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染矽尘大鼠肺组织匀浆一氧化氮含量、一氧化氮合酶活力的研究
研究表明[1],当暴露于矽尘等炎性刺激物作用时,肺泡巨噬细胞和肺中性粒细胞一氧化氮(nitricoxide,NO)生成增加,并上调诱导型一氧化氮合酶(inducible nitric oxide,iNOS)基因表达.但是,有研究[2]认为矽尘并不能够直接增加培养的肺泡巨噬细胞产生NO;还有研究认为NO可能是肺纤维性结节形成的调节因子[3].这些研究提示NO及NOS的变化与矽尘对肺的作用有关.本研究测定了染尘后不同处理时点肺匀浆NO含量和NOS活力,并进行相关分析,以期能有助于解释矽尘对肺的作用.
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To study the therapeutic effect of Chinese herbal medicines (CHM) in treating ascites and to elucidate its mechanism in regulating the lymphatic stomata and promoting the absorption of ascites from the peritoneal cavity. Methods: Using scanning electron microscope (SEM), computerized image processing and quantitative analytic assay, the effect of CHM extract, consisting of Atractylodes macrocephala, Salvia miltiorrhiza, Codonopsis pilosula, Alismatis orientale and Leonurus heterophyllus, was studied. Results: Intraperitoneal injection of nitric oxide (NO) supplier (Sodium nitroprussiate) or CHM administration could cause the average area of lymphatic stomata obviously enlarged (P<0.05), and the numbers of opening stomata significantly increased (P<0.01) in normal healthy mice. When L-notroarginine, a NO synthetase suppressor, was injected after CHM administration, the regulating effect of CHM on lymphatic stomata was inverted obviously, i.e. the average area and the density of lymphatic stomata were markedly reduced (P<0.01). Conclusion: CHM might treat ascites through increasing the endogenous NO concentration to open the lymphatic stomata and in turn to conduct the peritoneal water through lymphatic path.
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一氧化氮与糖尿病周围神经病变及中药干预的研究
糖尿病周围神经病变(Diabetic Peripheral Neuropathy, DPN)是糖尿病(DM)常见的慢性并发症之一, 文献报道患病率在40%~90%不等.DPN的发展常导致糖尿病足的发生, 是造成糖尿病患者致残的主要原因之一[1].
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慢性阻塞性肺病患者血浆一氧化氮、内皮素和降钙素基因相关肽的含量变化
慢性阻塞性肺病(COPD)是一种重要而常见的慢性呼吸系统疾病,患病人数多,死亡率高,而且随着COPD病情进展,逐渐合并肺原性心脏病,呼吸衰竭,严重影响了患者的身体健康和生活质量.近年来,人们逐渐认识到血管内皮合成释放的某些重要血管活性物质如ET-1、CGRP与COPD密切相关,参与了COPD、肺心病、呼吸衰竭的病理生理过程.本研究观测了COPD各病情组患者的血浆NO、ET-1和CGRP的含量变化.
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压力超负荷大鼠左心室一氧化氮和环磷酸鸟苷含量的变化
心肌肥厚是心血管疾病发病率和死亡率的独立危险因子,压力超负荷是触发心肌肥厚反应重要的因素.一氧化氮(NO)作为一种新型的信使分子,有着广泛的心血管效应.在自发性高血压大鼠,内皮依赖性血管舒张有缺陷,L-精氨酸--NO通路异常.环磷酸鸟苷(cGMP)是血管活性因子NO和钠尿肽类等胞内信号的主要介导者.本实验用大鼠腹主动脉缩窄压力超负荷模型,观察在心肌肥厚的发生和发展过程中左心室NO和cGMP含量的变化.
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血小板L-Arg/NO系统与高血压研究进展
高血压是人类死亡的重要原因之一,其发病机制仍未完全阐明.近年来的研究表明,血小板除参与止血和凝血过程外,在血栓形成、动脉粥样硬化及高血压发病过程中的作用也逐渐得到重视.现已证实,血小板内含有一氧化氮合酶(nitric oxide synthase,NOS),能利用左旋精氨酸(L-Arg)合成血小板一氧化氮(platelet-derived nitric oxide,PDNO),PDNO通过使细胞内环磷酸腺苷(cGMP)升高,抑制血小板的黏附与聚集作用.而原发性高血压时血小板存在一系列功能的异常,其中血小板L-Arg/NO系统功能改变是其血栓性并发症发生的原因之一.
