神经生长因子对小鼠腹腔巨噬细胞释放一氧化氮的影响

目的 :研究神经生长因子对小鼠腹腔巨噬细胞释放一氧化氮的影响。方法 :Griess试剂检测小鼠腹腔巨噬细胞一氧化氮浓度。结果 :游离氨基酸浓度为0 73～5 83mg/ml的神经生长因子能显著抑制小鼠腹腔巨噬细胞一氧化氮释放。结论 :抑制一氧化氮释放可能是神经生长因子保护神经元的作用机制之一     

糖萜素对小鼠腹腔巨噬细胞产生一氧化氮的影响

目的:探讨糖萜素对小鼠腹腔巨噬细胞产生NO的影响。方法:在饲料中添加不同剂量糖萜素喂养NIH小鼠,以基础饲料为对照,检测环磷酰胺免疫抑制组与非抑制组不同时间段小鼠腹腔巨噬细胞产生NO的含量。结果:含糖萜素饲料组于不同时间测得NO含量均较基础饲料组显著增高(P<0.05)。免疫抑制状态下,含糖萜素饲料组NO含量也较基础饲料组高(P<0.05)。体外糖萜素不能直接影响NO的生成。结论:糖萜素能显著提高小鼠体内巨噬细胞产生NO。体外则不能直接影响NO的生成     

糖萜素对小鼠腹腔巨噬细胞产生一氧化氮的影响

目的：探讨糖萜素对小鼠腹腔巨噬细胞产生NO的影响。方法：在饲料中添加不同剂量糖萜素喂养NIH小鼠,以基础饲料为对照,检测环磷酰胺免疫抑制组与非抑制组不同时间段小鼠腹腔巨噬细胞产生NO的含量。结果：含糖萜素饲料组于不同时间测得NO含量均较基础饲料组显著增高（P＜0．05）。免疫抑制状态下,含糖萜素饲料组NO含量也较基础饲料组高（P＜0．05）。体外糖萜素不能直接影响NO的生成。结论：糖萜素能显著提高小鼠体内巨噬细胞产生NO。体外则不能直接影响NO的生成。     

神经生长因子对小鼠腹腔巨噬细胞神经胶质细胞释放一氧化氮的影响

目的研究神经生长因子(NGF)对正常小鼠、非肥胖性糖尿病小鼠(NOD小鼠)腹腔巨噬细胞、神经胶质细胞释放一氧化氮(NO)的影响。方法实验分对照组和不同浓度NGF实验组,NO试剂盒检测细胞培养液中NO浓度。结果①与正常小鼠相比,NOD小鼠巨噬细胞、神经胶质细胞NO释放量均明显增高(P<0.05)。②与各自对照组相比,正常小鼠、NOD小鼠各实验组巨噬细胞、神经胶质细胞NO释放量均减小。③不同浓度的NGF对小鼠巨噬细胞、神经胶质细胞释放NO的影响差异无统计学意义。结论NOD小鼠可以释放高水平的NO;NGF对正常小鼠、NOD小鼠离体培养的腹腔巨噬细胞、神经胶质细胞NO的释放有显著的抑制作用。     

库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮生成的影响

目的研究库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮(NO)生成的影响。方法用G riess法测定巨噬细胞一氧化氮的生成量。结果库拉索芦荟多糖在25～400μg/mL浓度范围可显著促进正常巨噬细胞的NO生成,在50～400μg/mL浓度范围可抑制LPS激活的巨噬细胞的NO生成。结论库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮的生成具有双向调节作用。     

库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮生成的影响

目的研究库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮(NO)生成的影响。方法用G riess法测定巨噬细胞一氧化氮的生成量。结果库拉索芦荟多糖在25~400μg/mL浓度范围可显著促进正常巨噬细胞的NO生成,在50~400μg/mL浓度范围可抑制LPS激活的巨噬细胞的NO生成。结论库拉索芦荟多糖对小鼠腹腔巨噬细胞一氧化氮的生成具有双向调节作用。     

灵芝多糖肽对小鼠腹腔巨噬细胞一氧化氮产生的影响

目的　研究灵芝多糖肽 (GLPP)对小鼠腹腔巨噬细胞一氧化氮产生的影响并探讨其作用机制。方法　以Griess法 ,观察GLPP对LPS诱导小鼠腹腔巨噬细胞一氧化氮(NO)产生的影响 ;以免疫组化法检测诱导型一氧化氮合成酶 (iNOS)的表达 ,观察GLPP对iNOS的影响。结果　GLPP(2 5～ 2 0 0mg·kg-1)灌胃给药 5d或体外给药 (3 12 5～ 2 0 0mg·L-1)均可促进巨噬细胞NO释放 ,但对LPS刺激NO的释放影响不大 ;GLPP(10 0mg·kg-1)灌胃给药 5d或体外给药 (10mg·L-1)均可使巨噬细胞iNOS含量增加。结论　GLPP可增加小鼠腹腔巨噬细胞NO产生 ,其机制可能与其促进巨噬细胞iNOS合成有关。     

雷公藤多甙抑制小鼠腹腔巨噬细胞产生一氧化氮

雷公藤多甙（ｐｏｌｙｇｌｙｃｏｓｉｄｅｏｆＴｒｉｐｔｅｒｙｇｉｕｍｗｉｌｆｏｒｄｉＨｏｏｋ．ｆ．,ＴＷＰ）临床广泛用于治疗类风湿性关节炎等多种自身免疫性疾病,既可抑制细胞免疫又可抑制体液免疫［１］．但其在免疫抑制过程中对一氧化氮合酶（ＮＯＳ）的影响却...     

