维生素C联合维生素E对慢性乙型肝炎表面抗原转阴的影响

目的观察维生素C联合维生素E对慢性乙型肝炎表面抗原转阴的效果。方法2001年至2004年诊治的慢性乙型肝炎患者108例,随机分为对照组54例,给予保肝治疗,治疗组54例,应用维生素C和维生素E,疗程1年,比较前后2组ALT、AST水平变化,比较乙肝两对半在治疗前后的变化,分析疗程结束时,2组乙肝两对半的变化情况。结果2组治疗后ALT[治疗组为（56．8±25．9）U／L,对照组为（89．3±32．3）U／L]、AST[治疗组为（49．9±35．3）U／L,对照组为（76．5±34．5）U／L]均较治疗前[ALT治疗组为（176．3±65．2）U／L,对照组为（169．5±59．8）U／L,AST治疗组为（132．3±44．4）U／L,对照组为（121．4±38．6）U／L]有明显好转（P均〈0．05）;治疗组HBsAg94．4％转阴,对照组无明显变化。结论维生素C联用维生素E对乙型肝炎表面抗原（HBsAg）转阴疗效明显。     

维生素E和维生素C对大豆磷脂脂质体的抗氧化作用

利用分光光度法，研究了不同含量维生素Ｅ或维生素Ｃ对大豆磷脂脂质体的抗氧化保护作用及维生素Ｃ的存在和温度的变化对维生素Ｅ抗氧化作用的影响。结果表明，适量维生素Ｅ可明显抑制磷脂脂质体的氧化，含量越高，抑制作用越强；大量维生素Ｃ虽可起到抗氧化作用，但少量维生素Ｃ在铁离子的存在下却可起到促氧化作用；维生素Ｃ的存在对维生素Ｅ的抗氧化作用具有明显的协同作用；温度的升高有利于磷脂脂质的氧化。     

维生素C与维生素E联合应用的实验研究

维生素C是一种水溶性维生素。在体内抗坏血酸（维生素C或Vit C）和脱氢抗坏血酸形成可逆的氧化还原系统,此系统在生物氧化及还原作用中和细胞呼吸中起重要作用。维生素为一种脂溶性维生素。它具有增强细胞的抗氧化作用,抑制脂质过氧化等作用。现就两者联合应用的实验研究进行综述分析,以便在临床中更好地应用这两种药物。     

维生素E联合维生素C对急行军后骨骼肌损伤的保护作用

目的观察维生素E联合维生素C对新兵新训期间徒步行军后骨骼肌的保护作用。方法将平素身体健康且无正规体育锻炼史的60名男性新兵随机分为3组(每组20例):A组(对照组)、B组(维生素E干预组)、C组(维生素E+维生素C干预组)。行军前,B组、C组连续服用维生素E 4 mg/(kg·d),共14 d。在此基础上,C组给予口服维生素C 10 mg/(kg·d),A组服用相同体积的0.9%Na Cl溶液。14 d后,60名新兵进行120 km(40 km/d)徒步行军,行军过程中给予腿部热敷及按摩(20 min/次,2次/d),徒步行军结束后2、3、6、24 h抽取外周静脉血,检测肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)、活性氧类物质(ROS)及丙二醛(MDA)浓度的变化。结果 A组新兵外周血清各个时间点的CK、LDH、ROS、M DA值均高于B组、C组,而GSH-PX、SOD活性值均低于B组、C组,差异均有统计学意义(P<0.05);B组外周血清CK、LDH、ROS、M DA值高于C组,而GSH-PX、SOD活性值低于C组,差异有统计学意义(P<0.05)。行军后,三组外周血清GSH-PX、SOD活性下降,于6 h达到最低值,24 h后开始升高,且差异均有统计学意义(P<0.05);行军后,三组外周血ROS、MDA升高,并于行军结束后6 h达到高峰,24 h后开始下降,且差异有统计学意义(P<0.05)。结论维生素E联合维生素C通过调节氧化与抗氧化平衡来抑制长时间运动所导致的肌肉损伤。     