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雷公藤内酯醇对内毒素激活小鼠腹腔巨噬细胞分泌促炎症介质NO和IL-6的影响
Objective Tripterygium wilfordii Hook. f. has been used for centuries in traditional Chinese medicine to treat autoimmune disease associated with increased production of the pro-inflammatory cytokine. Triptolide( TP) is a compound originally purified from T. wilfordii Hook f. and it has potent anti- inflammatory and immunosuppressant activities. In this study, we investigated the effect of TP on secretion of NO and IL-6 in celiac macrophages ( MΦ) activated by lipopolysaccharide ( LPS) in Kunming mice. Methods Celiac MΦ of mice were separated, purified, and activated by LPS, then cultured in vitro with TP of different concentrations. The level of NO in cellular supematants was determined by Griess reagent, and that of IL-6 was determined by ELISA. Results We found that pro-inflammatory cytokine NO activity in MΦ induced by LPS was significantly inhibited by TP ( 10-3-10 μg/ml) from 4-24 h in a time and dose- dependent manner (P < 0. 01). The level of IL-6 in MΦ was significantly inhibited by TP (10-3-10 μg/ml) at 12 h in a dose-dependent manner (P <0. 01). Conclusions We demonstrated that TP can inhibit levels of NO and IL-6 in celiac MΦ of Kunming mice activated by LPS.
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AIM To determine NO, NO synthase (NOS) and NOSmRNA of the esophageal carcinoma cells (SHEEC1)in apoptotic process induced by As2O3 and to explore the relationship between NO and apoptosis.METHODS The apoptosis of the cell line (SHEEC1) was induced by arsenite (As2O3, 5 μmol/L and10 μmol/L). In the process, at 2 h, 4 h, 8 h, 16 h and 24 h after administration of As2O3, NO production incultural medium was detected quantitatively by spectrophotometry; NOS Ⅱ was detected byimmunohistochemistry and NOS mRNA by in situ hybridization (ISH). The cells at endpoint of theexperiment were examined under transmitted electron microscope (TEM) for apoptosis.RESULTS The amount of NO released from SHEEC1 were increased from the basal condition (0.68×10-2μmol/L) up to the high level (2.38×10-2μmol/L) at h 16. The increment of NOS Ⅱ was found afteradministration of As2O3; the intracytoplasmic ISH signals of NOSmRNA in small size was found firstly at4 h, and then became highly predominant. Apoptotic changes of SHEEC1 occurred at 24 h under TEM.CONCLUSION After administration of As2O3, NO released from cultured SHEEC1 cells was detected withincreasing amount up to 16 h. The expression of NOS H and transcription of NOSmRNA are upregulated.The present findings suggest a concept that the NO may be a mediated and effective factor in apoptosisinduced by As2O3,
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AIM To observe the effect of acupuncture and moxibustion on the expression of IL-1β and iNOSmRNA inrats, with ulcerative colitis.METHODS Surgical samples of fresh human colonic mucosa was homogenized by adding appropriateamount of normal saline and centrifuged at 3000 r/min. Protein content of the supernatant was measuredand then mixed with Freund adjuvant, and injected into the plantae of the rats models, then into theplantae, dorsa, inguen and abdominal cavities (no Freund adjuvant for the last injection) on the 10th, 17th,24th and 31st day respectively. When serum titer of anti-colonic antibody has reached to a certain level,20 mL/L formalin and antigen fluid (no Freund adjuvant) were administered by enema to set up ulcerativecolitis rat mode. The animals were randomly divided into four groups: model control group (MC = 8),electroacupuncture group (EP=8), herbs partition moxibustion group (HPM= 8) and normal control group(NC=8). HPM: Mosa cones made of refined mugwort floss were placed on the medicinal pads (medicinalpad dispensing: Radix Aconiti Praeparata, cortex Cinnamomi, etc. ) for qihai (RN6) and tianshu (ST25,bilateral) and ignited. Two moxa cones were used for each acupuncture once a day and 14 times in all. EP:tisnshu (bilateral) and qihai were stimulated by the intermittent pulse with 2Hz frequency, 4mA intensity for20 minutes once a day and 14 times in all. After treatment, all rats were killed simultaneously. The spleenwas separated and distal colon was dissected. Total tissue RNA was isolated by the guanidinium thiocyanate-phenol-chloroform extraction method. RT-PCR technique was used to observe the expression of IL-1β andiNOSmRNA no Freund adjuvant.RESULTS IL-1β and iNOSmRNA were not detected in the spleen and colonic mucosa of NC rats, whilethey were significantly expressed in those of MC rats. IL-1β and iNOSmRNA were markedly lower in EF andHPM rats than those in MC rats. There were no significant difference in the levels of IL-1β and iNOSmRNAbetween EP and HPM rats. The amount of IL-1β and iNOSmRNA was nearly the same between the spleenand colon in different groups.CONCLUSION Acupuncture and moxibustion greatly inhibited the expression of IL-lβ and iNOSmRNA inthe ulcerative colitis rats.
