普恩复治疗缺血性脑血管疾病的临床研究

探讨普恩复对缺血性脑血管疾病患者的疗效。对治疗组６８例服用普恩复，对照组４０例服阿斯匹林，１４天为一疗程。结果６８例患者经普 复治疗后有效率为９０．１％。本研究提示普恩复对治疗缺血性脑血管疾病有显著疗效。     

巴曲酶治疗缺血性脑血管疾病

目的：探讨巴曲酶（ｂａｔｒｏｘｏｂｉｎ）可否治疗缺血性脑血管疾病（ＩＣＶＤ）及其安全性。方法：随机选择，并经ＣＴ及（或）ＭＲＩ证实的急性ＩＣＶＤ３８例，男性２３例，女性１５例，年龄６５±ｓ１０ａ。用巴曲酶溶于１００ｍＬ生理盐水中静脉滴注，首次剂量１０ＢＵ，维持剂量５ＢＵ，隔日１次，１个疗程共３次。结果：４ｗｋ显效率５３％，总有效率８４％，作用迅速，用药后７２ｈ内出现疗效８７％，同时使血清凝血因子     

巴曲酶治疗缺血性脑血管疾病

目的：探讨巴曲酶（ｂａｔｒｏｘｏｂｉｎ）可否治疗缺血性脑血管疾病（ＩＣＶＤ）及其安全性。方法：随机选择，并经ＣＴ及（或）ＭＲＩ证实的急性ＩＣＶＤ３８例，男性２３例，女性１５例，年龄６５±ｓ１０ａ，用巴曲酶溶于１００ｍＬ生理盐水中静脉滴注，首次剂量１０ＢＵ，维持剂量５ＢＵ，隔日１次，１个疗程共３次。结果：４ｗｋ显效率５３％，总有效率８４％，作用迅速，用药后７２ｈ内出现疗效者８７％，同时使血清凝血因子１显著降低，交链纤维蛋白降解物显著增高。治疗期间未发现任何不良反应。结论：巴曲酶是一种新型强力单成分溶栓剂，治疗急性ＩＣＶＤ安全可行。     

葛根素治疗缺血性脑血管疾病的疗效观察

应用葛根素注射液治疗缺血性脑血管疾病患者４１例。结果显示：显效６３．４％,有效３４．１％,无效２．５％,总有效率９７．５％。     

藻酸双酯钠治疗缺血性脑血管疾病142例

缺血性脑血管疾病142例(男104例,年龄58±5a;女38例,年龄57±5a)用藻酸双酯钠(PSS)100mg溶于6％羟乙基淀粉500mL,静滴,qd,10d为一个疗程。经1-3个疗程后改为片剂PSS50-100mg,po,tid,维持治疗3mo后判断疗效。其中脑血栓71例中总有效率96％,脑动脉硬化59例及短暂性缺血发作12例全部有效。副作用轻微。     

那屈肝素钙治疗缺血性脑血管疾病

目的：探讨那屈肝素钙在缺血性脑血管疾病中的溶栓、抗凝作用。方法：６０例缺血性脑血管疾病病人，随机分成那屈肝素钙组３０例，予那屈肝素钙０．４ｍＬ腹部皮下注射，ｑ１２ｈ，共用８￣１０ｄ，另给脱水、扩容等常规治疗（甘露醇，羟乙基淀粉、曲克芦丁、胞磷胆碱）；对照组３０例只给常规治疗，观察治疗前、治疗后ｄ１０和１ｍｏ２组病人临床评分，出、凝血时间及副作用。结果：那屈肝素组在治疗１ｍｏ后，临床评分明显好于对照     

抗氧化药物治疗铅中毒的研究进展

铅中毒已成为危害我国公共健康的一个较大因素,传统的螯合剂药物副作用较大,且对损伤修复效果甚微,需要发现更理想的药物。抗氧化剂效果明显,副作用较小,且疗效较为持久,因而越来越多的研究关注此类药物的铅中毒治疗作用。本文综述国内外关于铅中毒的抗氧化药物治疗进展,介绍葛根素、槲皮素、姜黄素、大蒜素和褪黑素5种抗氧化药物治疗铅中毒的的实验研究进展,这5种药物能有效降低血铅含量,提高体内抗氧化酶活性并降低氧化应激水平,修复铅对细胞、器官组织的损伤,具有很高的临床应用价值。     