维生素C和维生素E单用及联用对慢性酒精性肝损伤模型大鼠的预防性保护作用

目的:观察维生素C(VC)和维生素E(VE)单用及联用对慢性酒精性肝损伤模型大鼠的预防性保护作用。方法:取60只大鼠,随机均分为对照组、模型组、VC组(150mg·kg-1)、VE组(250mg·kg-1)和同剂量联合用药组(VC+VE组),除对照组给予等量生理盐水灌胃外,其余各组连续灌胃56°白酒建立慢性酒精性肝损伤模型,同时给予相应药物,每天1次,6周后检测各组大鼠血清丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST),肝匀浆中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,并观察肝组织病理学变化,免疫组织化学法检测肝组织中Ⅰ和Ⅲ型胶原的表达情况。结果:与模型组比较,VC组、VE组、VC+VE组ALT和AST活性、MDA含量、Ⅰ和Ⅲ型胶原表达均显著性降低(P<0.05),SOD活性显著性升高(P<0.05),肝脏炎症反应和纤维化明显减轻,且单用组和联用组之间无显著性差异。结论:VC和VE可能通过清除自由基和抑制脂质过氧化过程对慢性酒精性肝损伤模型大鼠发挥预防性保护作用。     

公众对维生素C和维生素E的错误认识及危害

维生素C和维生素E是维持机体正常代谢和生理功能不可缺少的营养物质之一。一般情况下机体是不会缺乏的,仅在饮食不当导致摄入维生素不足或机体吸收维生素的能力发生障碍时才会出现。一些公众对维生素缺乏应有的认识,误把维生素C和维生素E当成补药、美容药,滥用现象比较普遍。现对滥用维生素C和维生素E的错误认识及危害浅析如下。     

维生素 C 联合维生素 E 对 COPD 患者氧化应激的影响

目的：探讨维生素C联合维生素 E对COPD患者氧化应激的影响。方法从贵阳医学院附属医院2011年6月6日至2014年3月20日住院患者中选择符合条件的30例COPD患者将其作为实验组,在予以COPD常规治疗方法的基础上加用维生素C及维生素E治疗10 d（维生素C注射液2．0 g＋NS 250 mL ,1次／d静滴,疗程10 d;维生素E胶丸100 mg ,1次／d口服,疗程10 d）。另外30例患者作为对照组仅予以COPD常规治疗,观察并比较两组在治疗前后体内SOD与MDA变化。结果无论实验组还是对照组在治疗前血清MDA及SOD水平均差异均有统计学意义,实验组在使用维生素C、E治疗后体内SOD及MDA水平与未使用维C及维E的对照组治疗后体内SOD及MDA水平比较均有差异性,且差异有统计学意义（P＜0．05）。结论维生素C联合维生素E治疗能显著改善慢性阻塞性肺疾病患者体内氧化应激水平,维持体内氧化／抗氧化水平的平衡。     

维生素C、维生素E联合作用对慢性阻塞性肺疾病患者脂质过氧化的影响

慢性阻塞性肺疾病(chronic obstructive pulmonary diseases,COPD)是呼吸系统最常见的疾病之一,是指具有气流阻塞为特征的慢性支气管炎和(或)肺气肿,气流阻塞不完全可逆,呈进行性发展,可伴有气道高反应性,其发生与肺部对有害气体和有害颗粒的反应有关,居当前世界死亡原因的第四位[1],对其治疗目前主要集中在氧疗、气管扩张、抗炎等方面.COPD的发病机制尚未完全明了,目前普遍认为COPD以气道、肺实质和肺血管的慢性炎症为特征,炎性介质参与其致病过程,而最新研究,该病患者体内存在着过度的脂质过氧化与抗脂质过氧化之间的不均衡[2,3].     

