帕金森病患者血液抗氧化功能的变化及多巴制剂与VitE对 …

目的 探讨帕金森病（ＰＤ）的抗氧化酶（ＳＯＤ）活性和过氧化脂质（ＬＰＯ）代谢水平的变化和多巴药物及ＶｉＴ对其的影响，找出反映氧化异常的客观生化指标。方法 对９６例ＰＤ患者动态检测了服用Ｌ－多巴和ＶｔＥ前后的血浆及红细胞膜超氧化物岐化酶（Ｐ－ＳＯＤ、Ｅ－ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性，血浆及红细胞过氧化脂质（Ｐ－ＬＰＯ、Ｅ－ＬＰＯ）及丙二醛（ＭＤＡ）的变化，并与２０例正常３人对照。     

东菱克栓酶对全脑缺血再灌流损伤脑保护作用的实验研究

本文采用Ｐｕｌｌｓｉｎｅｌｌｉ的４ＶＯ方法制作了大鼠全脑缺血再灌流动动物模型，采用ＴＢＡ法、ＤＴＮＢ直接法测定全脑缺血１０ｍｉｎ再灌流后４８ｈ海马区的过氧化脂质（ＬＰＯ）和谷光甘肽过氧化物酶（ＧＳＨ－Ｐｘ）含量变化，计量病理和电子显微镜观察病理变化及东菱精纯克栓酶对其含量变化和病理改变的影响。结果显示：（１）东菱克栓酶可降低海马区ＬＰＯ含量（Ｐ〈０．０１），使ＧＳＨ－Ｐｘ活性上升（Ｐ〈０．０１）。     

氧化、脂质过氧化与脑梗死关系的探讨

目的:探讨一氧化氮、氧化、脂质过氧化与脑梗死的关系。方法:检测了１４６例急性脑梗死患者(ＣＩ)和１００例健康志愿者(ＨＶ)血浆中的一氧化氮(Ｐ－ＮＯ)、维生素Ｃ(Ｐ－ＶＣ)、维生素Ｅ(Ｐ－ＶＥ)、β－胡萝卜素(Ｐ－β－ＣＡＲ)和过氧化脂质(Ｐ－ＬＰＯ)含量及红细胞中的超氧化物歧化酶(Ｅ－ＳＯＤ)、过氧化氢酶(Ｅ－ＣＡＴ)、谷胱甘肽过氧化物酶(Ｅ－ＧＳＨ－Ｐｘ)活性和过氧化脂质(Ｅ－ＬＰＯ)含量并作分析比较;同时,检测了其中４４例患者治疗前后的上述生化指标,并作分析比较。结果:与ＨＶ组比较,ＣＩ组的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著升高(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著降低(Ｐ＜０．００１);与治疗前比较,治疗后的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著降低(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著升高(Ｐ＜０．００１)。结论:脑梗死患者体内ＮＯ代谢异常,一系列自由基连锁反应病理性加剧,氧化抗氧化平衡严重失调,ＮＯ、氧化和脂质过氧化损伤加剧。     

自由基代谢与精神分裂症临床症状和药物治疗的关系

目的：探讨自由基代谢与精神分裂症临床症状和药物治疗的关系。方法：是否治疗的慢性精神分裂症患者各４０例分别评定定阳性和阴性症状量表（ＰＡＮＳＳ）,并测定膜脂质过氧化物丙二醛（ＭＤＡ）含量、铜／锌超氧化物歧化酶（Ｇｕ－ＺｎＳＯＤ）和谷胱苷肽过氧化物酶（ＧＳＨ－Ｐｘ）活性。结果：与健康对照组相比,未治疗组患者ＭＤＡ含量和ＧＳＨ－Ｐｘ活性显著增加,治疗组患者无显著改变;而两组患者ＳＯＤ活性显著降低;未治疗     

