一氧化氮合酶对大黄游离蒽醌提取物致小鼠腹泻的影响

目的研究大黄游离蒽醌的致泻作用及与NO的相关性。方法分别测定小鼠在给药后的排稀便时间和次数;在给小鼠预防性ip 40 mg.kg-1NO合酶抑制剂NAME后30 min,分别ig不同剂量的大黄游离蒽醌或等容量蒸馏水,30 min后处死小鼠,分别测定其胃、小肠及结肠内容物的重量和总蛋白,以及小肠和结肠内容物中K 、Na 、Cl-的含量。结果100、200 mg.kg-1游离蒽醌均可引起小鼠腹泻。L-NAME可显著对抗游离蒽醌致小鼠腹泻及增加小鼠胃、小肠及结肠的内容物、蛋白质浓度,调节电解质水平。结论大黄游离蒽醌的致泻作用与NO合酶通路的活性改变有关。     

Edible safety requirements and assessment standards for agricultural genetically modified organisms.

This paper describes the background, principles, concepts and methods of framing the technical regulation for edible safety requirement and assessment of agricultural genetically modified organisms (agri-GMOs) for Shenzhen Special Economic Zone in the People's Republic of China. It provides a set of systematic criteria for edible safety requirements and the assessment process for agri-GMOs. First, focusing on the degree of risk and impact of different agri-GMOs, we developed hazard grades for toxicity, allergenicity, anti-nutrition effects, and unintended effects and standards for the impact type of genetic manipulation. Second, for assessing edible safety, we developed indexes and standards for different hazard grades of recipient organisms, for the influence of types of genetic manipulation and hazard grades of agri-GMOs. To evaluate the applicability of these criteria and their congruency with other safety assessment systems for GMOs applied by related organizations all over the world, we selected some agri-GMOs (soybean, maize, potato, capsicum and yeast) as cases to put through our new assessment system, and compared our results with the previous assessments. It turned out that the result of each of the cases was congruent with the original assessment.     

利湿化痰健脾法对高脂血症大鼠一氧化氮合酶、血管内皮素基因表达的影响

目的观察利湿化痰健脾法对高脂血症大鼠血脂的影响及对血管内皮的保护作用。方法动物随机分成6组，高脂饲料喂养15d，于第16日眼眶取血查血脂，待证实造模成功后分别按不同实验要求灌胃给药。第37日检测一氧化氮合酶及血管内皮素基因表达。结果用药后各组实验大鼠一氧化氮合酶表达与正常组比较，P〈0．01；治疗组与模型组比较，P〈0．01。用药后各组大鼠血管内皮素基因RT—PCR产物光密度值与正常组比较，P〈0．01；治疗组与模型组比较，P〈0．01。结论利湿化痰健脾法通过升高高脂血症大鼠动脉壁内一氧化氮合酶的活性、降低血管内皮素基因的表达而达到调节实验大鼠的血脂水平、保护血管内皮的作用。     

通心贴外敷心俞穴对冠心病心绞痛NO、NOS、SOD、MDA的影响

目的:观察通心贴外敷心俞穴治疗冠心病心绞痛的NO、NOS、SOD、MDA影响.方法:对120例冠心病心绞痛患者,随机分为2组,其中治疗组60例,用通心贴外敷心俞穴,每日1次,30 d为1疗程;对照组60例,给予口服单硝酸异山梨酯片(山东鲁南制药厂生产),每次1片(每片20mg),每天1次,30 d为1疗程.结果:通心贴外敷心俞穴治疗后,病人心绞痛总有效率为90%,心电图改善总有效率为71.7%,动态心电图检测显示,缺血发作次数通心贴穴位治疗组从(7.62±0.34)降至(2.67±0.37).通心贴外敷心俞穴治疗组治疗后,病人N0、NOS、SOD明显升高,MDA明显下降,NO(umol/L)由(46.98±8.63)改善为(71.78±13.05),NOS(u/ml)由(1.59±0.24)改善为(2.30±0.30),SOD(u/ml)由(45.88±5.47)改善为(64.68±9.09),MDA(urn/ml)由(9.01±1.78)改善为(6.68土1.42);与单硝酸异山梨酯片对照组相比,有明显差异(P＜0.05).结论:通心贴外敷心俞穴治疗冠心病心绞痛疗效明显,能明显升高NO、NOS、SOD,降低MDA,且没有明显的毒副作用.     

