一氧化氮及一氧化氮合酶与乙肝病毒

目的:通过检测含有不同乙肝病毒血清标志物的感染者血中一氧化氮及一氧化氮合酶的含量,进一步证实一氧化氮与乙肝病毒损伤肝细胞的关系。方法:采用化学比色法测定不同组别的乙肝病毒感染者血中一氧化氮和一氧化氮合酶的含量,从而进行统计学处理及分析。结果:乙肝病毒复制活跃及肝功能不良的感染者血中一氧化氮和一氧化氮合酶的含量明显高于仅有乙肝病毒复制活跃但肝功能尚好的感染者,后者血中一氧化氮和一氧化氮合酶的含量又明显高于含有保护性抗体抗—HBs的既往感染者,它们之间均存在显著性差异。结论:一氧化氮与乙肝病毒损伤肝细胞有密切关系。     

运动与一氧化氮

一氧化氮作为一种自由基和信息传递因子，在运动中起了重要的调节作用；运动训练也会引起一氧化氮合酶的适应性变化．     

不同强度健步走锻炼对中老年人血清一氧化氮含量的影响

探讨不同强度的运动对中老年人血清一氧化氮和一氧化氮合酶的影响,进而寻找预防心血管疾病最适宜的运动强度。通过实验分析,认为中老年人在进行健身运动时,比较适宜的运动强度是100-120次/分。此种强度的运动可以增加体内NO含量,进而有效地预防心血管疾病的发生。     

运动对NO及NOS影响的研究综述

通过梳理近年有关一氧化氮双重生物学作用及一氧化氮与运动关系的研究,重点阐述不同运动方式对一氧化氮及其限速酶一氧化氮合酶的影响。     

二甲基精氨酸-二甲胺水解酶在疾病中的表达和功能

非对称性-二甲基精氨酸(ADMA)抑制一氧化氮合酶(NOS),是内皮功能损伤、心血管疾病和慢性肾脏疾病的危险因素.二甲基精氨酸-二甲胺水解酶(DDAH)可以代谢ADMA,主要分为两种.DDAH-1主要分布于肾小管、肝脏,从循环中摄取ADMA;DDAH-2主要存在于血管中,分布于内皮细胞胞膜交界处及胞内颗粒、血管平滑肌细胞肌纤维及核被膜中.DDAH的表达、调节和分布均具有特异性.可以特异地调节NO的产生.本文总结了DDAH在心血管疾病和肾脏疾病导致的内皮功能受损中所起的作用.     

纽虫神经系统结构及一氧化氮合酶的组织化学定位

运用硫辛酸脱氢酶(NADPH—d)组织化学方法研究了两种纽形动物一氧化氮合酶的分布情况，实验结果表明，短无头沟纽虫(Baseodiscus curtus)的阳性反应位于体表上皮细胞和神经系统的脑神经节和侧神经索中，纵沟纽虫(Lineus sp．)的阳性反应只位于体表上皮细胞中．比较了纽形动物与扁形动物和环节动物一氧化氮合酶组织化学定位的异同．     

沙蚕一氧化氮合酶的NADPH-d组织化学研究

用依赖还原型辅酶Ⅱ的黄递酶(NADPH-d)组织化学方法研究了环节动物门多毛纲动物沙蚕(Nerds)脑神经节及部分外周器官中NADPH-d阳性反应的分布．结果表明，沙蚕脑神经节中有少量阳性反应细胞及部分呈较强阳性反应的纤维束，触角中央有一束呈强阳性反应的纤维束通向脑神经节．在口前叶、口腔上皮、咽部上皮、体表皮肤中都呈现一定阳性反应．这表明一氧化氮合酶在沙蚕的神经系统和外周器官中都有分布，可以推测一氧化氮作为一种重要的信息分子参与了沙蚕多种生理调节过程．     

一氧化氮合酶阳性神经元在鱼脑的分布

应用还原型尼克酰胺腺苷二核苷酸—黄递酶组化法，研究了一氧化氮合酶阳性神经元在鱼脑内的分布。结果显示，一氧化氮合酶阳性神经元存在于硬骨鱼纲的鳙鱼脑内不同部位，数量较少，集中分布；胞体呈圆形或三角形，着色较深，发出突起。由此可见，低等脊椎动物鱼类脑中也存在一氧化氮合酶阳性神经元，较哺乳动物而言分布集中且数量少，表明一氧化氮的存在与动物脑的进化有一定的关系。     

一氧化氮合酶在猕猴中枢神经系统中的表达

研究神经元型一氧化氮合酶(NOS1)在灵长类动物中枢神经系统中的表达．方法：采用免疫组织化学技术，观察了一氧化氮合酶在正常猕猴脑和脊髓中的表达．结果表明NOS1阳性神经元分布于中枢神经系统的广泛区域，包括大脑皮质、海马、齿状回、尾壳核、纹状体、小脑皮质、脊髓前角、后角和中央灰质与中枢神经系统的诸多功能有关．     