脑血管病分类亚型与血脂关系的研究

目的：阐明血脂与脑血管病分类亚型的关系。方法：检测了２０８例脑血管病患者血清血脂７项指标含量。并与对照组５０例结果进行比较。ＴＧ、ＴＣ及ＨＤＬ－Ｃ采用酶法测定，ＡＰＯＡ－１、ＡＰＯＢ１００及ＬＰ（ａ）用免疫多点定标法测定，ＬＤＬ－Ｃ由ＴＧ、ＨＤＬ－Ｃ结果按公式计算。结果：脑梗塞（ＣＩ）患者ＴＧ、ＴＣ、ＬＤＬ－Ｃ、ＡＰＯ１００及ＬＰ（ａ）含量显著高于对照组，其ＴＧ、ＡＰＯＢ１００、含量也显著高于脑出血组，且ＬＰ（ａ）与ＡＰＯＢ１００，ＨＤＬ－Ｃ相关，复发ＣＩ亚组ＴＣ、ＬＤＬ－Ｃ、ＡＰＯＢ１００含量，首发及老年ＣＩ亚组ＴＧ、ＴＣ、ＡＰＯＢ１００含量显著高于对照组。结论：血清ＴＧ、ＴＣ、ＬＤＬ－Ｃ、ＡＰＯＢ１００及ＬＰ（ａ）水平升高是ＣＩ的危险因素，其中ＴＣ、ＬＤＬ－Ｃ、ＡＰＯＢ１００对复发ＣＩ危险性大，而首发及老年ＣＩ可能主要与ＴＧ、ＴＣ、ＡＰＯＢ１００有关     

羧乙基锗倍半氧化物对大鼠脑缺血再灌注损伤的保护作用

采用结扎双侧颈总动脉后再通的方法复制大鼠脑缺血再灌注损伤模型，通过测定再灌注后大鼠海马组织中脂质过氧化产物丙二醛（ＭＤＡ），超氧化物歧化酶（ＳＯＤ）与谷胱甘肽过氧化物酶（ＧＳＨ—Ｐｘ）及ＡＴＰａｓｅ的活性，观察了有机锗─羧乙基锗倍半氧化物（ＣＧＳ）对大鼠脑缺血再灌注后大鼠海马组织中ＭＤＡ水平，明显保护ＳＯＤ、ＧＳＨ─Ｐｘ、Ｎａ＋Ｋ＋─ＡＴＰａｓｅ及Ｃａ２＋─ＡＴ─Ｐａｓｅ活性。表明ＣＧＳ对大鼠脑缺血再灌注损伤具有保护作用。     

实验性迟发性脑血管痉挛时痉挛动脉的自由基代谢

为探讨蛛网膜下腔出血（ＳＡＨ）后迟发性脑血管痉挛（ＤＣＶＳ）时痉挛动脉的自由基代谢变化。通过了对ＤＣＶＳ时痉挛动脉的自由基含量、自由基清除酶超氧化物岐化酶（Ｃｕ－ＺｎＳＯＤ）与过氧化氢酶（Ｃａｔ）活性以及自由基代谢产物脂质过氧化物（ＬＰＯ）含量的测定。结果显示：（１）痉挛动脉的自由基含量比对照组明显升高（Ｐ＜０．０１）；（２）Ｃｕ－ＺｎＳＯＤ活性明显降低（Ｐ＜０．０５），Ｃａｔ活性明显升高（Ｐ＜０．０１）；（３）ＬＰＯ含量明显升高（Ｐ＜０．０１）。本实验结果证实ＳＡＨ后ＤＣＶＳ时痉挛动脉存在自由基的代谢紊乱，自由基介导的病理作用可能在ＤＣＶＳ发病机理中起重要作用。     

载脂蛋白E与脑动脉硬化症

本文观察７８例脑动脉硬化症患者与对照组４４例，对其血清载脂蛋白Ｅ（ＡＰＯＥ）和高密度脂蛋白（ＨＤＬ－Ｃ）、低密度脂蛋白（ＬＤＬ－Ｃ）、胆固醇（ＴＣ）、甘油三脂（ＴＧ）、载脂蛋白ＡＩ（ＡＰＯＡＩ）、载脂蛋白Ｂ（１００）（ＡＰＯＢ（１００））进行含量测定，并将ＡＰＯＥ与ＨＤＬ－Ｃ、ＬＤＬ－Ｃ、ＴＣ、ＴＧ、ＡＰＯＡＩ、ＡＰＯＢ（１００）逐一进行相关比较，结果发现：脑动脉硬化症病人（ＣＡＳ）血清ＡＰＯＥ、ＬＤＬ－Ｃ、ＴＣ、ＴＧ、ＡＰＯＢ（１００）明显高于正常对照组（Ｐ＜０．０１），ＨＤＬ－Ｃ显著低于正常对照组（Ｐ＜０．０１），ＡＰＯＡＩ无明显变化（Ｐ＞０．０５），且ＡＰＯＥ与ＨＤＬ－Ｃ呈负相关；与ＬＤＬ－Ｃ、ＴＣ、ＴＧ、ＡＰＯＢ（１００）呈正相关；与ＡＰＯＡＩ无直线相关关系。提示ＡＰＯＥ可做为诊断脑动脉硬化症的重要指标。     

