清抗氧化酶活性,减轻氧化应激水平。     

绿原酸对糖尿病大鼠肾脏氧化应激作用的实验研究

目的 探讨绿原酸对糖尿病大鼠肾脏氧化及抗氧化系统的影响.方法 将36只大鼠随机分成N组(正常组)、DM组(糖尿病组)及CA组(绿原酸干预组).DM组和CA组造糖尿痛模型,分别给予腹腔注射生理盐水和绿原酸,饲养10周后,测定血糖、肾脏重量、体重变化,肾皮质超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-PX)、丙二醛(MDA)含量及尿微量白蛋白排泄率(UAER).结果 与DM组大鼠相比,CA组大鼠血糖无明显差别,而肾重、体重明显增加,肾皮质SOD、GSH-PX活性明显上升,MDA含量及UAER则明显减少(均P<0.05).结论 绿原酸有改善糖尿病大鼠的一般状况,提高抗氧化能力,抑制氧化应激.减少尿蛋白的作用.     

紫外线照射充氧自血回输对梭曼中毒家兔氧自由基代谢的影响

目的 探讨紫外线照射充氧自血回输（UBIO）对家兔急性梭曼中毒后氧自由基代谢的影响。方法 将家兔100只随机分为5组，即正常对照组、中毒组、常规治疗组、UBIO治疗组及复合治疗组，每组20只。各组家兔于14d后检测血清中丙二醛（MDA）含量、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSHPx）及过氧化氢酶（CAT）活性。结果 与正常对照组相比，家兔梭曼中毒后，中毒组血清MDA含量及CAT活性明显升高（P〈0．01），SOD、GSH-Px活性明显降低（P〈0．05）。但经UBIO或复合治疗后，与中毒组比较，UBIO组及复合治疗组血清MDA含量明显降低（P〈0．01），SOD、GSH-Px及CAT活性明显升高（P〈0．05）。结论 家兔梭曼急性中毒后可伴有明显的氧自由基损伤，UBIO能明显提高机体抗氧化损伤能力，可以应用于梭曼急性中毒的治疗。     

联合抗氧化微量营养素对T1DM小鼠心、脑、肾、肝组织氧化应激状态的影响

目的比较不问抗氧化微量营养紊组合对实验性糖尿病小鼠心、脑、肾、肝组织氧化应激状态的干预作用。为应用抗氧化微量营养索防止糖尿病合并症提供科学依据。方法应用MLDS方法制备小鼠T1DM模型，分别添加4种（Se、VE、V、Cr）或7种（Sc、VE、V、Cr、VC、烟酰胺、赖氨酸）抗氧化微量营养紊，比较不同抗氧化微量营养索组合对糖尿病时心、脑、肾、肝组织抗氧化酶GSH-Px、SOD活性及自由基代谢产物MDA的影响。结果联合添加微量营养素的两组糖尿病小鼠心、脑、肾、肝组织GSH-Px、SOD活性不同程度地明显增高，MDA含量降低，但4种微量营养素添加组与7种微量营养素添加组之间酶活力水平与MDA含量未见明显差别。结论联合添加抗氧化微量营养素可明显减轻糖尿病小鼠心、脑、肾、肝组织氧化应激状态，可能对糖尿病合并症具有防治作用。     

大豆皂甙对实验性糖尿病大鼠肾脏自由基防御机能的影响

目的探讨大豆皂甙对实验性糖尿病大鼠肾脏自由基防御机能的影响。方法以Wistar雄性大鼠为研究对象,将实验动物分为三组即对照组、糖尿病模型组和大豆皂甙给药组,三组动物分别每日给予生理盐水、生理盐水、大豆皂甙（SS,10mg/Kg）灌胃3个月,然后处死取肾脏,采用组织匀浆生化测定法,检测肾组织中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、脂质过氧化物（LPO）和谷胱甘肽过氧化物酶（GSH-Px）含量的变化。结果与对照组和糖尿病治疗组相比较,糖尿病模型组肾组织中SOD和CAT含量显著降低（P〈0.01）;而LPO和GSH-Px含量显著增加（P〈0.01）。结论口服大豆皂甙能抑制自由基的产生,降低体内过氧化物的含量,提高机体抗氧化能力。     