补气通络针剂加小剂量甲基强的松龙对脊髓损伤后脊髓组织及血液中NO合成酶的影响

为探讨早期静脉滴注补气通络针加小剂量甲基强的松龙(methylprednisolone MP)对急性脊髓损伤的疗效和作用机制。取65只新西兰大白兔,随机分为空白组、生理盐水组、中药组、大剂量MP组、小剂量MP加中药组,采用改良Allen's重物打击法,致伤能量为120g.cm。通过观察动物脊髓神经功能的恢复和脊髓组织及血清中MOS的含量变化情况。结果显示中药组、大剂量MP组、小剂量MP加中药组均可促进脊髓神经功能的恢复,尤以大剂量MP组、小剂量MP加中药组为著;伤段脊髓及血清中NOS急剧升高且在6小时升至最高,以后逐渐下降,中药组、大剂量MP组和小剂量MP加中药组在不同时间均能降低血清及脊髓组织中NOS,大剂量MP组和中药加小剂量MP组在不同时间伤段脊髓及血清NOS变化比较无明显差异;但均比中药组显著。表明该方法可通过调节脊髓组织及血清NOS的含量变化,促进脊髓神经功能的恢复。     

红曲降低肾血管型高血压大鼠血压的生化机制

目的:初探红曲降低肾血管型高血压大鼠(Renovascular Hypertensive Rats,RHR)血压的生化机制.方法:通过试剂盒测定灌胃红曲4周后RHR肺组织ACE活性和主动脉NOS活性,以及灌胃红曲前后血浆ET和CGRP的变化.结果:灌胃4周后.红曲高剂量组和低剂量组肺ACE与阴性对照组相比显著下降(P＜0.01);红曲高和低剂量组血浆ET均比阴性对照组低20个单位(P＜0.01);红曲高剂量组血浆CGRP比灌胃前增高9个单位(P＜0.01),比阴性时照组高7个单位(P＜0.05).结论:红曲的降压途径可能是多方面的:在RHR上可能主要通过抑制肺ACE起到降压作用,同时也能降低血浆ET和升高血浆CGKP.     

依达拉奉对原代海马神经元缺氧复氧损伤的保护作用

目的:研究依达拉奉对原代培养海马神经元缺氧复氧损伤的保护机制.方法:建立离体海马神经元缺氧复氧的细胞损伤模型,实验分组为正常对照组、缺氧复氧组、依达拉奉干预组,其中依达拉奉干预浓度分为1、10、100和300 μmol/L.观察海马细胞四甲基偶氮唑盐(MTT)代谢率、丙二醛(MDA)含量及一氧化氮合酶(NOS)活性的变化,流式细胞仪观察细胞凋亡.结果:与缺氧复氧组相比,依达拉奉100μmol/L组和300 μmol/L组的MTT代谢率显著增高(P＜0.01),MDA含量降低(P＜0.05),NOS活性降低(P＜0.05),细胞凋亡率降低(P＜0.01).结论:依达拉奉能够有效地抑制脂质过氧化作用,降低MDA及NOS活性,减少细胞凋亡率,对缺氧损伤的神经元具有显著的神经保护作用.     

血管内皮生长因子、碱性成纤维细胞生长因子和一氧化氮合酶3在恶性黑素瘤的表达及其意义

目的研究血管内皮生长因子（VEGF），碱性成纤维细胞生长因子（b-FGF），一氧化氮合酶3（NOS3）在恶性黑素瘤中的表达及其生物学意义，并探讨其与肿瘤血管形成及淋巴结转移的关系。方法用免疫组化（S-P法）染色技术对45例黑色素瘤石蜡组织标本的VEGF、b-FGF、NOS3及肿瘤内微血管密度（MVD）进行检测和分析。结果VEGF、b-FGF表达与TNM分期、MVD及淋巴结转移有关（P〈0.05），两者共表达与MVD有关（P〈0．01）。NOS3与MVD及淋巴结转移有关（P〈0.05）；相关分析显示促血管形成因子（VEGF、b-FGF）与NOS3的表达呈正相关（r=0．2298，P〈0.05）。结论VEGF和b-FGF在促进肿瘤血管形成和转移方面可能起协同作用，并且有NO3的参与；VEGF、b-FGF、NOS的检测对于判断黑色素瘤转移和预后及治疗具有临床应用价值。     

Evidence for the involvement of L-citrulline but not nitric oxide in the proconvulsant action of the precursor L-arginine on picrotoxin-induced convulsions in rats

To determine the role of the metabolites of L-arginine in its actions on picrotoxin-induced convulsions in rats, the concentrations of nitric oxide (NO) and L-citrulline were measured in the brain 30 and 60 min after the administration of L-arginine (1000 and 2000 mg/kg) or of N-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg), an inhibitor of NO synthase. Animals treated similarly were challenged 30 and 60 min later with picrotoxin (5mg/kg), and the time of onset of myoclonus and clonic convulsions and the frequency of convulsions were determined. These parameters were also determined 30 and 60 min after administering L-arginine in L-NAME-pretreated (30 min) animals. Thirty minutes after the administration of L-arginine, the concentrations of both NO and L-citrulline were raised, the onset of myoclonus and clonic convulsions was delayed, and the frequency of convulsions was decreased, indicating the anticonvulsant property of L-arginine. A 60-min treatment of L-arginine produced a further increase in the concentration of L-citrulline but not that of NO and promoted the frequency of picrotoxin-induced convulsions. Pretreatment with L-NAME prevented L-arginine from raising the concentrations of both NO and L-citrulline; it also promoted the anticonvulsant actions and prevented the proconvulsant actions of L-arginine. These results lead to the conclusion that NO has no involvement in the time-dependent anti and proconvulsant actions of L-arginine on the picrotoxin convulsion model, and that L-citrulline seems to have a role in the proconvulsant action of L-arginine.