辛伐他汀对高胆固醇喂养大鼠血清一氧化氮含量的影响

通过观察内源性胆固醇合成抑制剂辛伐他汀(Simvastatin)对高胆固醇喂养大鼠血清一氧化氮含量的影响,以探讨其抗动脉粥样硬化的机理.结果表明,喂养8周后实验大鼠与喂养前相比,大鼠的体质量、胆固醇、一氧化氮均有显著的提高(P<0 01).其中辛伐他汀干预组胆固醇水平低于对照组,而一氧化氮含量高于对照组(P<0 05).结果提示辛伐他汀能够降低血清胆固醇的含量,提高大鼠血清一氧化氮的浓度,可能是其抗动脉粥样硬化的机理之一.     

2型糖尿病肾病患者血清一氧化氮、超氧化物歧化酶的变化及相关分析

对2型糖尿病肾病(diabetic nephropathy,DN)不同时期血清一氧化氮(nitric oxide,NO)、血清总超氧化物歧化酶(superoxi dedismutase,SOD)进行检测,探讨二者间的相互关系,为临床诊断、治疗提供理论依据。按尿白蛋白排泄率(urinary albumin excretion rate,UAER)将已确诊为2型糖尿病的51例患者分为3组：糖尿病正常白蛋白尿组(DM1组);微量白蛋白尿组(DM2组);大量白蛋白尿组(DM3组)。20例健康人作为对照组,对照组及实验组抽血做血清NO、SOD检测。结果显示：DM1、DM2组血清NO较对照组显著增高(均为P=0．000),DM3组较对照组降低(P=0．024),DM1、DM2组较DM3组血清NO水平增高(均为P=0．000);DN各组血清总SOD均较对照组降低,但以DM2、DM3组降低显著(均为P=0．000);NO与SOD正相关(r=0．607,P=0．000)。表明,1)NO在DN早期增高,晚期降低。在DN早期减少NO合成,晚期增加NO合成,对减缓DN进展有重要意义。2)血清总SOD在DN是降低的,抗氧化治疗可能在DN防治中占重要地位。3)DN患者血清NO与总SOD间存在密切相关性。     

幼龄大鼠内毒素血症时一氧化氮和一氧化氮合成酶变化

基层编号 996103 完成单位及南京市红十字医院: 主要人员孙克娅 一氧化氮(NO)作为一种时空细胞信息分子,在80年代末和90年代初成为医学界的研究热点.在Szabo建立的成年大鼠内毒素血症模型的基础上,我们对内毒素进行减量预试(5mg/kg、4mg/kg、3mg/kg体重腹腔注入),最后确定2mg/kg体重腹腔注入,在国内率先成功地建立幼龄大鼠内毒素血症模型,并且率先用生化方法测定组织匀浆NOS和NO含量,较全面地反映了在内毒素血症时,多器官和多细胞中多元NOS的水平,同时用免疫组织化学(ABC-Method)检测了在内毒素血症时小肠、肺、脾和肝脏组织中INOS的免疫活性表达,揭示INOS阳性细胞有参与非特异免疫功能的可能性.该研究对临床上G菌引起的肠道传染病的治疗有重要的理论指导价值,具有潜在的社会效益和经济效益.     

运动对人体血清一氧化氮含量和一氧化氮合酶活性影响的研究

为了探讨人体在不同功能状态下一氧化氮（NO）和一氧化氮合酶（NOS）的变化，应用跑台提供运动负荷，分别在36名大学生进行了安静，亚极量负荷和力竭性运动后血清中NO和NOS的测定。结果发现，亚极量负荷下血清中NO含量显著高于安静状态时（P＜0．001），NOS活性极显著地低于安静状态时（P＞0．001），力竭性运动后，NO含量和NOS活性极显著低于亚极量负荷时（P＜0．001），并且NO已降至低于安静时的水平（P＞0．05），提示，人体血清中NOS活性随运动负荷的增大而持续下降；NO含量在运动的开始阶段随运动负荷的增大而升高，但当达到一定水平时，则随运动负荷的继续增大而下降。     