单宁酸对糖尿病大鼠血清及肾脏C反应蛋白表达的影响

目的观察单宁酸(tannic acid,TA)对链脲佐菌素(STZ)诱发糖尿病(DM)大鼠血清及肾脏C反应蛋白(CRP)表达的影响。方法 70只雄性Wistar大鼠随机分为正常对照组、模型组、氨基胍(AG)组和TA低高剂量组,给药10周后处死大鼠。ELISA法检测各组大鼠血清CRP水平,免疫组织化学染色观察CRP在肾组织中的表达。结果 DM大鼠血清及肾组织CRP表达增加,单宁酸可降低DM大鼠血清CRP水平,下调肾组织CRP蛋白的表达。结论单宁酸可改善糖尿病大鼠微炎症状态,对保护糖尿病大鼠的肾脏损害具有一定的积极作用。     

低剂量γ射线照射外周血对抗氧化系统的兴奋作用

目的探讨低剂量γ射线照射外周血对抗氧化功能的影响。方法对10份人全血采用γ射线照射，照射剂量1Gy，分别于照射前及照射后1、2h检测血清还原型谷胱甘肽（GSH）、丙二醛（MDA）含量及超氧化物歧化酶（SOD）、谷胱甘肽过氧化酶（GSH-Px）和总抗氧化能力（T-AOC）及过氧化氢酶（CAT）活性。结果γ射线照射后1h与照射前比较，血清GSH含量升高（P〈0．01）、MDA含量降低（P〈0．01），而SOD、GSH-Px、T-AOC及CAT活性升高（P〈0．01）。照射后2h与照射后1h比较，GSH含量进一步升高（P〈0．01），MDA含量进一步降低（P〈0．01）；除SOD外，GSH-Px、T-AOC及CAT活性进一步升高（P〈0．01）。结论低剂量γ射线辐射可明显提高抗氧化能力，即对抗氧化系统有兴奋作用。     

紫外线照射充氧自血回输对梭曼中毒家兔氧自由基代谢的影响

目的 探讨紫外线照射充氧自血回输（UBIO）对家兔急性梭曼中毒后氧自由基代谢的影响。方法 将100只家兔随机分为5组，即正常对照组、中毒组、常规治疗组、UBIO治疗组及复合治疗组，各组于14d后检测家兔血清中丙二醛（MDA）含量、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）及过氧化氢酶（CAT）活性。结果 与正常对照组相比，家兔梭曼中毒后，血清MDA含量及CAT活性明显升高（P〈0.01），SOD、GSH—Px活性明显降低（P〈0．05）。但经UBIO或复合治疗后，与中毒组血清MDA含量比较明显降低（P〈0.01），SOD、GSH—Px及CAT活性明显升高（P〈0．05）。结论 家兔梭曼急性中毒后可伴有明显的氧自由基损伤，UBIO能明显提高机体抗氧化损伤能力，可以应用于梭曼急性中毒的治疗。     

复方血栓通对1型糖尿病大鼠氧化应激的影响及机制探讨

目的观察复方血栓通胶囊(XST)减轻糖尿病大鼠肾脏损伤的作用,探讨其保护机制。方法通过腹腔注射链脲佐菌素(STZ)60 mg/kg制作糖尿病大鼠模型,成模大鼠随机分为糖尿病组(DM组,10只)、糖尿病α-硫辛酸干预组(ALA组,10只)、糖尿病血栓通干预组(XST组,10只),另设正常对照组(10只)。ALA组大鼠予以α-硫辛酸0.1 g/kg灌胃,血栓通组大鼠予以XST 1 g/kg灌胃,DM组和正常对照组均每日同时间给予同体积蒸馏水灌胃。12周后比较各组肾脏/体重,24 h尿蛋白,尿蛋白/肌酐比,尿素氮(BUN)。测定各组大鼠肾皮质中超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活性,脂质过氧化产物丙二醛(MDA)和诱导型一氧化氮合酶(i NOS)的mRNA含量。结果和正常对照组相比,DM组、XST组、ALA组24 h尿蛋白、左肾重/体质量比、尿白蛋白/肌酐比、BUN均升高,GSHPx降低,MDA升高,i NOS表达上调(P0.05);与DM组相比,XST组和ALA组肾皮质GSH-Px活性增加,MDA含量降低,i NOS明显下降(P均0.05)。各组SOD比较差异无统计学意义(P0.05)。XST组和ALA组各指标变化相似,差异均无统计学意义(P0.05)。结论复方血栓通胶囊可通过抗氧化应激,降低i NOS的表达改善糖尿病大鼠肾脏损伤。     

