Beneficial effects of spin-labelled nitrosourea on CCNU-induced oxidative stress in rat blood compared with vitamin E

This study was carried out to determine the effects of a recently synthesized 1-ethyl-3-[4-(2,2,6,6-tetra-methylpiperidine-1-oxyl)]-1-nitrosourea (SLENU), compared with vitamin E as a positive control, on 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU)-induced oxidative stress in rats. We determined plasma malonyl dialdehyde (MDA) levels and the activities of erythrocyte superoxide dismutase (SOD) and catalase (CAT). Forty two white albino healthy rats were treated once daily for 30 days with oral preparations of CCNU (12.5 mg/kg and 25 mg/kg), SLENU (25-200 mg/kg), and combinations of these. The CCNU-induced increase in plasma MDA level and the usual decrease in erythrocyte SOD and CAT activities were reversed by SLENU, but not by vitamin E. We have previously demonstrated that SLENU is a superoxide scavenger. A combination of our present findings with previous results thus leads us to proposing a new chemotherapeutic combination of CCNU and SLENU that is devoid of high toxicity.     

Hippophae rhamnoides attenuates nicotine-induced oxidative stress in rat liver

The effects of vitamin E and Hippophae rhamnoides L. (Elaeagnaceae) extract (HRe-1) on nicotine-induced oxidative stress in rat liver were investigated. Four groups, eight rats each, were used in this study, and the supplementation period was 3 weeks. The groups were: nicotine (0.5?mg/kg/day, intraperitoneal (i.p.)); nicotine plus vitamin E (75?mg/kg/day, intragastric (i.g.)); nicotine plus HRe-1 (250?mg/kg/day, i.g.); and the control group. The malondialdehyde and nitric oxide levels, glutathione peroxidase, glutathione S-transferase, glutathione reductase, superoxide dismutase, and total and non-enzymatic superoxide scavenger activities were measured spectrophotometrically in supernatants of the tissue homogenates. Nicotine increased the malondialdehyde level in liver tissue compared with control. This nicotine-induced increase in lipid peroxidation was prevented by both vitamin E and HRe-1. Superoxide dismutase activity was higher in the nicotine plus vitamin E-supplemented group compared with nicotine and control groups. Glutathione reductase activity was higher in the nicotine group compared with the control group. However, glutathione peroxidase activity in the control group was higher than the levels in the nicotine, and the nicotine plus HRe-1 supplemented groups. The nitric oxide level was higher in the nicotine group compared with all other groups. Total and non-enzymatic superoxide scavenger activities and glutathione S-transferase activity were not affected by any of the treatments. Our results suggest that Hippophae rhamnoides extract as well as vitamin E can protect the liver against nicotine-induced oxidative stress.     

Vitamin E but not Hippophea rhamnoides L. prevented nicotine-induced oxidative stress in rat brain

Oxidant effects of nicotine in the central nervous system is not clear. The aim of this study was to investigate whether nicotine induces oxidative stress in rat brain, and if it does, to test the effects of Hippophea rhamnoides L. extract (HRe-1) and also vitamin E as a positive control. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine+vitamin E [75 mg/kg/day, intragastric (i.g.)]; nicotine+HRe-1 (250 mg/kg/day, i.g.); and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. Malondialdehyde (MDA) level was increased by nicotine in brain tissue, which was prevented by vitamin E whereas not affected by HRe-1. Brain tissue glutathione S-transferase activities of nicotine administered and HRe-1 supplemented groups were lower than control and vitamin E supplemented groups, while glutathione peroxidase (GSH-Px) activities of vitamin E and HRe-1 supplemented groups were lower than the nicotine administered group. Superoxide dismutase activity was not affected by any of the treatments. Total glutathione level was higher in the vitamin E supplemented group compared with control and nicotine administered groups. Vitamin E might have easily diffused to rat brain as a lipid soluble antioxidant, however, the plant extract, HRe-1, would not have sufficiently diffused to the brain to exert its antioxidant effect.     