牦牛血清和组织中一氧化氮合成酶活性的测定

对生活在海拔4300多m玛多牦牛和3500m左右循化牦牛血清和肝、肺、肾、心肌、骨骼肌中的一氧化氮合成酶(NOS)活性进行了测定,结果分别为:(28 21±2 99)U/mL和(24 35±4 64)U/mL,(2 05±0 70)U/mgprot和(2 55±0 58)U/mgprot,(0 98±0 56)U/mgprot和(1 52±0 40)U/mgprot,(0 72±0 35)U/mgprot和(1 61±0 57)U/mgprot,(0 73±0 46)U/mgprot和(0 70±0 21)U/mgprot,(1 10±0 73)U/mgprot和(0 66±0 33)U/mgprot。     

犊牦牛血清和组织中一氧化氮含量测定

测定1日龄和1月龄犊牦牛血清和肺、肾、骨骼肌、心肌、脾中NO含量,结果分别为:97.68±29.69和64.47±7.46(μmol/L),2.32±0.45和3.12±0.78(μmol/gprot,下同),3.04±0.53和5.36±1.22,3.03±1.10和4.49±0.83,5.87±2.41和6.31±2.92,1.56±0.25和1.72±0.72。结果表明,血清中NO的含量1日龄显著高于1月龄犊牦牛(P<0.05)。     

晚期糖基化终产物对大鼠阴茎海绵体组织中一氧化氮含量及其合成酶活性的影响

通过观察大鼠阴茎海绵体组织中晚期糖基化终产物(AGEs)含量的变化对一氧化氮(NO)含量及其合成酶(NOS)活性的影响,探讨AGEs在糖尿病性勃起功能障碍(DMED)发生发展中的作用.成年雄性SD大鼠60只,随机取40只用于制作糖尿病模型,造模成功的大鼠分为两组:糖尿病(DM)组和糖尿病 氨基胍给药(DM AG)组;另20只大鼠亦分为两组:正常对照(CONTROL)组和正常对照 氨基胍给药(CONTROL AG)组;氨基胍(AG)给药组大鼠造模后即在其饮水中按1 g/L剂量加入AG.饲养8周后取各组大鼠阴茎海绵体组织,匀浆后检测AGE-肽(AGE-P)含量、NO含量及各型NOS酶活性.DM组阴茎海绵体组织中AGE-P含量、NO含量及诱导型NOS(iNOS)活性明显高于CONTROL组(P＜0.05),而结构型NOS(cNOS)活性则明显低于后者(P＜0.05),而AG则明显减少了DM大鼠阴茎海绵体组织中AGE-P、NO的生成和减弱了iNOS活性,增强了cNOS活性;CONTROL组与CONTROL AG组间比较在各项指标上则无明显差异(P＞0.05).糖尿病状态下AGEs可以引起大鼠阴茎海绵体组织中cNOS活性减弱,iNOS活性增强,过量的NO生成,可能引起阴茎组织细胞的凋亡,导致阴茎勃起功能的损伤.     

糖尿病老年性白内障血清、房水中一氧化氮与抗氧化能力的改变

目的探讨糖代谢与年龄相关性白内障发生发展的关系。方法测定糖尿病合并年龄相关性白内障患者血清及房水中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)含量;分析糖尿病合并年龄相关性白内障患者房水、血清中抗氧化酶及一氧化氮含量变化。结果糖尿病年龄相关性白内障患者超氧化物歧化酶、丙二醛含量与正常组存在明显差异,一氧化氮含量明显高于正常组。结论糖尿病患者高血糖及氧化应激状态,增加了体内氧化损伤及蛋白糖基化反应;一氧化氮显著增加和自由基的增多,可能影响到房水代谢及晶状体代谢,从而加速了年龄相关性白内障的发生发展。     

大鼠端脑神经元型一氧化氮合酶免疫阳性神经元的分析

目的：观察大鼠端脑神经元一氧化氮合酶（nNOS）免疫阳性神经元的分析。方法：ABC免疫细胞化学显示大鼠端脑nNOS阳性神经元。结果：nNOS阳性神经元呈棕褐色，胞体的形态多样化，呈梭形、三角形、圆形等多种形状，突起一个或多个；阳性纤维呈棕色串珠状，个别脑区阳性纤维相互交织成网。端脑nNOS免疫阳性神经元主要分布于嗅结节（包括海马回）、梨状区（包括梨状皮质和梨状核）、斜角带、隔区、杏仁复合体、海马结构、尾壳核和苍白球，以及大脑皮质等各个部位，其中以大脑皮质、梨状区和斜角带、尾壳核等部分最为丰富。结论：大鼠端脑内分布有丰富的nNOS阳性神经元，它们可能通过调节神经递质的分泌，参与脑的高级整合功能。     

