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1.
目的观察寿聪胶囊对老年性痴呆大鼠脑组织及血清中总抗氧化力(TAOC)、脂褐质(LIP)及脑组织形态学的影响,以进一步探讨寿聪胶囊防治老年性痴呆的作用机制。方法选用Wistar雄性大鼠,随机分成空白对照组、模型对照组、脑复康组及寿聪胶囊低、高剂量组,每组9只。大鼠颈部注射D-半乳糖合并腹腔注射东莨菪碱制备老年性痴呆(AD)大鼠复合模型,应用中药复方寿聪胶囊进行防治,采用分光光度法测定脑组织及血清中TAOC、LIP的含量,光镜下观察脑组织形态学的变化。结果与模型组相比,寿聪胶囊能显著提高AD大鼠脑匀浆及血清中TAOC的活性,降低LIP的含量;而且明显减轻AD的病理损害。结论提示增强脑组织及血清中TAOC活性、降低LIP含量可能是寿聪胶囊防治AD的作用机制之一。  相似文献   
2.
Using two luminescence-inducing cocktails, two distinct patterns of inhibition of light by different anti-oxidants have been identified, comprising Group A, in which a complete inhibition of light emission which is then followed by re-emergence of light, forming apparent S-shaped curves or similar shapes. This light pattern is induced by the “classical” anti-oxidants, ascorbate, vitamin E, uric acid, thiols, deferoxamine, as well as by anti-oxidant agents present in plasma, saliva, urine and in extracts derived from black coffee, and Group B, in which a gradually emerging “mound”-shaped pattern of light was seen with extracts from the Tibetan plant mixture PADMA-28, elderberry (Sambucol), grape seeds, green and black teas, apple, parsimony, red wines, edible oils and SOD. While the results with the Group A agents point to the presence of probably a single, major, anti-oxidants relatively sensitive to oxidation, Group B agents probably include a mixture of anti-oxidants which are more resistant to oxidation. It was also shown that agents from Group B could protect agents from Group A against consumption by the oxidants generated by the cocktails. It is proposed that these simple to use cocktails which probably generate a multiplicity of oxidants mimicking those generated by activated phagocytes, can rapidly assess the total anti-oxidant capacities (TAOC) in body fluids derived from patients suffering of excessive oxidative stress. Also, this technique may be useful in determining the content of dietary anti-oxidants recommended as supplements to enhance the resistance against excessive oxidation of lipids.  相似文献   
3.
[目的]探讨天麻和阿胶联合应用对染铅大鼠海马总抗氧化能力和学习记忆的影响.[方法]大鼠经口染铅并分别单独及联合给予天麻4.0g/(kg@d)和阿胶1.0g/(kg@d)灌胃,连续3个月;每月用Y型迷宫测试学习记忆1次,最后处死大鼠,测定海马组织总抗氧化能力.[结果]高铅对照组和低铅对照组在Y型迷宫中学习达9/10所受电击次数(错误次数)多于空白组(P<0.01);单用天麻或单用阿胶即可明显减少染铅大鼠在迷宫中学习所受电击次数(P<0.01);天麻和阿胶联合应用时这种作用更强(P<0.01).海马总抗氧化能力,高铅对照组和低铅对照组低于空白组(P<0.01);单用天麻或单用阿胶即可明显提高总抗氧化能力(P<0.01),二者联合应用时这种作用更强(P<0.01).[结论]天麻和阿胶单用即可对铅引起的学习记忆的损害产生明显的拮抗作用,二者联用拮抗作用更为显著.  相似文献   
4.
目的 观察安宫牛黄丸联合丙种球蛋白治疗重症病毒性脑炎患儿的临床效果。方法 选择2017年2月—2020年2月青海省妇女儿童医院收治的94例重症病毒性脑炎患儿,随机分为对照组和治疗组,每组各47例。对照组静脉滴注静注人免疫球蛋白0.4 g/(kg·d),1次/d,连用5 d。在对照组的基础上,治疗组鼻饲或口服安宫牛黄丸,3岁患儿每次1/4丸,4~6岁患儿1/2丸/次,>6岁患儿1丸/次,将安宫牛黄丸加于生理盐水(15 mL)中制成匀浆,1次/d,连用5 d。观察两组患儿临床疗效,比较治疗前后两组患儿症状体征消失时间,细胞免疫指标CD3+、CD4+、CD4+/CD8+水平,氧化应激因子丙二醛(MDA)、总抗氧化能力(TAOC)和超氧化物歧化酶(SOD)水平。结果 治疗后,治疗组总有效率为95.74%,较对照组的80.85%显著升高(P<0.05)。治疗后,治疗组患儿症状消失时间明显短于对照组(P<0.05)。治疗后,两组CD3+、CD4+、C...  相似文献   
5.
目的探讨增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)患者玻璃体液中色素上皮衍生因子(pigment epithelium-derived factor,PEDF)与总抗氧化能力(total anti-oxidant capacity,TAOC)的关系。方法选择行玻璃体切割术的增殖性糖尿病视网膜病变患者20例(20眼),其中PDR合并玻璃体出血组12眼,PDR无玻璃体出血组8眼。非糖尿病患者18例(18眼)作为对照组。采用ELISA方法测定玻璃体液中PEDF和TAOC的水平,并行统计学分析。结果与对照组比较,PDR患者玻璃体液中的TAOC明显降低(P<0.01)。玻璃体液中PEDF水平与TAOC呈正相关(r=0.35,P<0.05),和对照组呈正相关(r=0.39,P<0.05)。无玻璃体出血组PDR患者玻璃体液中PEDF水平与对照组和合并玻璃体出血组比较明显降低(P<0.05)。结论玻璃体液中PEDF水平与TAOC密切相关。PEDF可作为眼内源性抗氧化物并对PDR起到保护作用。  相似文献   
6.
阿胶对染铅大鼠海马损害的拮抗作用   总被引:2,自引:0,他引:2       下载免费PDF全文
目的:观察和探讨阿胶对铅所致大鼠学习记忆损害的拮抗作用。方法:选用36只Wistar雄性大鼠随机分为对照组、铅组、阿胶铅组,每组12只。大鼠经口染铅并给予阿胶灌胃。每月用Y型迷宫试验测试学习记忆1次。3个月后处死大鼠,分别测定海马组织一氧化氮(NO)和总抗氧化能力(TAOC)并做病理检查。结果:(1)在Y型迷宫试验中,铅组大鼠学习记忆达标前所受电击次数(错误次数)显著高于对照组(P<0.01);阿胶铅组大鼠所受电击次数显著低于铅组(P<0.05;2、3月P<0.01)。(2)铅组大鼠海马NO和TAOC显著低于对照组(P<0.01),阿胶铅组大鼠海马NO和TAOC显著高于铅组(P<0.05或P<0.01)。(3)病理检查,铅组大鼠海马显著萎缩,细胞形态不规则、排列紊乱,细胞变性、脱失显著,轴突溶解、消失、阿胶铅组海马病理变化不明显。结论:铅可损害海马细胞结构和功能,降低海马组织NO和TAOC水平,降低学习记忆能力;阿胶对铅所海马损害和学习记忆障碍具有拮抗作用。  相似文献   
7.