镁和β-胡萝卜素对2型糖尿病大鼠胰岛素抵抗及抗氧化能力影响的研究

目的通过补充镁、β-胡萝卜素及其联合制剂,探讨镁、β-胡萝卜素及联合补充对实验型2型糖尿病大鼠胰岛素抵抗及抗氧化能力的影响。方法利用链脲佐菌素建立2型糖尿病大鼠动物模型,将其随机分为糖尿病模型组（B组）、镁组（C组）、β-胡萝卜素组（D组）及镁＋β-胡萝卜素组（E组）,并设正常对照组（A组）,实验期8周,分析血糖含量、胰岛素抵抗指数、超氧化物歧化酶（SOD）,丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH-Px）含量及活性。结果C、D和E组胰岛素抵抗指数均较B组明显降低（P〈0.05）;D组和E组SOD和GSH-Px水平均较B组明显升高,MDA水平明显降（P〈0.05）;C组SOD和GSH-Px水平较B组升高,MDA水平降低,但差别无统计学意义（P〉0.05）;同时,E组SOD和GSH-Px水平较C组升高,MDA水平降低（P〈0.05）;其余各组间差异无显著性。结论β-胡萝卜素可有效提高糖尿病大鼠抗氧化能力,减少脂质过氧化产物的生成;镁可改善大鼠胰岛素抵抗;联合补充镁及β-胡萝卜素,对大鼠抗氧化能力及胰岛素抵抗的改善有一定的协同作用。     

Effects of caffeic acid phenethyl ester on lipid peroxidation and antioxidant enzymes in diabetic rat heart

OBJECTIVES: The risk for cardiovascular disease is significantly high in diabetes mellitus. Experimental evidence suggests that oxidative stress plays a dominant role in the pathogenesis of diabetes mellitus. Caffeic acid phenethyl ester (CAPE), an active component of propolis, has several biological and pharmacological properties, including antioxidant, anti-inflammatory, anti-carcinogenic, antiviral, and immunomodulatory activities. In light of the antioxidant ability of CAPE, the effects of CAPE on the antioxidative status of cardiac tissue were investigated in streptozotocin (STZ)-induced diabetic rats. DESIGN AND METHODS: Twenty-six rats were randomly divided into three groups: group I, control, nondiabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 7); and group III, STZ-induced, CAPE-treated diabetic rats (n = 10). In groups II and III, diabetes developed 3 days after intraperitoneal (ip) administration of a single 35 mg kg(-1) dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10 mumol kg(-1) ip dose of CAPE per day. After 8 weeks, the levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the cardiac tissues of all groups were analyzed. RESULTS: In untreated diabetic rats, MDA markedly increased in the cardiac tissue compared with the control rats (P < 0.05). However, MDA levels were reduced to the control level by CAPE. The activities of SOD and CAT in the untreated diabetic group and the CAPE-treated diabetic group were higher than those of the control group (P < 0.05). Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats in the untreated diabetic group (P < 0.05). There were no significant differences in the activity of GSH-Px between the rats in the untreated diabetic group and the control group. However, the activity of GSH-Px was increased in CAPE-treated diabetic rats compared with the control and untreated diabetic rats (P < 0.05). CONCLUSION: These results reveal that diabetes mellitus increases oxidative stress in cardiac tissue and CAPE has an ameliorating effect on the oxidative stress via its antioxidant property.     