大鼠端脑神经元型一氧化氮合酶免疫阳性神经元的分布

目的 :观察大鼠端脑神经元型一氧化氮合酶 (nNOS)免疫阳性神经元的分布。方法 :ABC免疫细胞化学法显示大鼠端脑nNOS阳性神经元。结果 :nNOS阳性神经元呈棕褐色 ,胞体的形态多样化 ,呈梭形、三角形、圆形等多种形状 ,突起有一个或多个 ;阳性纤维呈棕色串珠状 ,个别脑区阳性纤维相互交织成网。端脑nNOS免疫阳性神经元主要分布于嗅结节 (包括海马回 )、梨状区 (包括梨状皮质和梨状核 )、斜角带、隔区、杏仁复合体、海马结构、尾壳核和苍白球 ,以及大脑皮质等各个部位 ,其中以大脑皮质、梨状区和斜角带、尾壳核等部位最为丰富。结论 :大鼠端脑内分布有丰富的nNOS阳性神经元 ,它们可能通过调节神经递质的分泌 ,参与脑的高级整合功能。     

糖尿病大鼠脑干听觉诱发电位波幅间比率的动态变化

目的：探讨脑干听觉诱发电位(BAEP)的波幅问比率在糖尿病大鼠中的动态变化。方法：采用链脲佐菌素(SIZ)腹腔注射法，建立实验性糖尿病(ED)动物模型。在成模前后按时间顺序连续10周动态观测BAEP的波幅间比率的变化。结果：与正常对照组相比，ED组大鼠在病程2周时出现BAEP Ⅰ、Ⅲ、Ⅳ、Ⅴ波幅增高；在病程4周时出现BAEP各波波幅增高；病程6周时BAEP Ⅰ、Ⅱ、Ⅲ、Ⅳ波幅增高；病程8～10周时：BAEP Ⅰ、Ⅲ、Ⅳ、Ⅴ波幅增高。病程8周后BAEPⅤ／Ⅰ波幅比率下降；病程10周后BAEPⅢ与Ⅴ波幅比率降低；Ⅴ与Ⅰ、Ⅳ与Ⅰ波幅比率明显降低。结论：糖尿病大鼠BAEP的波幅和波幅比率有明显变化，这有助于糖尿病中枢神经病变的早期诊断。     

益寿调脂片对实验性动脉粥样硬化家兔血脂、一氧化氮和脂质过氧化物的影响

目的：观察益寿调脂片治疗用药对实验性动脉粥样硬化家兔血脂、一氧化氮（ＮＯ） 和过氧化脂质的影响。方法：将３２ 只新西兰兔随机分为正常组（８ 只） 、造模组（２４ 只） 。正常组喂普通饲料,造模组喂高脂饲料,８ 周后造模组再随机分为模型组、益寿调脂片治疗组（ 加服益寿调脂片,每只每天每ｋｇ 体重４ ｇ） ,舒降之治疗组（ 加服舒降之,每只每天每ｋｇ 体重２－５ ｍｇ） 。用药４ 周后,抽血测生化指标。结果：益寿调脂片能提高超氧化物歧化酶（ＳＯＤ） 的活性,抑制高脂所致的血清ＮＯ降低和脂质过氧化物的升高,降低血清总胆固醇（ＴＣ） 、甘油三酯（ＴＧ） 水平,且提高ＳＯＤ活性方面优于舒降之（ Ｐ＜ ０－０５） ,对升高血清ＮＯ 和降低丙二醛（ＭＤＡ） 方面也优于舒降之,但无统计学意义。结论：益寿调脂片可能通过提高ＳＯＤ、ＮＯ的含量及活性,抑制脂质过氧化物的形成,而起到抗动脉粥样硬化形成的作用。     