静脉注射海洛因对一氧化氮及红细胞免疫功能的影响

目的 :探讨静脉注脉射海洛因者血中一氧化氮、一氧化氮合酶与红细胞免疫功能变化的关系。方法 :检测静脉注射海洛因者血中一氧化氮、一氧化氮合酶及红细胞 C3b受体活性等水平。结果 :静脉注射海洛因者血中一氧化氮及一氧化氮合酶的含量显著高于对照组 ,治疗组与非治疗组亦存在显著性差异 ,红细胞C3b受体活性明显下降且与一氧化氮含量呈负相关 ,治疗组一氧化氮及红细胞 C3b受体活性等指标有所恢复。结论 :静脉注射海洛因影响血中一氧化氮及一氧化氮合酶的含量 ,高浓度的一氧化氮 ,可能是红细胞免疫功能低下的重要原因之一 ,戒毒有望恢复其红细胞免疫功能。     

下丘脑室旁核NOS／NO系统对心血管活动的调节（综述）

下丘脑室旁核（PVN）是重要的心血管活动调节中枢。PVN分布有一氧化氮（NOS）神经元,合成并释放一氧化氮（NO）。NO通过抑制各级交感神经中枢,以及影响神经内分泌活动,对心血管活动进行调节。     

氯胺酮的镇痛作用及其对大鼠大脑皮层NO/NOS的影响

为了观察大鼠切口疼痛模型中皮下注射氯胺酮对大鼠的镇痛作用,及其对大脑皮层一氧化氮(NO)和一氧化氮合酶(NOS)的影响。采用体重(250±20)g雄性SD大鼠80只,其中行为学评分分生理盐水组,氯氨酮组(5m g/kg组,10m g/kg组、20m g/kg组)和吗啡组共5组,每组8只;NO和NOS测定分正常对照组、生理盐水组、氯胺酮组(10m g/kg组、20m g/kg组)和吗啡组共5组,每组8只。按B rennan法制成切口疼痛模型,以累积疼痛评分和冷刺激评分确定疼痛行为。给药后30m in取大脑皮层,测定NO含量、NOS(总NOS和iNOS)活性。结果表明,氯胺酮组(10m g/kg组、20m g/kg组)、吗啡组累积疼痛评分和冷刺激评分均低于生理盐水组(P<0.05);氯胺酮组(10m g/kg组、20m g/kg组)、吗啡组NO含量及NOS活性均低于生理盐水组(P<0.05)。说明在大鼠切口疼痛模型中,皮下注射不同剂量氯胺酮能产生镇痛作用,NO和NOS可能在氯胺酮的中枢神经系统的镇痛作用中发挥了重要作用。     

Nitric oxide involved in signal transduction of Jasmonic acid-induced stomatal closure of Vicia faba L.

Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JAinduced stomata closuring: ( i ) JA enhances NO synthesis in guard cell; ( ii ) both JA and NO induced stomatal closure, and had dose response to their effects; ( iU ) there are synergetic correlation between JA and lower NO concentration in regulation of stomatal movement; (iV) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (PTIO), a specific NO scavenger. An inhibitor of NO synthase (NOS) in mammalian cells, N^G-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.     

NO及其生成调节与运动

一氧化氮作为重要的细胞信使和效应分子,具有广泛的生物学效应,在介绍NO的生理功能基础之上,阐述了NO的调节机制以及运动对NO的影响,最后展望了NO在运动医学领域中的应用前景,并对今后的研究方向提出一些建议.     

Nitration of a peptide phytotoxin by bacterial nitric oxide synthase

Nitric oxide (NO) is a potent intercellular signal in mammals that mediates key aspects of blood pressure, hormone release, nerve transmission and the immune response of higher organisms. Proteins homologous to full-length mammalian nitric oxide synthases (NOSs) are found in lower multicellular organisms. Recently, genome sequencing has shown that some bacteria contain genes coding for truncated NOS proteins; this is consistent with reports of NOS-like activities in bacterial extracts. Biological functions for bacterial NOSs are unknown, but have been presumed to be analogous to their role in mammals. Here we describe a gene in the plant pathogen Streptomyces turgidiscabies that encodes a NOS homologue, and we reveal its role in nitrating a dipeptide phytotoxin required for plant pathogenicity. High similarity between bacterial NOSs indicates a general function in biosynthetic nitration; thus, bacterial NOSs constitute a new class of enzymes. Here we show that the primary function of Streptomyces NOS is radically different from that of mammalian NOS. Surprisingly, mammalian NO signalling and bacterial biosynthetic nitration share an evolutionary origin.     