Effect of vitamin E and vitamin C supplementation on antioxidative state and renal glomerular basement membrane thickness in diabetic kidney

The aim of this study was to analyze the effect of vitamins C and E on malondialdehyde (MDA) content and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) as well as glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. Wistar male rats were divided into following groups (12 rats each): the control, diabetic rats, diabetic rats whose drinking water was supplemented with vitamin C in a dose of 1.0 g/l or diet was supplemented with 200 mg of vitamin E/100 g fodder. Body weight, blood glucose and HbA1C levels and 24-hour urinary albumin excretion (UAE) were studied every week (0-12 weeks). After 6 and 12 weeks, MDA content and activities of SOD, CAT and GSH-Px were measured in the kidney homogenate supernatants. Electron micrographs of glomeruli were scanned and morphometric investigations were performed by means of computer image analysis system to compare GBM thickness. The blood glucose and HbA1C concentrations and UAE in diabetic rats were significantly higher than in the control group. An increase in the MDA level and decrease in the SOD, CAT and GSH-Px activities in the kidney of diabetic rats were observed after 6 and 12 weeks of experiment. Administration of vitamins C and E did not affect body weight, blood glucose and HbA1C levels. Both vitamin C and vitamin E decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of diabetic rats as well as reduced UAE, decreased kidney weight and GBM thickness. The results indicate the potential utility of antioxidant vitamins in the protection against the development of diabetic nephropathy.     

Caffeic acid phenethyl ester as a protective agent against doxorubicin nephrotoxicity in rats

BACKGROUND: Nephrotoxicity is one of the important side effects of antracycline antibiotics. The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, against nephrotoxicity induced by doxorubicin (DXR). METHODS: The rats were divided into control, CAPE alone, doxorubicin (20 mg/kg, i.p.) and doxorubicin plus CAPE (10 micromol/kg/day, i.p.) groups. At the end of the 10th day, kidney tissues were removed for light microscopy and analysis. The levels of tissues protein carbonyl content (PC), malondialdehyde (MDA) and nitric oxide (NO) as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) were determined. Plasma oxidants and antioxidants were also measured. RESULTS: The activities of CAT and GSH-Px were decreased as well as myeloperoxidase, NO, MDA and PC were increased in renal tissue of doxorubicin group compared with the other groups. Plasma GSH-Px activity was higher in doxorubicin plus CAPE group than the others and plasma MDA level was higher in doxorubicin group than the other groups. There were glomerular vacuolization, tubular desquamation, loss of brush border, and adhesion to Bowman's in the light microscopy in the kidneys of doxorubicin group. The tubules and brush border were almost normal and some of the glomerulus was filled with fine vacuoles in CAPE treated rats. CONCLUSION: Doxorubicin caused renal injury and CAPE treatment prevented lipid peroxidation and protein oxidation in renal tissue and partially preserved glomerulus and tubules.     

Plasmatic homocysteine concentration and its relationship with complications associated to diabetes mellitus

BACKGROUND: The aim of this study was to examine the effect of verapamil (VP) on lipid peroxidation and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px); as well as on glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. METHODS: Wistar male rats were divided into three groups, 12 rats each: the control (C), diabetic rats (DR), and DR receiving VP, 7 mg/kg body weight in drinking water (DR + VP). Blood glucose (BG) and HbA(1c) levels, 24-h urinary albumin excretion (UAE) and body weight (BW) were measured every week (0-12 weeks). After 6 and 12 weeks, the animals were sacrificed and malondialdehyde (MDA) content and activities of SOD, CAT and GSH-Px were determined in the kidney homogenate supernatants. Electron micrographs of the glomeruli were scanned and morphometric investigations were performed by means of a computer image analysis system to compare the glomerular basement basal membrane (GBM) thickness. RESULTS: The levels of BG, HbA(1c) and UAE in DR were significantly higher than in the C group. A progressive increase in the MDA level and a decrease in the SOD, CAT and GSH-Px activities in the kidney of DR were observed after 6 and 12 weeks. VP administration did not affect BW changes, BG and HbA(1c) levels in DR. VP decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of DR as well as decreased kidney weight, GBM thickness and albuminuria in DR. CONCLUSIONS: These results confirm the role of oxidative stress in the development of diabetic nephropathy and point to the possible antioxidative mechanism of the nephroprotective action of VP.     

