去势对大鼠阴茎组织细胞凋亡的影响

目的 :探讨雄激素对阴茎海绵体结构和功能的影响以及细胞凋亡与 NOS活性在阴茎勃起中的关系。方法 :将 30只成年雄性大白鼠随机分为 3组 ,阉割组、替代组及假手术组 ,阉割组与替代组分别切除双侧睾丸 ,其中替代组在切除睾丸后给予睾酮替代。于 1周后取阴茎海绵体 ,用紫外分光光度计测定其一氧化氮合酶 (NOS)活性 ,同时用 ISEL 法检测其细胞凋亡情况。结果 :阉割组海绵体 NOS活性下降 70 % ,并出现细胞凋亡 (P <0 .0 1) ,睾酮替代组和对照组 NOS活性及细胞凋亡差异无显著性 (P >0 .0 5 ) .结论 :雄激素可通过调节 NOS活性及细胞的增殖与凋亡而维持阴茎海绵体的结构与功能。     

肝硬化患者一氧化氮、一氧化氮酶、肿瘤坏死因子、内皮素、内毒素水平的相关性研究

目的：探讨肝硬化患者血NO、TNF、ET与EPS的关系。方法：分别应用酶法和放射免疫分析法测定了84例肝硬化患者血NO、NOS、ET和EPS含量，并与35名正常健康人作对照。结果：肝硬化患者血NO、TNF、EPS含量高于正常人组（P＜0．05－0．01），ET水平低于正常人组（P＜0．01－0．01），且与内毒素含量的高低密切相关。结论：肝硬化患者血NO、TNF、ET水平的高低其内毒素为主要诱因。     

针刺对吗啡戒断大鼠脑组织一氧化氮合酶基因表达的影响

目的 :观察针刺对吗啡戒断大鼠脑组织神经元一氧化氮合酶基因 (nNOSmRNA)表达的影响 ,探讨针刺改善戒断症状的分子生物学机理。方法 :建立大鼠吗啡自然戒断模型 ,运用逆转录聚合酶链反应 (RT PCR)测定戒断大鼠脑组织nNOSmRNA的表达。观察戒断后 ,针刺“足三里”和一氧化氮合酶 (NOS)抑制剂L N 硝基精氨酸 (L NAME)对吗啡戒断大鼠戒断症状和脑组织nNOSmRNA表达的影响。结果 :戒断组nNOSmRNA表达增加 ,针刺组和L NAME组nNOSmRNA表达比戒断组减少。针刺组戒断积分比戒断组少 ,组间差异显著 (P <0 .0 1 )。结论 :针刺“足三里”穴具有抑制吗啡戒断大鼠脑组织nNOSmRNA表达的作用 ,提示这可能是针刺改善吗啡戒断症状的一个重要机制。     

电针“足三里”对酸化乙醇致胃黏膜损伤大鼠的胃组织总NOS、iNOS影响的时效关系研究

目的 :通过电针“足三里”对酸化乙醇致大鼠胃黏膜损伤模型胃黏膜影响的实验 ,探讨针刺的时效关系。方法 :将动物随机分组、造模 ,造模成功后针刺组进行电针。在电针后 7个不同时刻各组进行取材 ,检测胃组织总NOS、iNOS ,将各针刺组与其对应模型组的实验结果进行两两比较。结果 :针刺组与对应时间模型组动物指标均值有一定变化趋势 ,其中针刺 0组比其对应模型 0组总NOS、iNOS活性相对增高。结论 :本实验各针刺组治疗 1次后 ,不同的时段对损伤的胃组织总NOS、iNOS活性的影响不同 ,针刺后即刻可在一定程度上提高胃组织总NOS、iNOS活性 ,因而可能对胃黏膜起一定的保护作用。     

颜面皮肤癌VEGF和NOS表达及相关性

[目的]研究血管内皮生长因子(VEGF)、诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)在颜而皮肤癌的表达及其相关性.[方法]应用免疫组化方法检测47例颜面皮肤癌标本VEGF、iNOS和eNOS的表达,并对其相关性进行统计分析.[结果]47例颜面皮肤癌组织中,表达iNOS、eNOS、VEGF的分别为63.83%、74.47%、68.09%;VEGF与iNOS的表达具有明显相关性(P＜0.01),VEGF与eNOS的表达无明显相关性(P＞0.05);VEGF的表达与颜面皮肤癌肿瘤分化程度呈正相关,与临床分期及病理分型无关.iNOS表达与颜面皮肤癌的分化程度及临床分期呈正相关,与病理分型无关.eNOS表达与颜面皮肤癌病理分型、临床分期和分化程度均无关.[结论]VEGF与iNOS的表达具有明显相关性,iNOS和VEGF在肿瘤生成过程中起重要作用.     