抗氧化酶类对大鼠感染性脑损伤的内源性防护作用

目的 通过测定脑组织丙二醛（ＭＤＡ）、超氧化物歧化酶（ＣｕＺｎ－ＳＯＤ和Ｍｎ－ＳＯＤ）、过氧化氢酶（ＣＡＴ）及谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）活性的变化,探讨抗氧化酶类在大鼠感染性脑损伤内生防护机制听作用。方法 向大鼠左颈内动脉注射百日咳菌悬浮液,诱发感染性脑损伤模型。４０只大鼠随机分为生理盐水对照组（ＮＳ）和右日咳杆菌悬浮液组（ＢＰＳ）,观察时间为４ｈ和２４ｈ。用可见光和紫外分光光度法分别测定     

神经症患者超氧化物歧化酶、谷胱甘肽超氧化物酶及脂质超氧化物含量的变化

为研究氧自由基与神经症之间的关系，分别采用邻苯三酚自氧化法、二硫对硝基苯甲酸直接法、硫代巴比妥酸比色法，测定了８７例神经症和５５名健康人超氧化物歧化酶（ＳＯＤ）、谷胱甘肽超氧化物酶（ＧＳＨ－Ｐｘ）和脂质超氧化物（ＬＰＯ）含量。结果显示，神经症组ＳＯＤ与ＧＳＨ－Ｐｘ两种酶含量均低于对照组，神经症组治疗前低于治疗后；ＬＰＯ为治疗前高于治疗后，差异均有显著性。从单胺类的代谢与生成氧自由基的生化联系以及机体内ＳＯＤ、ＧＳＨ－Ｐｘ、ＬＰＯ之间的相互关系上对结果进行了分析，提示体内单胺类物质代谢过程中产生的氧自由基在神经症的病理过程中可能发挥一定的作用。     

帕金森病血抗氧化系统的变化及临床意义

探讨帕金森病（ＰＤ）患者体内抗氧化系统水平及其在ＰＤ发病中的可能作用。方法观测了７０例ＰＤ患者和７０例正常人的血浆维生素Ｃ、Ｅ浓度（Ｐ－ＶＣ，Ｐ－ＶＥ），血浆及红细胞膜超氧化物歧化酶（Ｐ－ＳＯＤ，Ｅ－ＳＯＤ）活性，血浆及红细胞过氧化脂质（Ｐ－ＬＰＯ，Ｅ－ＬＰＯ）水平的变化。结果与正常对照组相比，ＰＤ患者的Ｐ－ＶＣ、Ｐ－ＶＥ浓度及Ｐ－ＳＯＤ、Ｅ－ＳＯＤ活性均明显降低，而Ｐ－ＬＰＯ、Ｅ－ＬＰＯ水平则显著增高。并且Ｐ－ＶＣ、Ｐ－ＶＥ、Ｅ－ＳＯＤ水平与ＰＤ患者的病情和病程呈负相关。结论提示ＰＤ患者可能存在血抗氧化系统缺陷而使内源性氧自由基堆积，导致黑质神经元退变     

维生素E、C在CVD与PD患者中抗氧化作用的临床研究

目的 探讨维生素E（Vit E)与维生素C（Vit C)在脑血管病（CVD）与帕金森病（PD）中的抗氧化作用。方法 检测CVD162例和PD77例共239例患者服用VitE和VitC前后血浆Vit E、Vit C、过氧化脂质（LPO）水平和红细胞超氧化物歧化酶（SOD）活性,并与对照组进行了比较。结果 服药前两组患者血浆Vit E、Vit C水平和红细胞SOD活性明显低于正常对照组;服药后两组患者的Vit E、Vit C水平和SOD活性无明显变化,而CVD组的LPO值升高。结论 CVD和PD患者可能有Vit E、Vit C水平和SOD活性降低,服用Vit E、Vit C后仅见CVD患者的LPO值升高,但匀不能象健康对照组那样提高Vit E、Vit C水平和SOD活性。     