Protective effects of Hippophae rhamnoides L. juice on lead-induced neurotoxicity in mice

We examined the effect of Hippophae rhamnoides L. (HRL) juice on lead-induced memory impairment and neuronal damage in the brains of adult mice. Kunming mice were exposed to lead acetate 10 mg/kg body weight for 20 d. Twenty percent and 40% HRL prevented the lead-induced decrease in step-through latency. In the water maze test, the swimming time was lengthened in mice treated with lead acetate, but this time was decreased in mice that received 20% and 40% HRL. The malondialdehyde (MDA) levels were increased in lead-treated mice, which were reduced by 20% and 40% HRL in dose-dependent manner. The activities of acetylcholinesterase (AchE) and monoamine oxidase-A and -B were significantly increased in the lead-treated group, which were decreased by 40% HRL but not by 20% HRL. The levels of norepinephrine, serotonin, and 5-hydroxyindole acetic acid were decreased significantly in the lead-treated mice, and the decreases were antagonized by 40% HRL, except for than in dopamine, but 20% HRL had no effect on this change. These data suggest that the different doses of the HRL juice protect against the lead acetate-induced deficits in learning and memory and changes in neurobiochemical parameters.     

Protection of mitochondrial system by Hippophae rhamnoides L. against radiation-induced oxidative damage in mice

The whole extract of the fresh berries of Hippophae rhamnoides L. (RH-3), which has been reported to provide protection to whole mice, various tissues, cells and cell organelles against lethal irradiation, was further investigated for its effects on mitochondria isolated from mouse liver. Superoxide anion, reduced (GSH) and oxidized glutathione (GSSG) levels, NADH-ubiquinone oxidoreductase (complex I), NADH-cytochrome c oxidoreductase (complex I/II), succinate-cytochrome c oxidoreductase (complex II/III), mitochondrial membrane potential (MMP), lipid peroxidation (LPx) and protein oxidation (PO) were determined for RH-3-mediated radioprotective manifestation. Pre-irradiation treatment of mice with RH-3 (30 mg kg(-1,) i. p.; single dose; -30 min) significantly inhibited the radiation-induced increase in superoxide anions, GSSG, thiobarbituric acid reactive substances (TBARS), complex I, complex I/III activity and MMP maximally at 4 h (P < 0.05). This treatment inhibited the oxidation of proteins (P < 0.05) at all the time periods studied here. This study suggests that pre-irradiation treatment of mice with RH-3 protects the functional integrity of mitochondria from radiation-induced oxidative stress.     

Modulation of N-nitrosodiethylamine (NDEA) induced oxidative stress by vitamin E in rat erythrocytes

Nitrosamines, such as N-nitrosodiethylamine (NDEA), induced oxidative stress due to the generation of reactive oxygen species, which are capable of initiating peroxidative damage to the cell. The present study was designed to establish whether pre-treatment with vitamin E (40 mg/kg body wt, intraperitoneally (ip), twice a week for 4 weeks) to NDEA induced rats provides protection against oxidative stress caused by NDEA. A single necrogenic dose of NDEA (200 mg/kg body wt) was administered intraperitoneally (ip) to the rats with or without vitamin E pre-treatment and the animals were sacrificed on Day 7, 14 or 21 after NDEA administration. Lipid peroxidation (LPO) and the activities of antioxidant enzymes were determined in erythrocytes as indices of oxidative damage. The result showed elevated levels of LPO in erythrocytes with NDEA treatment, however, vitamin E pre-treated rats administered NDEA showed decreased LPO (Day 14 and 21). Superoxide dismutase (SOD) enzyme activity and the glutathione (GSH) content increased with NDEA treatment and remained high in vitamin E pre-treated group. Catalase (CAT), glutathione reductase (GSH-R) and glutathione-S-transferase (GST) enzyme activities declined with NDEA treatment; however, vitamin E pre-treated rats administered NDEA, showed elevation in the enzyme activities. Glutathione peroxidase (GSH-Px) activity increased in erythrocytes in vitamin E pre-treated rats administered NDEA, while Se-GSH-Px activity was not affected significantly. This study demonstrates that the pre-treatment with vitamin E prior to the administration of NDEA was effective in counteracting and modulating oxidative stress in rat erythrocytes in a time-dependent manner.     