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Chronic gastritis ( CG ) and peptic ulcer ( PU ) are frequently-occurring diseases. It is now well recognized that Helicobacter pylori (Hp) is a major factor that leads to CG and PU[1-8] In order to study the relationship among T lymphocyte subsets, NO, Hexosamine and Hp infection in patients with chronic gastric diseases, the levelsof blood T lymphocyte subsets, plasma NO and hexosamine in gastric mucosa were measured respectively in 30 patients with CG and 32 patients of PU + CG.
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AIM To study relationship of injury induced by nitric oxide, oxidation, peroxidation, lipoperoxidation with chronic cholecystitis. METHODS The values of plasma nitric oxide (PNO), plasma vitamin C (P-VC), plasma vitamin E ( P-VE ), plasma β-carotene ( P-β-CAR ), plasma lipoperoxides (P-LPO), erythrocyte superoxide dismutase (E-SOD), erythrocyte catalase (ECAT), erythrocyte glutathione peroxidase (E-GSHPx) activities and erythrocyte lipoperoxides (ELPO) level in 77 patients with chronic cholecystitis and 80 healthy control subjects were determined, differences of the above average values between the patient group and the control group and differences of the average values between preoperative and postoperative patients were analyzed and compared, linear regression and correlation of the disease course with the above determination values as well as the stepwise regression and correlation of the course with the values were analyzed. RESULTS Compared with the control group, the average values of P-NO, P-LPO, E-LPO were significantly increased ( P < 0.01 ), and of P-VC, P-VE, P-β-CAR, E-SOD, E-CAT and E-GSH-Px decreased ( P < O. 01 ) in the patient group. The analysis of the linear regression and correlation showed that with prolonging of the course, the values of P-NO, P-LPO and E-LPO in the patients were gradually ascended and the values of P-VC, P-VE, P-β-CAR, E-SOD, E-CAT and E-GSH-Px descended (P < 0. 01 ). The analysis of the stepwise regression and correlation indicated that the correlation of the course with P-NO, P-VE and P-β-CAR values was the closest. Compared with the preoperative patients, the average values of PNO, P-LPO and E-LPO were significantly decreased (P < 0.01 ) and the average values of PVC, E-SOD, E-CAT and E-GSH-Px in postoperative patients increased ( P < 0.01) in postoperative patients. But there was no significant difference in the average values of P-VE, P-W-CAR preoperative and postoperative patients. CONCLUSION Chronic cholecystitis could induce the increase of nitric oxide, oxidation, peroxidation and lipoperoxidation.
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一氧化氮调节大鼠主动脉平滑肌细胞基质金属蛋白酶的表达
血管重构是血管壁结构变化的活跃过程,主要包括细胞生长、迁移、死亡及细胞外基质(exrtacellular matrix,ECM)产生和降解等.腹主动脉瘤(abdominal aortic aneurysm,AAA)是血管重构的典型,其以血管平滑肌细胞(smooth muscle cell, SMC)减少ECM破坏及其水解酶基质金属蛋白酶(metalloproteinases,MMPs)表达增高为主要特征.一氧化氮(NO)作为重要的生物学分子,介导多种血管疾病的血管壁重构过程.我们前期研究已证实人AAA组织中诱生型一氧化氮合酶(inducible nitric oxide sythase,iNOS)的蛋白表达高于正常人腹主动脉,提示NO可能参与AAA的重构过程.本研究观察NO的生成变化对MMP表达的调节作用,为研究NO在AAA发病中的作用奠定体外实验基础.
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气体类神经递质与神经系统疾病
新发现的气体类神经递质一氧化碳(CO)和一氧化氮(NO)在神经系统疾病中的作用愈来愈受到重视.自20世纪90年代以来,由血红素氧合酶(HO)催化血红素分解代谢产生的内源性一氧化碳(CO),和由一氧化氮合成酶(NOS)催化精氨酸产生的一氧化氮(NO)的生物学研究取得了重要进展.近的研究表明,与NO分子结构类似的CO不仅是1种重要的信使分子,而且可能是1种新型的神经递质,与NO一道在神经系统参与了复杂的多种生理病理过程,这2种气体分子不仅在呼吸系统、心血管系统、免疫系统中发挥信使分子和递质的作用,也在神经系统疾病的病生理过程中起了重要的作用.