维生素E对胃黏膜损伤模型小鼠的保护作用研究

目的:观察维生素E(VE)对胃黏膜损伤模型小鼠的保护作用。方法:取小鼠50只随机均分为正常对照组、模型组、西咪替丁(25mg·kg-1)组和VE低、高剂量(25、50mg·kg-1)组,灌胃给予相应药物30min后,后4组灌胃给予吲哚美辛25mg·kg-1,4h后处死小鼠,检测各组小鼠胃黏膜损伤程度及血清中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量。结果:与正常对照组比较,模型组小鼠胃黏膜损伤指数和SOD活性、MDA含量均明显升高(P<0.01);与模型组比较,西咪替丁组和VE低、高剂量组小鼠胃黏膜损伤指数和SOD活性、MDA含量均明显降低(P<0.01);与西咪替丁组比较,VE高剂量组小鼠胃黏膜损伤指数和SOD活性均明显降低(P<0.01)。结论:VE可能通过抗氧化、清除氧自由基和抑制脂质过氧化过程发挥预防胃黏膜损伤的作用,且VE高剂量(50mg·kg-1)组对胃黏膜损伤的保护作用强于西咪替丁(25mg·kg-1)组。     

维生素C、E预防阿霉素对心肌毒性的观察

阿霉素（ADM）属蒽醌类抗生素、具有抗瘤谱广、作用强的特点,对多生肿瘤都有较好疗效。但因基潜在的心肌毒辣性（主要表现为用药早期出现各种心律失常、、晚期出现剂量依赖性充血性心衰,此时病死率可主50％）使其临床使用受到一定限制。大量动物实验及临床研究资料显示,维生素C和维生素E（简和VC、VE）在预防ADM心肌毒性方面有一定效果。因此我院自1996年至1999年,对以ADM为主的联化化疗病人大量补充VC和VE,通过临床观察发现,二者共同应用时,对预防和减轻ADM心肌毒性有定效果。     

The Role of Vitamin C,Vitamin E,and Selenium on Cadmium-Induced Renal Toxicity of Rats

The aim of this study was to determine whether vitamin C, vitamin E, and selenium have protective effects against cadmium-induced renal toxicity of rats. Vitamin C (250 mg/kg/day), vitamin E (250 mg/kg/day), and sodium selenate (0.25 mg/kg/day) were given to rats orally for 8 days. Cadmium (2 mg/kg/day CdCl₂) was given to rats intraperitoneally. Vitamin C, vitamin E, and selenium (in the same dose and time) were given 1 h prior to the administration of cadmium every day. The tissue and blood samples were taken from the rats for histological evaluation and biochemical analyses on the Day 9. Lipid peroxidation (LPO) and glutathione (GSH) determination were made in kidney tissue. In addition, urea and creatinine levels were determined in serum. The damage to the kidney tissue was moderate in the rats given cadmium. In this group, the distinctive changes in the proximal tubules were observed. Degenerative changes in kidney tissue were also observed in rats given vitamin C, vitamin E, selenium, and cadmium. LPO levels significantly increased and GSH levels decreased in kidney tissues following cadmium administration. Serum urea and creatinine levels were also increased in rats given cadmium. The administration of vitamin C, vitamin E, and selenium caused a significant decrease in LPO levels and an increase in GSH levels in the kidney of rats given cadmium. Serum urea and creatinine levels were decreased in rats given both the antioxidant and cadmium. It is concluded that vitamin C, vitamin E, and selenium showed some protective effect on the rat kidney.     

Effects of acute and chronic administration of olanzapine in comparison to clozapine and haloperidol on extracellular recordings of substantia nigra reticulata neurons in the rat brain