Purpose

Major depressive disorder (MDD) is a devastating disease that afflicts large populations and has also been accepted to be an independent risk factor for cardiovascular disease (CVD). Oxidative stress seems to play an essential role in the relationship of MDD and CVD. We aimed to determine the level of oxidative stress in patients with MDD and to investigate the effects of long-term antidepressant (AD) treatment on the oxidative-antioxidative system parameters and CVD risk factors.

Method

Fifty patients who fully met the fourth Diagnostic and Statistical Manual of Mental Disorders criteria for MDD and 44 healthy control subjects were included in the study. Control visits of the patients were repeated 6 weeks, 12 weeks and 24 weeks after beginning of the AD treatment. Lipid profiles, oxidation and oxidizability of apolipoprotein B-containing lipoproteins (expressed as apo B-b-MDA and apo B-Δ-MDA, respectively), levels of plasma malondialdehyde (p-MDA), total antioxidative capacity (TAOC), antioxidant molecules and antioxidant enzyme activities including paraoxonase/arylesterase, red blood cell superoxide dismutase (RBC-SOD) and glutathione peroxidase were determined during 24-week of follow-up period.

Results

According to the results of the study, p-MDA, apo B-b-MDA and RBC-SOD activity were increased and arylesterase activity was decreased in MDD patients. Body mass index (BMI), vitamin A and total cholesterol levels in MDD patients increased after 24-weeks of AD treatment. RBC-SOD activity, TAOC, p-MDA and apo B-b-MDA levels were decreased; paraoxonase/arylesterase activities and apo B-Δ-MDA were increased at the end of 24th week.