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正确认识呼出气一氧化氮对哮喘诊断与管理的临床价值
呼出气一氧化氮(exhaled nitric oxide,eNO)自1991年被发现后,经多年广泛而深入探索,近年学术界对其认识逐渐明朗,因此,充分了解哮喘患者eNO的改变,明确其临床定位,有助于正确地选择使用该技术,指导临床实际工作.
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吸入一氧化氮对肺硝基酪氨酸形成及肺泡细胞凋亡影响的实验研究
吸入一氧化氮(inhaled nitric oxide, iNO)可以选择性扩张肺血管,降低肺动脉压,改善肺通气血流比例,改善氧合,已成功应用于新生儿胎粪吸入综合征(meconium aspiration syndrome, MAS)的治疗[1].但一氧化氮(nitric oxide, NO)是一种活性小分子,与超氧阴离子(O-2)快速反应形成高毒性的过氧亚硝酸盐(peroxynitrite,ONOO-),具有潜在的过氧化损伤作用[2].
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呼出气体中的一氧化氮检测与哮喘
哮喘的病理基础是慢性气道炎症.支气管镜下支气管灌洗液和支气管内膜活检的方法是检测评估气道炎症的金标准,因其有创伤性和较高的花费使其很难成为哮喘儿童常用的检查方法.其他无创伤性的方法如外周血嗜酸细胞计数、尿白三烯E4(leukotriene-E4)的检测、痰诱导细胞分析等也被用来评价气道炎症的程度,但这些方法缺乏敏感性和特异性,操作费时费力.近来,对呼出气体中的成分,尤其是呼出气中一氧化氮浓度(fractional concentration of exhaled nitric oxide, FENO)的测定,常用来评估气道炎症.FENO可以直接检测并立即得出结果.
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Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol-lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was tablished by 0.5 mmol/L 3-morpholinosyndnomine (SIN-1), a nitric oxide donor. The models were then cultured with 0.1 mmol/L of 4,4’-di sothiocyanostilbene-2,2’-disulfonic acid (DIDS;the chloride channel blocker) for 18 hours. Neuronal survival was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining. Western blot analysis and immunoche-nescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins. Real-time PCR was used to detect the mRNA expression of CIC-3. The results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted ClC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-1. Our findings indicate that the increased activities of the ClC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.
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Amentoflavone is a natural biflavone compound with many biological properties, including anti-inlfammatory, antioxidative, and neuroprotective effects. We presumed that amentolfavone exerts a neuroprotective effect in epilepsy models. Prior to model establishment, mice were intragastrically administered 25 mg/kg amentoflavone for 3 consecutive days. Amentoflavone effectively prevented pilocarpine-induced epilepsy in a mouse kindling model, suppressed nu-clear factor-κB activation and expression, inhibited excessive discharge of hippocampal neurons resulting in a reduction in epileptic seizures, shortened attack time, and diminished loss and apoptosis of hippocampal neurons. Results suggested that amentolfavone protected hippocampal neurons in epilepsy micevia anti-inlfammation, antioxidation, and antiapoptosis, and then ef-fectively prevented the occurrence of seizures.
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ENOS(Efficacy of Nitric Oxide in Stroke)试验分中心招募
什么是ENOS试验?有证据表明,卒中后高血压与卒中的预后不良有关.目前尚无大型的临床随机对照试验能全面的评价在卒中急性期的血压管理.已经证实:作为急性卒中的二线治疗,NO(nitric oxide)能在多个环节作用于卒中,如降低血压、舒张脑血管、改善中枢和周围的血液动力学等等.
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缺氧预适应过程中的小鼠脑一氧化氮下调
Downregulation of nitric oxide in the brain of mice during their hypoxic preconditioning.J Appl Physiol 91:1193~1198,2001.An animal model of hypoxic preconditioning was produced in mice by repeated exposure to autohypoxic condition.The animals' tolerance times to hypoxia were 1.7,1.8,2.1 and 2.3 times longer in runs 2,3,4 and 5,respectively,than that in run 1,and their oxygen consumption and heart and respiration rates were progressively and significantly slowed down during the repetitive exposure to hypoxia.L-arginine concentration,nitric oxide (NO) synthase-positive cells,NO synthase activity,and NO content in the whole brain and the subregions telencephalon,diencephalons,and brain stem were significantly increased during the first exposure and were,instead of continuing to increase,significantly decreased in run 4 after the second and third exposure.Tolerance times under the hypoxic condition were significantly shortened and prolonged when preadministration of L-arginine and its analog,respectively,was made.These results indicate that NO in the brain is downregulated under condition of hypoxic preconditioning and negatively involved in increased tolerance to hypoxia.