藻酸双酯钠治疗缺血性脑血管疾病100例

缺血性脑血管疾病100例(男60例,女40例;年龄55±s11a)用藻酸双酯钠(PSS)1-3mg/kg,加入10％葡萄糖液500mL,iv,静滴,30滴/min,qd,15d为一个疗程。1-3个疗程后改PSS片,50mg,tid,po,维持治疗。另设对照组50例用曲克芦丁治疗。结果:PSS治疗组总有效率96％;曲克芦丁组为90％(经ridit分析P<0.01)。25例脑梗死患者经PSS治疗后血液流变学与血脂均有显著改善(P<0.05-0.01)。     

抗氧化应激治疗糖尿病肾病研究进展

糖尿病肾病(Diabetic nephropathy,DN)是慢性肾脏病的一种,是糖尿病最常见的并发症之一,30％～40％糖尿病可出现肾脏损害,其发病机制尚不完全清楚.DN患者体内存在可能与局部趋化因子高表达有关的炎性细胞的浸润,机体氧化应激的增强及抗氧化应激能力的减弱与DN的发生发展有关,因此抗氧化应激目前已成为治疗DN的重要手段之一.     

The discovery and development of new potential antioxidant agents for the treatment of neurodegenerative diseases

Introduction: Several neurodegenerative disorders (NDs) including Alzheimer’s and Huntington’s diseases have had associations with the oxidative process and free radical damage. Consequently, in past decades, several natural and synthetic antioxidants have been assessed as therapeutic agents but have shown limitations in bioavailability, metabolic susceptibility and permeability to the blood brain barrier. Given these issues, medicinal chemists are hard at work to modify/improve the chemical structures of these antioxidants, thereby improving their efficacy.

Areas covered: In this review, the authors critically analyze several biological mechanisms involved in the generation of free radicals. Additionally, they analyze free radicals’ role in the generation of oxidative stress and in the progression of many NDs. Further, the authors review a collection of natural and synthetic antioxidants, their role as free radical scavengers along with their mechanisms of action and their potential for preventing neurodegenerative diseases.

Expert opinion: So far, preclinical studies on several antioxidants have shown promise for treating NDs, despite their limitations. The authors do highlight the lack of the adequate animal models for preclinical assessment and this does hinder further progression into clinical trials. Further studies are necessary to fully investigate the potential of these antioxidants as ND therapeutic options.     

Arsenic: toxicity, oxidative stress and human disease

Arsenic (As) is a toxic metalloid element that is present in air, water and soil. Inorganic arsenic tends to be more toxic than organic arsenic. Examples of methylated organic arsenicals include monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)]. Reactive oxygen species (ROS)‐mediated oxidative damage is a common denominator in arsenic pathogenesis. In addition, arsenic induces morphological changes in the integrity of mitochondria. Cascade mechanisms of free radical formation derived from the superoxide radical, combined with glutathione‐depleting agents, increase the sensitivity of cells to arsenic toxicity. When both humans and animals are exposed to arsenic, they experience an increased formation of ROS/RNS, including peroxyl radicals (ROO^?), the superoxide radical, singlet oxygen, hydroxyl radical (OH^?) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant‐induced DNA damage. Arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4‐hydroxy‐nonenal (HNE)] are the major end products. This review discusses aspects of chronic and acute exposures of arsenic in the etiology of cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders. The role of antioxidant defence systems against arsenic toxicity is also discussed. Consideration is given to the role of vitamin C (ascorbic acid), vitamin E (α‐tocopherol), curcumin, glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase in their protective roles against arsenic‐induced oxidative stress. Copyright © 2011 John Wiley & Sons, Ltd.     