Conclusion

Oxidative stress, demonstrated in MDD patients, was partly improved during 24 weeks of AD treatment. Increase in paraoxonase/arylesterase activities and decrease in p-MDA and apo B-b-MDA levels after 24 weeks seem to be beneficial for reduction of CVD risk in MDD patients. However increased BMI and apo B-Δ-MDA levels are negative cardiovascular effects of long-term AD treatment.  相似文献   
8.
It has been proved that oxidative stress increases when leukemia is accompanied by depression. This fact may indicate the role of oxidative stress in the development of depression in cancer patients. The aim of this study was to determine whether the acute myeloid leukemia of Brown Norway rats, which is accompanied by oxidative stress, evoked behavioral and receptor changes resembling alterations characteristic of rat models of depression. The rats were divided into two groups: leukemic rats and healthy control. Leukemia was induced through intraperitoneal injection of 107 promyelocytic leukemia cells to the Brown Norway rats. Depression-like behavior was evaluated in the forced swim test at 30 or 34 days after leukemic cells injection. The rats were killed after the evaluation and the spleen, brain cortex and hippocampus were excised. The red–ox state was assessed in homogenates of tissues by measuring total glutathione (GSH) content, the ferric ion reducing ability of plasma (FRAP) level, expression of heme oxygenase-1 (HO-1), biliverdin reductase (BvR) and ferritin mRNA, superoxide dismutase (SOD) activity, as well as malondialdehyde (MDA) concentration. Radioligand binding assay was used to assess of the effect of leukemia on cortical receptors. Leukemic cells were identified using RM-124 antibody by FACS Calibur flow cytometry. Leukemia influenced locomotory activity as well as forced swim test behavior in a 34-day series of experiments. Signs of oxidative stress in leukemic rats were observed in each examined stage of leukemia development. The FRAP values and glutathione contents, were significantly lowered whereas HO-1 mRNA expression, and malonodialdehyde concentrations were significantly increased in the spleen and brain structures of leukemic rats in comparison with the healthy controls. A significant increase in the potency of glycine to displace [3H]L-689,560 from the strychnine-insensitive glycine site of the N-methyl-D-aspartic (NMDA) receptors receptor complex in cortical homogenates of the leukemic rats in 30- and 34-day experimental series was observed in comparison with the control. Upregulation of 5-HT2A receptors was observed in rat cortex after 30 days of leukemia development but not in 34-days series compared with the control. It is concluded that disturbances in antioxidant system in brain cortex were accompanied by an activation of glycine sites of the NMDA receptor complex, regardless of stage of leukemia development, which are characteristic of model of depression. Findings of our study demonstrate the link between glutamatergic activity, oxidative stress and leukemia.  相似文献   
9.
Oxidative stress may be a contributing factor in the etiopathophysiology of schizophrenia, which may be exacerbated by the treatment with antipsychotics with pro-oxidant properties. Increased levels of S100 B are associated with neurodegenerative disorders, including schizophrenia. The aim of the present study was to investigate the role of oxidative cell damage in the pathogenesis of schizophrenia. Forty patients who fully met the fourth Diagnostic and Statistical Manual of Mental Disorders criteria for schizophrenia and 35 healthy control subjects were included in the study. Serum S100 B level was determined to investigate brain damage. Plasma malondialdehyde (MDA) levels and susceptibility of red blood cell (RBC) to oxidation were determined to investigate the oxidative status and plasma vitamin E, vitamin C, serum total carotenoid levels and total antioxidant capacity and RBC superoxide dismutase (SOD) and whole blood glutathione peroxidase activities were measured to investigate the antioxidative defence before and after 6 weeks of antipsychotic treatment. Plasma MDA and serum S100 B levels and RBC-SOD activity were significantly higher in the schizophrenia group than those of the control group. Treatment did not modify any of the oxidative-antioxidative system parameters or serum S100 B levels. S100 B level was significantly higher in patients with negative symptoms than the patients with positive symptoms and the control subjects. S100 B levels were significantly reduced after 6 weeks of treatment in patients with negative symptoms. The results of the present study might support the oxidative cell injury hypothesis of the schizophrenia. Furthermore, the underlying mechanisms of the subgroups of schizophrenia might be different as suggested by the increased S100 B levels and its decrement after treatment in patients with negative symptoms.  相似文献   
10.
目的 探讨桑枝总生物碱片联合达格列净片治疗2型糖尿病的临床疗效。方法 选取2020年4月1日—2021年12月31日三门峡市中医院收治的84例2型糖尿病患者,将所有患者按照随机数字表法分为对照组和治疗组,每组各42例。对照组每日早晨口服达格列净片,10 mg/次,1次/d。治疗组在对照组基础上口服桑枝总生物碱片,起始剂量1片/次,持续治疗4周后,剂量调整为2片/次,3次/d。两组患者连续治疗24周。考察两组临床疗效,比较两组的生活质量、血糖指标、氧化应激指标。结果 治疗后,治疗组患者的总有效率为95.24%,对照组的总有效率为80.95%,组间比较差异有统计学意义(P<0.05)。治疗后,两组的糖尿病生存质量特异性量表(DSQL)评分明显低于治疗前(P<0.05),且治疗组的DSQL评分明显低于对照组(P<0.05)。治疗后,两组的空腹血糖(FPG)、餐后2 h血糖(2 h PG)、糖化血红蛋白(HbA1c)均显著降低(P<0.05),且治疗组FPG、2 h PG、HbA1c明显低于对照组(P<0.05)。治疗后,两组的血清谷胱甘肽过氧化酶(GSH-Px)、总抗氧化能力(TAOC)水平高于治疗前,蛋白氧化终产物(AOPPs)水平低于治疗前(P<0.05);治疗组的血清GSH-Px、TAOC水平高于对照组,血清AOPPs水平低于对照组,组间差异具有统计学意义(P<0.05)。结论 桑枝总生物碱片联合达格列净片治疗2型糖尿病具有较好的临床疗效,能改善患者生活质量,显著降低血糖水平,降低氧化应激反应。  相似文献   
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