醋柳黄酮对家兔血液流变性、血小板及凝血功能的影响

目的:研究醋柳黄酮(TFH)对家兔血液流变性、血小板及凝血功能的影响.方法:测定醋柳黄酮灌胃给药对家兔血黏度、血小板聚集、血栓形成和凝血功能的影响.结果:醋柳黄酮灌胃1.5～10 mg·kg-1可显著降低家兔全血黏度、血浆黏度;抑制ADP诱导的家兔血小板聚集;抑制血栓形成;明显延长活化部分凝血酶原时间(APTT).结论:醋柳黄酮具有改善家兔血液流变性、抑制血栓形成作用.     

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。     

沙棘总黄酮对改善神经细胞损伤的作用

目的探讨沙棘总黄酮(TFH)对神经细胞的保护作用及其机制。方法采用培养PC12细胞NaCN及缺糖引起的细胞损伤模型,以及Na2S2O4、KCl分别诱导PC12细胞缺氧损伤和Ca2+超载损伤模型,研究TFH对神经细胞损伤的保护作用。结果TFH对PC12细胞损伤有明显的保护作用。结论TFH具有保护神经细胞的作用。     

沙棘总黄酮对豚鼠心室乳头状肌和培养大鼠心肌细胞的电生理作用(英文)

用传统微电技术研究了沙棘总黄酮(TFH)对心肌细胞的电生理作用,TFH 100—200 mg·L~(-1)使豚鼠心室乳头状肌APD缩短,收缩力下降,培养大鼠心肌细胞APD缩短及4相除极斜率降低。TFH 100 mg·L~(-1)可抑制毒毛花甙G诱发豚鼠乳头状肌心律失常。提示,上述作用主要与TFH抑制心肌细胞Ca~(2 )内流影响心肌细胞内Ca~(2 )储库有关。     

Antigenotoxic effects ofSatureja hortensis L. on rat lymphocytes exposed to oxidative stress

The protective properties of Satureja hortensis L. on the rat lymphocytes DNA lesions were tested. Lymphocytes were isolated from blood samples taken from healthy rats. DNA breaks and resistance to H2O2-induced damage were measured with the comet assay. Rat lymphocytes were incubated in S. hortensis ethanolic extract (SHE) (0.05, 0.1, 0.5, 1.0, and 2.5 mg/ mL), essential oil (SHEO)(0.05, 0.1, 0.5, 1.0, and 2.5 microL/mL), H2O2 (50, 100, and 200 microM), a combination of H2O2 (200 mM) with either SHE (1.0, 2.5 mg/mL) or SHEO (1.0, 2.5 microL/mL) at 4 degrees C for 30 min, and the extent of DNA migration was measured using a single-cell microgel electrophoresis technique under alkaline conditions. Treatment of rat lymphocytes with SHE or SHEO resulted in significant reduction of H2O2-induced DNA damage compared to controls. SHE exhibited a significant (P < 0.01) inhibitory effect on oxidative DNA damage at 2.5 mg/mL. SHEO (1.0 and 2.5 microL/mL) also showed significant inhibitory effects (P < 0.01) on H2O2 induced chromosomal damage. In conclusion both the ethanolic extract and the essential oil of the plant reversed the oxidative damage to rat lymphocytes induced by hydrogen peroxide.     

Protective effects of fruit extracts of Hippophae rhamnoides L. against arsenic toxicity in Swiss albino mice

Seabuckthorn (Hippophae rhamnoides L.) berry has a long history of applications as a food and medicinal ingredient in eastern countries. The present study was carried out to investigate the effect of different fruit extracts of H. rhamnoides on altered biochemical parameters indicative of haematological alterations, tissue oxidative stress, and arsenic concentration in arsenic-exposed mice (2.5 mg/kg body weight, intraperitoneally). Two aqueous extracts (at room temperature and under reflux condition) and an ethanolic extract of H. rhamnoides at a dose of 500 mg/kg body weight were co-administered daily during arsenic exposure in mice for 3 weeks. Exposure to arsenic led to a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity, suggesting disturbed haem synthesis pathway. Arsenic also caused significant depletion of reduced hepatic glutathione (GSH) level, glutathione S-transferase (GST) and glutathione peroxidase and catalase activities, while it increased the level of thiobarbituric acid reactive substance (TBARS), suggesting liver oxidative stress. Most of the altered biochemical variables responded favorably to the co-supplementation of H. rhamnoides, particularly the aqueous fruit extract, extracted at room temperature (HF-WRT). However, arsenic concentration in blood and tissues remained unchanged, suggesting the lack of chelating property of fruit extract of H. rhamnoides. The present study, thus, led us to conclude that the fruit extract of H. rhamnoides has a significant protective role against arsenic-induced oxidative injury. However, it lacks the ability to remove arsenic from the binding sites, suggesting that the herbal extract could be co-administered with a chelating agent of known efficacy during treatment of arsenic to achieve the optimum effect of chelation treatment.     