Tunisian radish extract (Raphanus sativus) enhances the antioxidant status and protects against oxidative stress induced by zearalenone in Balb/c mice

Radish (Raphanus sativus) is a food plant known worldwide. From antiquity it has been used in folk medicine as a natural drug against many toxicants. Zearalenone (zen) is a non-steroidal estrogenic mycotoxin present in corn and food mixture for farm animals and it is hepatotoxic, hematotoxic, immunotoxic, nephrotoxic and genotoxic. The objectives of the present study were to assess the biological activity of radish extract and to evaluate the protective role of radish extract against the toxicity of zen in female Balb/c mice. Animals were divided into seven groups and treated orally for 10 days as follows: a control, an olive oil group, groups treated with radish extract alone (5, 10 and 15 mg kg(-1) b.w.), a group treated with zen (40 mg kg(-1) b.w.) and a group treated with zen plus the lowest dose of radish extract. The results indicate that radish extract improved the antioxidant status and had no significant effects on hematological and biochemical parameters tested or histology of the liver and kidney. Treatment with zen results in a significant increase in ALT, AST, ALP, BILT, BILD, CRE accompanied with significant changes in most of hematological parameters and the antioxidant enzyme activities, co-treatment of zen and the radish extract results in a significant reestablishment of hematological, serum biochemical parameters, and the histology of the liver and kidney. These findings suggest that radish extract is safe and can be overcome or, at least, significantly diminish zen effects.     

Influence of vitamin C on markers of oxidative stress in the earliest period of ischemic stroke

Experimental studies have demonstrated that oxidative stress plays an essential role in the pathophysiology of ischemic stroke. The objective of the present study was to assess some serum markers of oxidative stress in patients in the early period of ischemic stroke and determine whether vitamin C supplementation affects the parameters of oxidative stress and the clinical status of patients. The study included 60 patients with ischemic stroke and 20 controls. Patients with ischemic stroke were divided into two groups: group I (n = 30), which did not receive vitamin C therapy, and group II (n = 30), which received vitamin C (500 mg/day, i.v.) for 10 days beginning on day 1 after ischemic stroke. Blood levels of bilirubin, creatinine, uric acid and total antioxidative capacity (TAC) were measured on stroke-days 1, 3, 5, and 10. Moreover, the neurological status of patients was evaluated on the same days using the NIHSS, Rankin and Bartel scales. Neurological status was also assessed with the Rankin scale after 3 months. Uric acid and TAC were decreased in group I on all measurement days. However, we did not observe any differences in the clinical status of patients receiving vitamin C during the first ten days of stroke or after 3 months. Although administration of vitamin C (500 mg/day, iv) to ischemic stroke patients since the first day ischemic stroke resulted in elevated serum levels of antioxidants, it did not substantially improve the clinical and functional status of patients after 3 months.     

神经保护剂治疗缺血性脑卒中的研究进展

脑卒中的治疗包括超早期溶栓和神经保护药物。溶栓治疗有时间限制,而无时间限制的神经保护治疗也陷入了困境。常规途径的神经保护药物治疗脑缺血性损伤的效果不理想。来自卒中动物模型中的阳性结果和来自人类试验的阴性结果所引起的惊人偏差普遍引起对神经保护治疗的怀疑。2008年的卒中圆桌会议对迄今耗资数百亿美元,而基本均宣告无效的神经保护药物治疗进行了全面的反思和分析。尽管目前神经保护治疗的现状惨淡,但仍有少数药物的神经保护疗效得到随机试验证实,新型抗氧化自由基清除剂依达拉奉就是其中的一种,在Ⅲ期临床试验中取得良好的结果,是目前临床试验证明惟一有效的自由基清除剂。脑活素是另外一个引起关注的药物,在不同的脑缺血动物模型中表现出神经保护和神经营养特性,在几个小规模针对缺血性卒中的对照临床试验中显示了临床有效性和安全性,目前正在进行Ⅲ期临床试验。神经保护治疗的时间窗、改变治疗模式可能是今后神经保护的研究方向。     