Rationale: Previously, we have shown that the atypical antipsychotics clozapine and risperidone, unlike haloperidol, decreased the firing rate of substantia nigra reticulata (SNR) neurons. As the SNR receives substantial input from the striatum, an area where motoric side-effects of antipsychotics are thought to be mediated, the SNR might be an interesting brain structure with regard to motor side-effects. Objective: The newly developed atypical antipsychotic olanzapine was studied for its effects on the firing rate of SNR cells. In addition, to gain insight in the implications of our experimental setup for clinical use, responses upon clozapine, olanzapine and haloperidol were studied after chronic treatment. Methods: In chloralhydrate-anaesthetized male Wistar rats, extracellular recordings were made from SNR neurons upon intravenously (IV) administered cumulative doses of the antipsychotics. Naive rats and rats that were subcutaneously (SC) injected for 21 days with an antipsychotic were used. Results: Olanzapine (50–1600 mg/kg; IV), significantly inhibited the firing rate of the SNR neurons. Upon 21 days of treatment with a daily SC injection of 20 mg/kg clozapine, the challenge on day 22 with cumulative injections of clozapine (200–6400 mg/kg; IV) significantly inhibited the firing rate of the SNR neurons. Olanzapine (50–1600 mg/kg; IV) also significantly inhibited the SNR activity when pretreated with olanzapine in an SC administered dose of 1 mg/kg, but not 5 mg/kg. Haloperidol (12.5–800 μg/kg; IV) did not significantly affect the SNR activity in rats pretreated with SC administered 0.5 mg/kg haloperidol. Conclusions: Upon acute and chronic administration of clozapine and olanzapine versus haloperidol, differential effects on SNR neuronal firing could be obtained. The experimental setup seem to be valid for further studies into the mechanism of action of typical versus (relatively low doses of) atypical antipsychotics. The implications of the inhibitory effect of atypical antipsychotics on the SNR firing rate are presently unknown, but could be associated with the lower propensity to induced motoric side-effects. On the other hand, the SNR activity might also reflect non-motoric activity possibly related to negative symptoms. Received: 11 December 1998/Final version: 20 January 1999     

Effect of chronic administration of methamphetamine on the responsiveness of substantia nigra zona reticulata neurons to GABA or a GABA agonist in rats

Summary The effects of chronic administration of methamphetamine on the responsiveness of neurons of the substantia nigra zona reticulata (SNR) to gammaaminobutyric acid (GABA) or to a GABA receptor agonist were examined. Neuronal activity was recorded from the SNR of rats that had been pretreated twice daily, for 6 consecutive days, with saline or with 5 mg/kg methamphetamine. Intravenous administration of the GABA receptor agonist, muscimol, caused a dose-dependent decrease in the unit activity of the SNR neurons and the SNR neurons became less sensitive to the depressant effects of the drug after chronic treatment with methamphetamine. Iontophoretic application, with increasing currents, of GABA produced a progressive inhibition of unit activity in control animals, an effect that was significantly reduced in rats pretreated with methamphetamine. These results support the hypothesis that long-term administration of methamphetamine increases the activity of the striatonigral GABA system and thereby reduces the sensitivity of postsynaptic GABA receptors in the SNR.     

Protective effects of vitamin E and C on cisplatin nephrotoxicity in developing rats

The kinetics of vitamin E was followed in serum, liver and kidney of 10- and 55-day-old rats after the administration of a single i.m. dose of 100 mg α-tocopherol acetate/100 g body wt. The basal levels without vitamin E administration were significantly higher in serum and liver of 10- than 55-day-old rats. The effect of vitamin E on cisplatin (CP; 0.6 mg/100 g body wt., i.p.) nephrotoxicity was investigated by determining urinary volume and protein excretion, as well as the concentration of blood urea nitrogen (BUN) and lipid peroxides in renal tissue (LPO). Previously described age differences in CP nephrotoxicity were confirmed. The administration of vitamin E, 12 h prior to CP, diminished the toxic effect of CP in young and adult rats. This effect could not be enhanced by a second administration of vitamin E. The simultaneous administration of vitamin E and C 12 h prior to CP intensified the protective effect of a single administration of vitamin E in 10- and 55-day-old rats without influencing the concentration of platinum in renal tissue. Received: 10 April 1997 / Accepted: 10 June 1997     

Voltammetric characterization of the effect of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse caudate-putamen and substantia nigra slices

Fast scan cyclic voltammetry is an electrochemical technique used to measure dynamics of transporter-mediated monoamine uptake in real time and provides a tool to evaluate the detailed effects of monoamine uptake inhibitors and releasers on dopamine and serotonin transporter function. We measured the effects of cocaine, methylphenidate, 2β-propanoyl-3β-(4tolyl) tropane (PTT), fluoxetine, amphetamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), phentermine and fenfluramine on dopamine and serotonin uptake following electrically stimulated release in mouse caudate-putamen and substantia nigra pars reticulata slices. We determined rank orders of uptake inhibition effects based on two variables; increases in apparent K_m for dopamine and serotonin uptake and inhibition constant (K_i) values. For example, the rank order of uptake inhibition based on apparent K_m values at the dopamine transporter was amphetamine ≥ PTT ≥ methylphenidate  methamphetamine = phentermine = MDMA > cocaine  fluoxetine = fenfluramine, and at the serotonin transporter was fluoxetine = methamphetamine = fenfluramine = MDMA > amphetamine = cocaine = PTT ≥ methylphenidate > phentermine. Additionally, changes in electrically stimulated release were documented. This is the first study using voltammetry to measure the effects of a wide range of monoamine uptake inhibitors and releasers on dopamine and serotonin uptake in mouse brain slices. These studies also highlight methodological considerations for comparison of effects between heterogeneous brain regions.     