沙棘属植物的ISSR-PCR反应体系的建立

目的 建立沙棘的简单重复序列区间聚合酶链反应(ISSR-PCR)优化反应体系.方法 对影响ISSR-PCR反应的各因子,如模板DNA用量、TaqDNA聚合酶浓度、镁离子浓度、dNTP浓度等进行单因素梯度实验.结果 筛选出了优化的反应条件.结论 建立的反应体系多态性高,系统稳定,可应用于沙棘属植物遗传多样性研究和亲缘关系分析.     

醋柳黄酮治疗中、重度高血压的随机对照研究

目的　探讨醋柳黄酮治疗中、重度高血压的疗效、特点和不良反应。方法　采用同期随机对照的方法。 78例合格的中、重度高血压病患者 (BP≥ 16 0 / 10 0mmHg)随机分为醋柳黄酮治疗组和依那普利对照组 (各 39例 ) ,治疗 6周 ,观察血压变化及其规律。结果　醋柳黄酮治疗 6周后血压下降 18.1± 8.2 / 12 .4± 10 .1mmHg ,与依那普利的降压水平相似。但醋柳黄酮对中、重度高血压病患者的降压速度稍慢 ,2～ 4周后与依那普利的降压水平基本一致。不良反应总发生率低 ,主要为头昏头晕 ,短期内可自行改善。结论　醋柳黄酮能降低中、重度高血压病的血压水平 ,安全性好。     

Beneficial role of diosgenin on oxidative stress in aorta of streptozotocin induced diabetic rats

The present study was designed to investigate the beneficial role of diosgenin on oxidative stress markers and histopathological changes in aorta of streptozotocin induced diabetic rats. Diabetes was induced in experimental rats by a single intraperitoneal injection of streptozotocin (55mg/kg body weight (b.w.)). From the sixth week, experimental rats received diosgenin at different doses (10, 20 and 40mg/kg b.w.) once daily for 4 weeks. At the end of the experimental periods, diabetic rats exhibited significant increase in the levels of plasma glucose, glycosylated hemoglobin with significant decrease in insulin and total hemoglobin. The activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and the levels of reduced glutathione were decreased while increases in the levels of lipid peroxidation markers were observed in aortic tissues of diabetic rats. Oral administration of diosgenin to diabetic rats significantly decreased the plasma glucose and increased the insulin level based on a dose dependent manner. Diosgenin at a dose of 40mg/kg b.w. was more pronounced effect than the other two doses and used for further studies. All the manifestations observed in diabetic rats were significantly reversed to near normal at a dose of 40mg/kg b.w. of diosgenin. These findings suggest that diosgenin could have a beneficial role against aortic damage induced by oxidative stress in diabetic state, which was evidenced by the propensity of diosgenin to modulate the antioxidant defense and to decrease the lipid peroxidation in aorta.     

Changes in vitamin C and vitamin E during oxidative stress in myocardial reperfusion

Injury to the myocardial tissue due to ischemia and reperfusion occurs because of imbalance between the formation of oxidants and available antioxidants in the heart. Levels of vitamin C (ascorbic acid) and vitamin E (alpha--tocopherol) were evaluated in 52 patients of acute myocardial infarction (AMI) treated by streptokinase. They were further divided into reperfused group (39 patients) and non-reperfused group (13 patients). Twenty normal healthy subjects served as controls. Vitamin C and vitamin E were estimated in study group before and after thrombolytic therapy and in controls. Vitamin C levels were low in AMI cases as compared to controls (8.74 +/- 1.87 and 10.63 +/- 3.26 mg/L, respectively, P < 0.001). Trend of fall in vitamin C levels in the two study groups was not statistically significant. Vitamin E levels declined from 12.19 +/- 6.71 to 9.96 +/- 6.50 mg/L by 4 hours which was significant (P < 0.01) in the reperfused group, but the change in non-reperfused group (9.28 +/- 6.37 to 9.35 +/- 6.07 mg/dL by 4 hours) was non-significant. This is because of increased consumption of this antioxidant in suppressing the oxidative stress which occurs with reperfusion. Vitamin E can be proposed as a valid marker for reperfusion.     