Changes in lipid peroxides and superoxide dismutase as incubation of in vitro erythrocytes with cerebrospinal fluids and the action of various scavengers of free radicals]

In this experiment, LPO increased and SOD reduced as the time pass when erythrocytes (RBC) and CSF were mixed and incubated. There was a negative relationship between LPO and SOD. LPO in RBC of arterial blood was higher than that of venous blood after incubation for 3 days (P less than 0.01). When arterial RBCs were incubated together with various scavengers of free radical (SOD catalase and histidine and mannitol), the production of LPO was less than that of arterial RBC incubation singly (P less than 0.01). The change of LPO was not reduced when sodium nitrite and arterial RBC incubated. The results demonstrated that the scavengers of free radicals could be eliminated free radical but failed with sodium nitrite.     

Hydroxyl radical and superoxide dismutase in blood of patients with Parkinson's disease: relationship to clinical data

Hydroxyl radical (·OH) levels in blood, superoxide dismutase (SOD) activity in plasma (plasma-SOD) and in red blood cells (RBC) relative to Cu,Zn-SOD (SOD1) protein (RBC-SOD/SOD1), SOD1 protein in RBC (SOD1/RBC) and plasma (SOD1/plasma), and Mn-SOD protein in plasma (SOD2/plasma) were measured in patients with Parkinson’s disease (PD), multiple-system atrophy (MSA) with parkinsonism, and in control subjects. Patients with PD had significantly higher ·OH and plasma-SOD values and significantly lower RBC-SOD/SOD1 and SOD1/RBC values than the corresponding MSA and control values. In PD, RBC-SOD/SOD1 values were significantly lower in older patients and were negatively correlated with age. ·OH levels were significantly higher in PD patients with early onset, a long period of illness or severe Yahr stage, and were negatively correlated with onset and positively correlated with duration of illness. RBC-SOD/SOD1 values in PD patients who received pergolide therapy were significantly higher than those in PD patients who received neither pergolide nor bromocriptine therapy. Therefore, the higher ·OH level and the lower SOD1 activity may play a role in the onset and progression of PD, and pergolide may act neuroprotectively by inducing SOD1 activity.     

丁基苯酞对血管性痴呆患者自由基及血液流变学的影响

目的研究丁基苯酞对血管性痴呆患者脑血流动力学及对神经功能的影响。方法将80例血管性痴呆患者按病情相匹配的原则分为治疗组46例,对照组34例,治疗组采用常规内科治疗和丁基苯酞治疗20d,对照组采用常规内科治疗20d,治疗前及治疗后4周行脑血流动力学检查、日常生活活动能力(ADL)量表测定、听觉P300测试。结果治疗后脑血流动力学检查ADL量表测定、听觉P300测试组间比较有显著性差异(P<0.05或P<0.01)。结论丁基苯酞能改善血管性痴呆患者脑血流动力学,促进神经功能康复。     

Peripheral markers for oxidative stress in Parkinson’s disease patients of Eastern India

Oxidative stress is thought to play a major role in the pathogenesis of Parkinson’s disease (PD). Neurons are highly susceptible to a defective antioxidant scavenging system, thus inducing oxidative changes in human red blood cells (RBCs), in vivo and in vitro. Previous studies on oxidative stress in RBCs in patients with PD have yielded controversial results claiming unaltered activity to reduced activity. We have thus undertaken this study to investigate the possibility of oxidative damage to the RBCs in PD by measuring the cytosolic antioxidant enzymes viz., catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (G-Px). The biochemical parameters were measured in erythrocytes of 80 PD patients and 80 normal age-matched healthy controls. The enzymes activities were correlated with age of patients, age of onset of disease, duration of disease, United Parkinson’s Disease Rating Scale (UPDRS) and Hoehn and Yahr stage. Patients with PD had higher red blood corpuscle (RBC) activity of SOD. The CAT, and G-Px activities were significantly lower in patients with PD compared to the controls. Erythrocyte SOD, CAT and G-Px were markedly lower in those PD patients who were suffering for a greater duration of the disease and in advanced cases of PD. A significant (P < 0.05) negative correlation of enzyme activities with disease duration, UPDRS score and Hoehn and Yahr stage of the disease was found. Results of our present study concludes the implication of oxidative stress as one of the risk factors, which can initiate or promote neurodegeneration in PD by playing a role in dopaminergic neuronal loss and was correlated to the severity of the disease.     