一氧化氮在植物体内的生理作用研究进展（综述）

从一氧化氮在植物体内的生物合成,在植物体中的分布,对植物生长发育的作用以及与植物激素的关系等方面综述了一氧化氮在植物体内的生理作用研究进展,并对今后的研究方向进行了展望。     

Regulation between nitric oxide and MAPK signal transduction in mammals

Nitric oxide (NO) is an important biological messenger in the regulation of tissue homeostasis. It exhibits a wide range of effects during physiological and pathophysiological processes. Typical beneficial properties of NO include the regulation of vascular tone,the protection of cells against apoptosis, the modulation of immune responses, and the killing of microbial pathogens. On the other hand,NO may cause severe vasodilation and myocardial depression during bacterial sepsis or act as a cytotoxic and tissue-damaging molecule in autoimmune diseases. Mitogen-activated protein kinase (MAPK) is a family of serine/threonine protein kinases that are widely distributed in mammalian cells. MAPK cascade plays pivotal roles in gene expression, cell proliferation, differentiation, neuronal survival and programmed cell death under a variety of experimental conditions. MAPKs transduce the signal for the cellular response to extracellular stresses or stimuli. The relation between them, however, has never been reviewed. Based on our researches and other reports in the field, we review their reciprocal regulatory functions.     

NO-independent regulatory site on soluble guanylate cyclase

Nitric oxide (NO) is a widespread, potent, biological mediator that has many physiological and pathophysiological roles. Research in the field of NO appears to have followed a straightforward path, and the findings have been progressive: NO and cyclic GMP are involved in vasodilatation; glycerol trinitrate relaxes vascular smooth muscles by bioconversion to NO; mammalian cells synthesize NO; and last, NO mediates vasodilatation by stimulating the soluble guanylate cyclase (sGC), a heterodimeric (alpha/beta) haem protein that converts GTP to cGMP2-4. Here we report the discovery of a regulatory site on sGC. Using photoaffinity labelling, we have identified the cysteine 238 and cysteine 243 region in the alpha1-subunit of sGC as the target for a new type of sGC stimulator. Moreover, we present a pyrazolopyridine, BAY 41-2272, that potently stimulates sGC through this site by a mechanism that is independent of NO. This results in antiplatelet activity, a strong decrease in blood pressure and an increase in survival in a low-NO rat model of hypertension, and as such may offer an approach for treating cardiovascular diseases.     

瑞舒伐他汀钙干预对高尿酸血症所致大鼠内皮功能紊乱的影响

 为探讨瑞舒伐他汀钙(rosuvastatin)对高尿酸血症大鼠模型及其内皮功能紊乱的影响,将72只Sprague-Dawley(SD)雄性大鼠随机分组,采用酵母膏和氧嗪酸钾腹腔注射方法,建立高尿酸血症动物模型.设别嘌呤醇干预为阳性对照,以2.5、5.0和10.0mg瑞舒伐他汀钙/kg剂量干预动物模型,采用专用试剂盒测定尿酸(UA)、一氧化氮(NO)、内皮素-1(ET-1)、血管紧张素II(AngII)的血清水平,免疫组织化学鉴定主动脉组织的一氧化氮合酶(eNOS)蛋白质表达水平变化.结果显示,与对照组比较,高尿酸血症动物模型组血清UA、ET-1和AngII显著升高,血清NO降低,主动脉内皮组织eNOS表达水平降低.瑞舒伐他汀钙干预动物模型后发现,随着药物剂量和干预时间的增加,该药改善以上内皮功能紊乱相关的指标,使之逐渐恢复至正常水平,当瑞舒伐他汀钙干预剂量为10mg/(kg·d)和干预6周时,与非药物干预的模型组有显著差异,其改善内皮功能效果明显高于嘌呤组(阳性对照组).由此表明,瑞舒伐他汀钙通过升高血清中NO和eNOS的蛋白表达,降低血浆ET-1及AngII,从而改善高尿酸血症大鼠的血管内皮功能,并且该作用呈剂量依赖性.     

一氧化氮与肺动脉高压的关系研究进展

肺动脉高压是肺心病发病过程中的中心环节,其产生及严重程度影响着慢性阻塞性肺疾病和肺心病的病程．虽然目前对其发病机制还没有全面清晰地了解,但众多细胞因子在其形成过程中的表达起重要作用已得到共识．一氧化氮作为一种信号物质,在血压调节、细胞凋亡、学习记忆过程形成等多个重大生命活动中起着积极的生物学意义,尤其对血管平滑肌舒张的作用机制显示了其在治疗肺动脉高压领域有着巨大潜力．