大鼠颅脑冷冻伤后一氧化氮的变化及其对脑水肿的影响

目的：探讨脑冷冻性损伤后一氧化氮(NO)与脑水肿的关系及其对脑水肿的影响。方法：建立大鼠脑冷冻伤脑水肿模型，测定伤后伤侧脑组织水的质量分数和颈静脉血NO量，并应用一氧化氮合酶(NOS)抑制剂进行治疗。结果：伤后伤侧颈静脉血NO浓度增加，但随着脑水肿的加重，NO浓度呈进行性下降。应用NOS抑制剂可以有效减少脑组织水的质量分数。结论：NO与创伤性脑水肿的发生和发展密切相关，NOS抑制剂也许可以用于治疗脑水肿。     

Effects of niacin on nitric oxide synthase expression in rat lungs exposed to silica

The aim of this study was to evaluate the effects of niacin in diet on the expression of nitric oxide synthase (NOS) in rat lungs of the animal model of silicosis established by direct tracheal instillation of silica particles into rat lungs surgically. The niacin concentration in serum was analyzed by high performance liquid chromatography (HPLC). The expression of inducible nitric oxide synthase (iNOS) protein in paraffin-embedded lung sections was determined by streptavidin/peroxidase (SP) staining. Quantitative analysis by Image-Pro Plus was also performed on the expression of iNOS. The results showed that niacin concentration in serum of the niacin-treated rats was significantly higher than that in the control and silica-treated rats. After 7 days of silica instillation, iNOS integrated optical density (IOD) in rat lungs and total NOS and iNOS activities in bronchoalveolar lavage fluid (BALF) in silica-treated rats rose by 273420.75, 2.61 units/mL and 1.89 units/mL respectively, when compared with those in the control rats. Niacin treatment significantly reduced silica-induced iNOS IOD in rat lung tissues and total NOS and iNOS activities in BALF supernatant by 248292.35, 1.50 units/mL and 0.91 units/mL, respectively, as compared with those in silica-treated rats. Therefore, niacin can effectively attenuate the pathological expression of NOS in rat lung tissues induced by silica particles.     

Regulation of embryo implantation by nitric oxide in mouse

Intrauterine injection and zymography were used to investigate the effect of nitric oxide (NO) on embryo implantation in mice. On day 3, one uterine horn of female pregnant mice was injected intraluminally with various doses of nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), while the contralateral horn served as control. Animals were sacrificed by cervical dislocation on day 7 of gestation, and the number of implanted embryos in each horn was calculated. The results showed that lower doses (0.05 mg L-NAME) did not inhibit implantation significantly (P > 0.05), but high doses (0.2 mg L- NAME) resulted in a significant reduction in the number of implanted embryos (P < 0.05). Co-administration of SNP, a generator of NO, with L-NAME would reverse the antiimplantation effect of L-NAME. To further understand the precise mechanism of NO in implantation, matrix metalloproteinase (MMPs) activities were detected by gelatin zymography. The reduction in the number of implanted embryos in 0.2 mg L-NAME treated group was associated with decreased MMP-9 activity but a stable MMP-2 activity. The activities of MMP-2 and MMP-9 were not changed in L-NAME and SNP treated group. These data suggest that NO acts as a mediator to regulate the activity of MMP-9, and facilitates embryo implantation.     

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.     

Influence of magnetic field on nitric oxide and neuropeptide Y in rat adrenal gland

We have investigated the effects of magnetic fields on nitric acid (NO) and neuropeptide Y (NPY) on adrenal glands of the rat using NO nitric acid reductase-spectrophotometry ↭d histochemistry techniques. We found that all cellular layers of the adrenal cortex, including zona glomerulosa, zona fasciculata and zona reticularis were stained by NADPH-d, and some chromaffin cells of the medulla were positive for NPY. Furthermore, magnetic fields increased NO so strongly that high NO levels could be maintained for several hours, as well as some neuroganglion cells in medulla that were double-stained for NPY and NADPH-d. Our data showed that the magnetic field can regulate endocrine and neuroendocrine directly by some action on parenchyma cells, or indirectly by action to NO-ergic, NPY-ergic neurons in the adrenal gland.