急性脑梗塞患者红细胞免疫功能与血清SOD,LPO的变化

测定了３１例急性脑梗塞患者红细胞Ｃ３ｂ受体花环率（ＲＢＣ—Ｃ３ｂＲＲ）和红细胞免疫复合物花环率（ＲＢＣ—ＩＣＲ）以及可能影响红细胞免疫粘附（ＲＣＩＡ）功能的血清脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）。结果表明，急性脑梗塞患者ＲＢＣ—Ｃ３ｂＲＲ明显降低，而ＲＢＣ—ＩＣＲ明显增高；血清ＳＯＤ含量减少，ＬＰＯ明显增高。ＲＢＣ—Ｃ３ｂＲＲ降低与血清ＬＰＯ增高呈显著负相关，与ＳＯＤ呈正相关。上述结果说明红细胞免疫功能降低与体内自由基代谢改变有关。     

自由基在大鼠全脑缺血再灌流损伤中作用机理及保精增智液的保护作用

本文采用大鼠４血管关闭方法制作了全脑血再灌流模型。于再灌流后２４ｈ取双侧海马，分别采用Ｐｒｏｇａｌｌｏｌ－ＮＢＴ和改良的ＴＢＡ法测定了ＳＯＤ活性和ＬＰＯ含量。结果ＳＯＤ明显低于对照组而ＬＰＯ明显高于对照组（Ｐ＜０．０１）。同时观察了一种新的中药方剂—保精增智液对自由基的拮抗作用，实验证明该药造模后给药效果不明显（Ｐ＞０．０５），造模前给药可使ＬＰＯ下降及ＳＯＤ上升，与对照组比较差异显著（Ｐ＜０．０１）。证明该药对全脑缺血再灌流损伤引起的自由基升高有保护作用。     

氯喹,SOD防治脑缺血再灌注损伤的实验研究

探讨氯喹、超氧化物歧化酶（ＳＯＤ）防治脑缺血再灌注损伤的效果。用４血管阻断法造成大鼠全脑缺血，３０ｍｉｎ后再恢复双侧颈总动脉血流３０ｍｉｎ，此时大鼠脑组织磷脂酶Ａ（ＰＬＡ）活性和内皮素（ＥＴ）、过氧化脂质（ＬＰＯ）含量显著增高，而ＳＯＤ活性和维生素Ｅ（ＶｉｔＥ）含量明显降低，大脑皮层神经细胞和血脑屏障明显损害。预防用氯喹或ＳＯＤ治疗，部分抑制了ＬＰＯ、ＥＴ含量的增高和ＳＯＤ活性下降，明显减轻脑神经细胞和血脑屏障损伤程度；但对ＶｉｔＥ含量都无明显影响。氯喹、ＳＯＤ对缺血再灌注脑损伤有一定的防治作用。     

Plasma lipid peroxidation in sporadic Parkinson's disease. Role of the L-dopa

Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease (PD). There are several methods to measure oxidative stress, being lipid peroxidation (LPO) one of the most frequently used. Endogenous plasma LPO was determined by a spectrofluorimetric method in fifty two patients with sporadic PD and in forty controls. To know the maximum capacity of lipids to peroxidate, LPO was also measured after co-incubation with Fe2+/H2O2 (exogenous LPO). All PD patients were taken L-dopa and the effect of this treatment on LPO levels was additionally studied. Urine catecholamines and their main metabolites were also analyzed, and their possible correlation to LPO statistically studied. Endogenous plasma LPO levels were 33% higher in PD group than in control group (P<0.001). Exogenous plasma or oxidizability was also higher in PD patients compared to controls (20%, P<0.05). The intake of L-dopa was negatively dose-related to endogenous and exogenous plasma LPO. In conclusion, plasma of PD patients has elevated levels of LPO and also is more prone to peroxidation than that in the control group. The results also suggest an antioxidant effect of L-dopa.