Protective effects of vitamin C, alone or in combination with vitamin A, on endotoxin-induced oxidative renal tissue damage in rats

This study was designed to investigate the protective effects of vitamin C and vitamin A on oxidative renal tissue damage. Male Wistar rats were given an intraperitoneal injection of 0.5 ml saline (control) or 0.5 ml solution of lipopolysaccharide (10 mg/kg), which caused endotoxemia. Immediately (within 5 min) after the endotoxin injection, the endotoxemic rats were untreated or treated with intraperitoneal injection of vitamin A (195 mg/kg bw), vitamin C (500 mg/kg bw) or their combination. After 24 hours, tissue and blood samples were obtained for histopathological and biochemical investigation. Endotoxin injection caused renal tissue damage and increased erythrocyte and tissue malondialdehyde (MDA) and serum nitric oxide (NO), urea and creatinine concentrations, but decreased the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared to the parameters of control animals. Treatment with vitamin C or with vitamins C and A significantly decreased the MDA levels and serum NO, urea and creatinine levels, recovered the antioxidant enzyme activities (SOD, GSH-Px and CAT), and prevented the renal tissue damage in endotoxemic rats. In contrast, vitamin A alone did not change the altered parameters except for creatinine levels. Notably, the better effects were observed when vitamins A and C given together. It is concluded that vitamin C treatment, alone or its combination with vitamin A, may be beneficial in preventing endotoxin-induced oxidative renal tissue damage and shows potential for clinical use.     

Protective role of caffeic acid phenethyl ester in the liver of rats exposed to cold stress

Cold exposure can induce a form of environmental stress. Cold stress (CS) alters homeostasis, results in the creation of reactive oxygen species and leads to alterations in the antioxidant defense system. The caffeic acid phenethyl ester (CAPE), an active component of propolis, has an antioxidant capacity. We investigated the effect of CS on oxidative stress and antioxidant defense system and the possible protective effect of CAPE in rat liver tissue. Twenty-four female Wistar Albino rats were divided into four groups: Control, CAPE-treated, CS, and CAPE-treated CS (CS + CAPE) group. Catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were measured. In addition, histological changes in liver tissue were examined by light microscopy. SOD, CAT and GSH-Px activities and total GSH level were significantly declined in the CS group. In the CS + CAPE group, the activities of these three enzymes and GSH level significantly raised with regard to the CS group. MDA levels increased in the CS group and decreased in the CS + CAPE group. The tissues of the CS group showed some histopathological changes such as necrosis, hepatocyte degeneration, sinusoidal dilatation, hemorrhage and vascular congestion and dilatation. In the CS + CAPE group, the histopathological evidence of hepatic damage was markedly reduced. Histological parameters were consistent with biochemical parameters. In this study, CS increased oxidative stress in liver tissue. CAPE regulated antioxidant enzymes, inhibited lipid peroxidation and reduced hepatic damage.     

糖尿病大鼠肾脏氧化应激的实验研究

目的　研究糖尿病大鼠肾脏氧化应激反应 ,求证氧化应激在糖尿病肾病发病机制中的作用。方法　将实验动物分为正常组与糖尿病组 ,用链脲佐菌素 (STZ)诱导糖尿病大鼠模型 ,8周后检测两组大鼠血糖、血脂、尿蛋白、肾重 体重等各指标的变化以及肾组织中丙二醛 (MDA)的含量 ,铜、锌超氧化物歧化酶 (Cu ,Zn SOD) ,谷胱甘肽过氧化酶(GSH Px)的活性。结果　与正常组相比 ,糖尿病组血糖、血脂、尿蛋白、肾重 体重等指标明显增高 ,肾皮质MDA含量亦增加 ,而肾脏抗氧化酶的活性则降低。结论　糖尿病大鼠肾脏存在氧化应激反应 ,肾组织抗氧化酶缺乏在糖尿病肾病发病机制中起重要作用     

Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats

Background: NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation.Objective: The aim of this study was to assess the potential protective effects of β-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model.Methods: Thirty-two male Wistar albino rats (200–250 g) were randomized into 4 groups consisting of 8 rats each. The β-glucan group received 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+β-glucan group was administered 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis.Results: The gastroprotective and antioxidant effects of β-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] μmol/L; NO, 8.04 [7.25–9.10] vs 30.35 [22.34–37.95] μmol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42–0.66] to 1.55 [1.19–1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [6] U/mL; P < 0.001). In the ASA+β-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001).Conclusion: β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.