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31.
MP Costi D Tondi M Rinaldi D Barlocco G Cignarella DV Santi C Musiu I Pudu G Vacca P La Colla 《European journal of medicinal chemistry》1996,31(12):1011-1016
A new series of N-(substituted)benzyl-1,8-naphthalimides 4, structurally related to the previously reported thymidylate synthase (TS) inhibitor naphthaleins 3, were synthesized and compounds tested for their inhibition of several species of TS. Moreover, their in vitro cytotoxicity together with antimycotic and antibacterial properties were assayed. While no activity was detected in the antibacterial tests, the m-nitro (4ae) and the p-nitro (4af) derivatives were found able to partially inhibit TS at low micromolar concentrations. Introduction of nitro or (substituted)-amino groups in position 4 of the naphthalic ring always led to less active compounds. 相似文献
32.
2型糖尿病患者外周血白细胞iNOSmRNA表达的变化及意义 总被引:1,自引:0,他引:1
目的研究2型糖尿病DM患者外周血白细胞中iNOSmRNA表达的变化及其与糖尿病肾病DN发生、发展的关系。方法101例2型DM患者,根据尿微量白蛋白排泄率和血肌酐水平分为单纯DM组和不同的DN组,用原位杂交法检测外周血白细胞iNOSmRNA表达的阳性细胞的百分率,并与21例健康体检者进行比较。结果早期DN组白细胞iNOSmRNA表达的百分率明显高于对照组、DM组及晚期DN组(P<0.001)。结论外周血白细胞iNOSmRNA表达的变化参与了DN的发生、发展。 相似文献
33.
乙醇毒染大鼠睾丸总抗氧化能力、一氧化氮和一氧化氮合酶的变化与生殖细胞凋亡的关系 总被引:3,自引:2,他引:1
目的:探讨饮酒大鼠睾丸总抗氧化能力(T-AOC)、一氧化氮(NO)含量和一氧化氮合酶(NOS)活性的变化与生殖细胞凋亡的关系。方法:20只成年健康SD雄性大鼠随机均分为对照组和实验组,实验组和对照组分别用50%的乙醇溶液和蒸馏水按10 m l/kg每晚灌胃1次连续26 d(两个生精周期)后,用硝酸还原酶法测定睾丸组织中NO含量;用化学比色法测定其T-AOC和NOS活性;原位缺口末端标记(TUNEL)法检测生殖细胞凋亡指数(AI)的变化。结果:与对照组相比,实验组生殖细胞AI增加(P<0.01);睾丸组织T-AOC极显著下降(P<0.01),而NO含量明显上升(P<0.01)、NOS活性显著增强(P<0.01)。结论:大量饮酒能诱导生殖细胞凋亡增加,NOS活性增强导致NO的过量产生及T-AOC的显著下降是其重要原因。 相似文献
34.
尼莫地平对阿尔茨海默病大鼠脑组织NO、NOS含量及行为学的影响 总被引:1,自引:0,他引:1
目的:探讨尼莫地平对阿尔茨海默病(AD)大鼠脑组织一氧化氮(NO)、一氧化氮合酶(NOS)浓度及行为学改变的影响。方法:SD大鼠30只,随机分为空白对照组,AD模型组和尼莫地平组,采用大鼠脑组织立体定位微量注射技术,尼莫地平组和AD模型组用鹅膏蕈氨酸(IBO)1μl(5μg)损毁大鼠双侧迈内特基底核(nbM)建立AD动物模型,空白对照组以0.1mol/L pH7.4PB液代替IBO。尼莫地平组给予尼莫地平0.5mg/kg,空白对照组和AD模型组以生理盐水代替尼莫地平,连续灌胃60d,每d2次,每次2ml。做迷宫试验及跳台试验测学习记忆能力,然后将大鼠断头处死,分离海马及大脑皮质,分别检测NO,NOS含量。结果:AD模型组较空白对照组学习记忆能力显著降低,海马及大脑皮质NO,NOS含量显著升高,尼莫地平较AD模型组学习记忆能力显著升高,海马及大脑皮质NO、NOS含量显著降低。结论:用IBO损毁大鼠双侧nbM可建立AD动物模型,尼莫地平可显著改变AD模型大鼠的学习记忆能力,降低海马及大脑皮质NO、NOS含量。 相似文献
35.
一氧化氮及一氧化氮合酶在遗传性癫痫易感大鼠惊厥发作中的作用 总被引:3,自引:0,他引:3
目的:探讨一氧化氮、一氧化氮合酶在遗传癫痫易感大鼠惊厥发作中的变化及作用。方法:选择惊厥评分在30-40的P77PMC大鼠35只,均分A-G7组,A组为对照组、G组预先30min腹腔注射一氧化氮合酶抑制剂L-NAME,分别于铃声刺激致惊后0.5、1、2、4,12h断头处死,取出脑组织分离双侧大脑皮层、海马等组织匀浆,测定一氧化氮及一氧化氮合酶,分别统计并进行t检验。结果:惊厥后0.5-1h皮层、海马一氧化氮、一氧化氮合酶逐渐升高,2h达峰值,4-12h恢复正常,应用L-NAME后,一氧化氮、一氧化氮合酶升高被抑制,但大鼠惊厥评分增高并致1例惊厥后死亡和明显延长惊厥持续时间。结论:惊厥后大鼠体内一氧化氮、一氧化氮合酶合成增加,给予合成酶抑制后能明显下降,但能加重惊厥程度和延长持续时间,提示一氧化氮于惊厥后升高,可能作为内源性抑制性性质,在惊厥发作自行终止机制中具有重要作用。 相似文献
36.
Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m–2min–1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p<0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p<0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes. 相似文献
37.
Dystonia is a common movement disorder which is thought to represent a disease of the basal ganglia. However, the pathogenesis of the idiopathic dystonias, i.e. the neuroanatomic and neurochemical basis, is still a mystery. Research in dystonia is complicated by the existence of various phenotypic and genotypic subtypes of idiopathic dystonia, probably related to heterogeneous dysfunctions.In neurological diseases in which no obvious neuronal degeneration can be found, such as in idiopathic dystonia, the identification of a primary defect is difficult, because of the large number of chemically distinct, but functionally interrelated, neurotransmitter systems in the brain.The variable response to pharmacological agents in patients with idiopathic dystonia supports the notion that the underlying biochemical dysfunctions vary in the subtypes of idiopathic dystonia. Hence, in basic research it is important to clearly define the involved type of dystonia.Animal models of dystonias were described as limited. However, over the last years, there has been considerable progress in the evaluation of animal models for different types of dystonia.Apart from animal models of symptomatic dystonia, genetic animal models with inherited dystonia which occurs in the absence of pathomorphological alterations in brain and spinal cord are described.This review will focus mainly on genetic animal models of different idiopathic dystonias and pathophysiological findings. In particular, in the case of the mutant dystonic (dt) rat, a model of generalized dystonia, and in the case of the genetically dystonic hamster (dtsz), a model of paroxysmal dystonic choreoathetosis has been used, as these show great promise in contributing to the identification of underlying mechanisms in idiopathic dystonias, although even a proper animal model will probably never be equivalent to a human disease.Several pathophysiological findings from animal models are in line with clinical observations in dystonic patients, indicating abnormalities not only in the basal ganglia and thalamic nuclei, but also in the cerebellum and brainstem. Through clinical studies and neurochemical data several similarities were found in the genetic animal models, although the current data indicates different defects in dystonic animals which is consistent with the notion that dystonia is a heterogenous disorder.Different supraspinal dysfunctions appear to lead to manifestation of dystonic movements and postures. In addition to increasing our understanding of the pathophysiology of idiopathic dystonia, animal models may help to improve therapeutic strategies for this movement disorder. 相似文献
38.
39.
杜仲对糖尿病大鼠扑捉行为和阴茎组织神经传导通路的影响 总被引:6,自引:1,他引:5
目的:探讨杜仲改善勃起功能的药效和病理学机制。方法:雄性糖尿病(DM)大鼠30只随机分为3组:A组(10只,DM大鼠赋形剂灌胃组)、B组(10只,DM大鼠西地那非灌胃组)、C组(10只,DM大鼠杜仲灌胃组)及10只正常对照组大鼠(赋形剂灌胃,D组);灌胃4周后观察4组大鼠扑捉行为,透射电镜检查阴茎组织有髓神经纤维超微特征;用免疫组化二步法显示阴茎组织中神经元型一氧化氮合酶(nNOS)的表达。结果:与A组比较,C组大鼠扑捉次数显著增多(P<0.05),阴茎组织中nNOS表达显著增强(P<0.001)。透射电镜显示:A组大鼠阴茎组织有髓神经纤维排布失序,部分变性、板层分离形成透明空泡或网络状,C组大鼠有髓神经纤维排列规整,板层结构清晰。结论:杜仲可通过减轻有髓神经的损伤、增强阴茎组织中nNOS表达改善ED。 相似文献
40.
Tetrahydrobiopterin Attenuates Microvascular Reperfusion Injury Following Murine Pancreas Transplantation 总被引:1,自引:0,他引:1
M. Maglione M. Hermann P. Hengster S. Schneeberger W. Mark P. Obrist G. Werner-Felmayer E. R. Werner R. Margreiter G. Brandacher 《American journal of transplantation》2006,6(7):1551-1559
In this study we investigated the effect of tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide synthases, on ischemia-reperfusion injury (IRI) following murine pancreas transplantation. Pancreatic grafts were exposed to prolonged cold ischemia times (CIT) and different treatment regimens: normal saline (S), S + 16 h CIT, BH4 50 mg/kg + 16 h CIT. Nontransplanted animals served as controls. Graft microcirculation was analyzed by means of functional capillary density (FCD) and capillary diameters (CD) after 2 h reperfusion using intravital microscopy. Quantification of inflammatory responses (mononuclear infiltration) and endothelial disintegration (edema formation) was done by histology (hematoxylin and eosin), and peroxynitrite formation assessed by nitrotyrosine immunostaining. FCD was significantly reduced after prolonged CIT, paralleled by increased peroxynitrite formation as compared with controls (all p < 0.05). Microcirculatory changes correlated significantly with intragraft peroxynitrite generation (Spearman: r = -0.56; p < 0.01). Pancreatic grafts treated with BH4 displayed markedly higher FCD values (p < 0.01) and abrogated nitrotyrosine staining (p = 0.03). CD were not significantly different in any group. Histology showed increased inflammation, interstitial edema, hemorrhage, acinar vacuolization and focal areas of necrosis after 16 h CIT, which was diminished by BH4 administration (p < 0.01). BH4 treatment significantly reduces post-ischemic deterioration of microcirculation as well as histologic damage and might be a promising novel strategy in attenuating IRI following pancreas transplantation. 相似文献