The Protective Effect of Rosuvastatin on Ischemic-Brain Injury and Its Mechanism

The statins, which lower plasma cholesterol levels, are 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors. To date, stains have developed to third generation, which include five commonly used stains: lovastatin, pravastatin, simvastatin, fluvastatin and atorvastatin. Recently, a new statin, named rosuvas-tatin, was used in the third stage of clinical trial. Rosu-vastatin, in contrast to most other statins, has the more powerful capability to lower plasma cholesterol levels,…     

参芪心复康对心气虚细胞模型ET和NOS基因表达的影响

目的研究参芪心复康对心气虚细胞模型内皮素(ET)和一氧化氮合酶(NOS)基因表达的影响.方法采取培养心肌细胞缺氧再给氧损伤的方法建立心气虚细胞模型.设参芪心复康组、人参组、水蛭组、丹参组、对照组、模型组,采用逆转录聚合酶链反应(RT-PCR)基因表达检测心气虚细胞模型和各中药治疗组的ET和NOS基因表达情况.结果各中药组ET和NOS mRNA表达与心气虚的细胞模型的ET和NOS表达有显著性差异(P＜0.01);参芪心复康组与其他中药组的ET和NOS mRNA表达情况有显著性差异(P＜0.01或P＜0.05).结论参芪心复康防治心气虚证的机制与其干预ET和NOS mRNA表达有关.     

The effect of divalent cations on neuronal nitric oxide synthase activity.

Neuronal nitric oxide synthase (NOS I) is a Ca(2+)/calmodulin-binding enzyme that generates nitric oxide (NO*) and L-citrulline from the oxidation of L-arginine, and superoxide (O(2)*(-)) from the one-electron reduction of oxygen (O(2)). Nitric oxide in particular has been implicated in many physiological processes, including vasodilator tone, hypertension, and the development and properties of neuronal function. Unlike Ca(2+), which is tightly regulated in the cell, many other divalent cations are unfettered and can compete for the four Ca(2+) binding sites on calmodulin. The results presented in this article survey the effects of various divalent metal ions on NOS I-mediated catalysis. As in the case of Ca(2+), we demonstrate that Ni(2+), Ba(2+), and Mn(2+) can activate NOS I to metabolize L-arginine to L-citrulline and NO*, and afford O(2)*(-) in the absence of L-arginine. In contrast, Cd(2+) did not activate NOS I to produce either NO* or O(2)*(-), and the combination of Ca(2+) and either Cd(2+), Ni(2+), or Mn(2+) inhibited enzyme activity. These interactions may initiate cellular toxicity by negatively affecting NOS I activity through production of NO*, O(2)*(-) and products derived from these free radicals.     

Pneumonia‐induced sepsis in mice: temporal study of inflammatory and cardiovascular parameters

The aim of the present work is to provide a better comprehension of the pneumonia‐induced sepsis model through temporal evaluation of several parameters, and thus identify the main factors that determine mortality in this model. Klebsiella pneumoniae was inoculated intratracheally in anesthetized Swiss male mice. Inflammatory and cardiovascular parameters were evaluated 6, 24 and 48 h after the insult. The results show that severity of infection and the mortality correlated with the amount of bacteria. Six, 24 and 48 h after inoculation, animals presented pathological changes in lungs, increase in cell number in the bronchoalveolar lavage, leukopenia, increase in TNF‐α and IL‐1β levels, hypotension and hyporesponsiveness to vasoconstrictors, the two latter characteristics of severe sepsis and septic shock. Significant numbers of bacteria in spleen and heart homogenates indicated infection spreading. Interestingly, NOS‐2 expression appeared late after bacteria inoculation, whereas levels of NOS‐1 and NOS‐3 were unchanged. The high NOS‐2 expression coincided with an exacerbated NO production in the infection focus and in plasma, as judging by nitrate + nitrite levels. This study shows that K. pneumoniae inoculation induces a systemic inflammatory response and cardiovascular alterations, which endures at least until 48 h. K. pneumoniae‐induced lung infection is a clinically relevant animal model of sepsis and a better understanding of this model may help to increase the knowledge about sepsis pathophysiology.     

Mussel oligopeptides ameliorate cognition deficit and attenuate brain senescence in d-galactose-induced aging mice

Dietary supplementation exerts beneficial effects in reducing incidence of chronic neurodegenerative diseases. The purpose of this study was to examine protective effects of mussel (Mytilus edulis) oligopeptides supplementation on brain function in d-galactose induced aging mice. Sixty female 8-month-old mice were randomly divided into five groups: vehicle control, d-galactose, and d-galactose combined with 200, 500, 1000 mg/kg mussel oligopeptides. The results showed that mussel oligopeptides could improve cognitive learning and memory ability and protect the hippocampal neurons. In addition, GSH, SOD and GSH-pX activities were increased and MDA level was significantly decreased in mice fed with mussel oligopeptides. It was also found that mussel oligopeptides supplementation prevented d-galactose-induced elevations of iNOS activity and NO production and lactate acid levels in brain. Moreover, PI3K and Akt genes were up-regulated by mussel oligopeptides supplementation. These findings suggest that mussel oligopeptides are able to enhance exercise capacity and protect against oxidative damage caused by d-galactose in aging model mice through regulating oxidation metabolism and PI3K/Akt/NOS signal pathway. Therefore, mussel oligopeptides are good materials for future development of healthcare products to combat age-related brain dysfunction and to improve healthy life span.