天山雪莲培养物含药血清对大鼠腹腔巨噬细胞一氧化氮释放的影响

目的探讨天山雪莲培养物的含药血清对大鼠腹腔巨噬细胞一氧化氯（N0）释放的影响。方法采用血清药理学方法，灌胃给予天山雪莲培养物3g／kg体重。结果天山雪莲培养物和原药材的醇提物0．5h含药血清对腹腔巨噬细胞NO释放的影响类似，能够抑制活化的腹腔巨噬细胞NO释放，且天山雪莲培养物醇提物（TCSauⅠ）的作用优于原药材醇提物（WSauⅠ），而2h和4h的含药血清药效则有所差别。     

依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶的影响

目的探讨人工合成的植物雌激素依普拉芬对去卵巢大鼠血清一氧化氮及一氧化氮合酶合酶的影响。方法6个月龄雌性SD大鼠60只分为假手术组（10只SD大鼠）和去卵巢组（50只）;再将去卵巢大鼠分为阴性对照组,依普拉芬高、中、低剂量组和雌激素对照组（各10只）,分别给予基础饲料和不同剂量的依普拉芬,12周后测定血清NO及NOS。结果与假手术组相比,去卵巢大鼠阴性对照组血清NO及NOS明显降低,依普拉芬组高于阴性对照组,与假手术组比较差异无统计学意义。同时低于雌激素组。结论NO及NOS参与了骨质疏松的病理生理过程;依普拉芬可以通过提高去卵巢大鼠血清NO及NOS浓度达到防治绝经后骨质疏松症的作用。     

用一氧化氮光学生物传感器研究供体药物体外释放的通路

目的研究一氧化氮(NO)供体药物体外释放的通路。方法用自制NO光学生物传感器通过模拟硝普钠(SNP)释放NO的3种通路所需要的体外环境,测定了不同条件的生理溶液中SNP释放的NO。结果光照和巯基化合物是引起SNP体外释放NO的主要因素。在酸化的生理液中,NO在40.0~360.0μmol.L-1的浓度范围内,线性关系良好(r=0.9992),检测限为4.0μmol.L-1,日内精密度RSD=2.3%,日间精密度RSD=3.4%。干扰试验发现,L-Cys和L-GSH在中性环境下对CytC膜有干扰,但在酸性条件下无干扰。与经典方法Griess比色法比较,无显著性差异。结论所用生物传感器系统为NO供体药物的体外释放研究提供了一种较好的手段。     

Enhancement by nitric oxide of neurogenic contraction in the mouse urinary bladder

In isolated detrusor strips from the mouse urinary bladder, contractile responses to electrical field stimulation were mostly mediated by neurally released acetylcholine and ATP. The aim of this study is to investigate the possible role of nitric oxide (NO) involved in the neurogenic detrusor contraction. Repetitive electrical field stimulation evoked muscle contractions of the isolated mouse detrusor strips, which could be abolished by tetrodotoxin (TTX). NO donors including sodium nitroprusside (SNP) and S-nitroso-N-acetyl-penicillamine (SNAP) as well as exogenous NO increased, while hemoglobin and NO synthase inhibitor N^G-nitro-L-arginine decreased the neurogenic detrusor contractions. The addition of L-arginine reversed the inhibitory effect of N^G-nitro-L-arginine. SNP failed to affect the contractions induced by carbachol and α,β-methylene ATP. These findings suggest that NO potentiated the excitatory neuromuscular transmission in electrically stimulated detrusor strips from the mouse. Received: 15 July 1997 / Accepted: 4 September 1997     

一氧化氮及一氧化氮合酶在成年与老年大鼠前列腺中的变化

目的:研究一氧化氮(NO)及一氧化氮合酶(NOS)在成年与老年大鼠前列腺中的变化,探讨在大鼠前列腺老年化过程中的临床意义。方法:取4月龄及20月龄SD雄性大鼠各6只,分别取前列腺组织匀浆,检测其NO与NOS活性。结果:老年组大鼠的NO与NOS活性明显低于成年组(P<0.05)。结论:老年大鼠前列腺组织中NO水平及NOS活性的降低可能与前列腺良性增生及功能减退有关。     

Dynamic changes in NADPH-diaphorase staining reflect activity of nitric oxide synthase: Evidence for a dopaminergic regulation of striatal nitric oxide release