硫化氢对局灶性脑缺血大鼠脑组织氧化应激的影响

目的：观察硫化氢（H2 S）对局灶性脑缺血大鼠脑组织氧化应激的影响。方法40只健康雄性 SD 大鼠,随机分为假手术（Sham）组、缺血模型（Ischemia）组、H2 S 低剂量（L-NaHS）组、H2 S 中剂量（M-NaHS）组和 H2 S 高剂量（H-NaHS）组。线栓法复制大鼠大脑中动脉闭塞模型。H2 S 低、中、高剂量组大鼠于缺血3 h 时分别腹腔注射0.7 mg/ kg、1.4 mg/ kg 和2.8 mg/ kg 的 NaHS,Sham 组和 Ischemia 组注射等容量的0.9%氯化钠溶液。5组大鼠均于缺血24 h 时断头取脑,测定脑组织中丙二醛（ MDA）的含量、超氧化物歧化酶（ SOD）的活性和谷胱甘肽过氧化物酶（GSH-PX）的活性;透射电镜观察脑组织的病理变化。结果与 Sham 组比较,Ischemia 组大鼠脑组织 SOD、GSH-PX 活性明显降低（ P ﹤0.01）,MDA 含量明显升高（ P ﹤0.01）;电镜观察显示神经元水肿,线粒体膜肿胀、线粒体嵴断裂甚至消失,线粒体大量空泡化,细胞器的数量减少;与 Ischemia 组比较,M-NaHS、H-NaHS 组大鼠脑组织中 SOD、GSH-PX活性明显升高（ P ﹤0.05）,MDA 含量明显降低（ P ﹤0.05）;电镜观察可见神经元轻度水肿,线粒体部分肿胀、内外膜结构清晰、部分嵴断裂消失,细胞器数量增多,脑缺血损伤程度明显减轻。结论 H2 S 可减轻大鼠局灶性脑缺血损伤,其机制与提高大鼠的抗氧化应激能力有关。     

Protective effects of emodin against cisplatin‐induced oxidative stress in cultured human kidney (HEK 293) cells

Emodin (a rhubarb anthraquinone) has strong antioxidant and anticancer actions, and recent studies indicated that it reduces cellular oxidative stress induced by various insults and drugs. Cisplatin is an anticancer drug that is associated with nephrotoxicity and induces oxidative stress in cultured human kidney (HEK 293) cells. This study aimed to assess the in‐vitro antioxidant properties of the emodin against cisplatin‐induced oxidative stress in HEK 293 cells. Our study revealed that emodin acted as a potent free radical scavenger and provided nephroprotection against cisplatin‐induced oxidative stress. Emodin as low as 0.5 µm did not decrease cell viability and restored the cisplatin‐induced glutathione depletion and total antioxidant capacity in a dose‐dependent manner. Emodin augmented the cisplatin‐induced inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S‐transferase, glutathione reductase and superoxide dismutase). These results suggest that emodin has the potential to be used as an adjunct therapeutic agent in patients receiving cisplatin treatment. Copyright © 2012 John Wiley & Sons, Ltd.     

Hydroxyl scavenging activity accounts for differential antioxidant protection of Plantago major against oxidative toxicity in isolated rat liver mitochondria

Objectives The aim of this work was to study the effects of P. major against the oxidative damage of isolated rat liver mitochondria. Methods The extracts were obtained using methanol (MeOH), ethyl acetate (EAc), dichloromethane (DCM), and hexane (Hex) as solvents. Key findings Hex, DCM, and EAc totally, and MeOH partially, inhibited ROS generation and lipid peroxidation of membranes induced by Fe²⁺ or t‐BOOH. However, only MeOH was able to prevent the t‐BOOH‐induced glutathione and NAD(P)H oxidation. All extracts chelated Fe²⁺ and reduced DPP Hradicals. EPR analysis revealed that P. major exhibited potent scavenger activity for hydroxyl radicals. Conclusions The potent antioxidant activity exhibited by P. major was able to prevent oxidative mitochondrial damage, contributing to the understanding of its hepatoprotective action against ROS‐mediated toxicity.