Oleoylethanolamide exerts partial and dose-dependent neuroprotection of substantia nigra dopamine neurons

Oleoylethanolamide (OEA), agonist of nuclear PPAR-α receptors and antagonist of vanilloid TRPV1 receptors, has been reported to show cytoprotective properties. In this study, OEA-induced neuroprotection has been tested in vitro and in vivo models of 6-OHDA-induced degeneration of substantia nigra dopamine neurons. First, PPAR-α receptors were confirmed to be located in the nigrostriatal circuit, these receptors being expressed by dopamine neurons of the substantia nigra, and intrinsic neurons and fibers bundles of the dorsal striatum. In the substantia nigra, their location was confined to the ventral tier. The in vitro study showed that 1 μM OEA exerted a significantly neuroprotective effect on cultured nigral dopamine neurons, effects following U-shaped dose-response curves. Regarding the in vivo study, rats were locally injected with OEA into the right striatum and vehicle into the left striatum 30 min before 6-OHDA-induced striatal lesion. In the short term, signals of heme oxygenase-1 (oxidation marker, 24 and 48 h post-lesion) and OX6 (reactive microglia marker, 96 h post-lesion) were found to be significantly less intense in the striatum pretreated with 5 μM OEA. In the long term (1 month), reduction in striatal TH and synaptophysin was less intense whether the right striatum was pretreated with 5 μM OEA, and nigral TH+ neuron death was significantly reduced after pretreatment with 1 and 5 μM OEA. In vivo effects also followed U-shaped dose-response curves. In conclusion, OEA shows U-shaped partial and dose-dependent neuroprotective properties both in vitro and in vivo models of substantia nigra dopamine neuron degeneration. The occurrence of U-shaped dose-response relationships normally suggests toxicity due to high drug concentration or that opposing intracellular pathways are activated by different OEA doses.     

In vivo evidence for GABAergic control of serotonin release in the cat substantia nigra

Push-pull cannulae were used for estimating the release of endogenously synthesized [3H]serotonin in both substantia nigra and caudate nuclei of halothane-anaesthetized cats. The unilateral nigral application of GABA (10-5 M) reduced the local release of [3H]serotonin picrotoxin induced an opposite effect. Both treatments failed to modify [3H]serotonin release in the caudate nuclei or in the contralateral substantia nigra. These results suggest that GABAergic neurons innervating the substantia nigra may regulate nigral serotonin transmission. The possibility that such a regulation could be presynaptic (direct or through other nigral neurotransmitters) or related to a change in the activity of the nigro-raphe projection is discussed.     

Opposed effects of locus coeruleus and substantia nigra lesions on social behavior in rat colonies

Rats were observed in enriched colony environments following radio-frequency lesions of the locus coeruleus (LC), zona compacta of substantia nigra (SN, or control operations. LC-lesioned animals were initially inactive, stayed in the burrows, and fell when climbing ropes and ramps. SN-lesioned rats were opposite to LC animals in many ways. They were hyperactive, had minimal motor disturbances, and were hyperaggressive. SN animals self-isolated and were not social-groomers, whereas LC rats socially-groomed and mounted other animals more than controls. These results provide evidence that the dopaminergic nigrostriatal pathway and the noradrenergic fibers innervating the cerebral cortex and limbic forebrain exert opposed effects upon behavior.     

正常和老年性白内障晶体VE Vc含量的测定

测定正常和老年性白内障晶体ＶＥ、Ｖｃ含量，发现老年性白内障晶体ＶＥ、ＶＣ含量比正常晶体明显减少，并讨论了这些改变的意义。