沙棘果实化学成分的分离与鉴定

目的对中药沙棘果实的化学成分进行分离与鉴定。方法用硅胶柱、Sephadex LH-20和HPLC柱色谱方法进行分离纯化,通过理化性质和核磁共振的氢谱和碳谱数据确定化合物的结构。结果得到9个化合物,分别鉴定为4-羟基苯甲酸(1)、苹果酸甲酯(2)、γ-N-(2-呋喃基-甲基-)丁胺酸(3)、5-羟甲基糠醛(4)、齐墩果酸(5)、3,4-二羟基苯甲酸(6)、β-谷甾醇(7)、豆甾醇(8)、胡萝卜苷(9)。结论化合物1-3为首次从沙棘属中分离得到。     

Oxidative stress induced by atrazine in rat erythrocytes: Mitigating effect of vitamin E

The present study investigates the propensity of atrazine to induce oxidative stress and its possible attenuation by vitamin E in rat erythrocytes, which is a convenient model to understand the oxidative damage induced by various xenobiotics. Experimental animals were administered atrazine (300?mg/kg body weight, daily) and/or vitamin E (100?mg/kg body weight, daily) orally for a period of 7, 14, and 21 days. Results indicated that the reduced glutathione (GSH) content of the erythrocytes of atrazine treated rats was significantly decreased as compared to the control group. Co-administration of vitamin E along with atrazine restored the GSH content of erythrocytes nearly to control levels. The activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione-s-transferase were found to be increased significantly in the erythrocytes accompanied by a decrease in the activity of the glucose-6-phosophate dehydrogenase, following atrazine exposure. On the other hand, when vitamin E was co-administered along with atrazine, activities of these enzymes were found to be restored significantly. In conclusion, results of the study demonstrated that atrazine induced oxidative stress in rat erythrocytes, in terms of increased activities of the various antioxidant enzymes, and decreased content of reduced glutathione. However, vitamin E administration ameliorated the effects of atrazine, suggesting that vitamin E is a potential antioxidant against atrazine-induced oxidative stress.     

Cypermethrin-induced oxidative stress in rat brain and liver is prevented by vitamin E or allopurinol

Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of various pesticides, this study was designed to investigate the possibility of oxidative stress induction by cypermethrin, a Type II pyrethroid. Either single (170 mg/kg) or repeated (75 mg/kg per day for 5 days) oral administration of cypermethrin was found to produce significant oxidative stress in cerebral and hepatic tissues of rats, as was evident by the elevation of the level of thiobarbituric acid reactive substances (TBARS) in both tissues, either 4 or 24 h after treatment. Much higher changes were observed in liver, increasing from a level of 60% at 4 h up to nearly 4 times the control at 24 h for single dose. Reduced levels (up to 20%) of total glutathione (total GSH), and elevation of conjugated dienes ( approximately 60% in liver by single dose at 4 h) also indicated the presence of an oxidative insult. Glutathione-S-transferase (GST) activity, however, did not differ from control values for any dose or at any time point in cerebral and hepatic tissues. Pretreatment of rats with allopurinol (100 mg/kg, ip) or Vitamin E (100 mg/kg per day, ig, for 3 days and a dose of 40 mg/kg on the 4th day) provided significant protection against the elevation of TBARS levels in cerebral and hepatic tissues, induced by single high dose of oral cypermethrin administration within 4 h. Thus, the results suggest that cypermethrin exposure of rats results in free radical-mediated tissue damage, as indicated by elevated cerebral and hepatic lipid peroxidation, which was prevented by allopurinol and Vitamin E.