In fixed tissue, neuronal NADPH-diaphorase staining results from nitric oxide synthase (NOS) activity. Neuronal NOS only synthesizes nitric oxide once activated by the binding of Ca²⁺/calmodulin. We show here that neuronal NADPH-diaphorase staining is also dependent on Ca²⁺/calmodulin, implying that only activated NOS is detected. In addition, in bovine pulmonary endothelial cells, carbachol and bradykinin dramatically and rapidly increase the intensity of NADPH-diaphorase staining. Furthermore, administration of MK801, an NMDA antagonist, decreases neuronal NADPH-diaphorase staining. This suggests that the intensity of the NADPH-diaphorase staining is related to the level of enzyme activation at the moment of tissue fixation. The potential of exploiting this observation to detect cellular activation of NOS is illustrated by the observations that the intensity of NADPH-diaphorase staining in rat striatal neurones is decreased following systemic treatment with the D1-like dopamine receptor antagonist SCH23390, and increased by the D2-like antagonist eticlopride. These results therefore provide strong evidence that the NADPH-diaphorase reaction can be used to monitor NOS activity at a cellular level of resolution, and reveal a dopaminergic regulation of NOS activity in the striatum mediated by D1-like and D2-like dopamine receptors.     

Inhibition of lipopolysaccharide-induced inducible nitric oxide (iNOS) mRNA expression and nitric oxide production by higenamine in murine peritoneal macrophages

Nitric oxide synthesized by inducible nitric oxide synthase (iNOS) has been implicated as a mediator of inflammation in rheumatic and autoimmune diseases. The effects of higenamine, a tetrahydroisoquinoline compound, on induction of NOS by bacterial lipopolysaccharide (LPS) were examined in murine peritoneal macrophages. LPS-induced nitrite/nitrate production was markedly inhibited by higenamine which at 0.01 mM, decreased nitrite/nitrate levels by 48.7+/-4.4%. This was comparable to the inhibition of LPS-induced nitrite/nitrate production by tetrandrin (49.51+/-2.02%) at the same concentration. Northern and Western blot analysis of iNOS expression demonstrated that iNOS expression was significantly attenuated following co-incubation of peritoneal macrophages with LPS (10 microg/ml; 18 hrs) and higenamine (0.001, 0.01 mM; 18 hrs). These results suggest that higenamine can inhibit LPS-induced expression of iNOS mRNA in murine peritoneal macrophages. The clinical implications of these findings remain to be established.     

The effects of extended nitric oxide release on responses of the human non-pregnant myometrium to endothelin-1 or vasopressin

BackgroundUterotonic mediators: endothelin-1 (ET-1), arginine vasopressin (AVP), and nitric oxide (NO) play important roles in the regulation of uterine contractility. We hypothesize that NO affects both ET-1 or AVP. Therefore, this study investigated the involvement of extended exogenous NO release in the regulation of responses of the human non-pregnant myometrium to ET-1 and AVP.MethodsSpecimens were obtained from 10 premenopausal women, undergoing hysterectomy for benign gynecological disorders. Responses of the myometrial strips to ET-1 or AVP in the absence and presence of an exogenous NO donor (diethylenetriamine; DETA/NO; 10⁻⁴ mol/L) were recorded under isometric conditions. To inhibit endogenous NO, a competitive inhibitor of NO synthase, L-N^G-nitroarginine (L-NNA) was added to the organ bath.ResultsET-1 enhanced the spontaneous contractile activity of the myometrium more powerfully (p < 0.01) than AVP. Preincubation with exogenous NO weakened ET-1- or AVP-induced increases in this contractile activity (p < 0.05). However, unexpected results were obtained after preincubation with L-NNA and with DETA/NO then added. Both ET-1 and AVP induced augmented contractile effects in almost all concentrations compared with the responses to these peptides alone or after NOS synthase inhibition (both p < 0.01).ConclusionsThis study demonstrated for the first time that extended incubation with a NO donor influences the uterine muscle response evoked by ET-1 and AVP. Both endogenous and exogenous NO is involved in the control of the uterine responses to ET-1 or AVP of non-pregnant myometrium. Furthermore, both peptides stimulate increased uterine contractility when the local imbalance between the constrictive and relaxing mediators takes place.     

吸入NO对高原人体运动后血液流变学的影响

探讨外源性一氧化氮 (NO)吸入对高原人体运动后血液流变学的影响。方法 :对进驻海拨 41 0 0m高原 2 0天的 2 0名健康青年随机分为吸入NO ( 1 0ppm)组和对照组 (口服炒面胶囊 ) ,每组 1 0人。在吸入NO前、吸入NO 6天后踏阶运动前后分别检测血中红细胞压积 (HCT)、血液粘度 ( ηb)、血浆粘度( ηp)、还原粘度 ( ηr)、红细胞刚性指数(IR)、红细胞变形系数 (TK)、红细胞聚集系数 (VAI)及血栓形成系数 (TFL)含量。结果 :吸入NO前运动后较运动前 ,对照组和吸入NO组HCT、ηb、ηp、ηr、IR、TK、VAI、TFL均降低 (P <0 0 5或 0 0 1 ) ;吸入NO后运动后较运动前对照组各指标均降低 ,吸入NO组HCT、ηb、ηp、ηr、TK、VAI降低 (P<0 0 5或 0 0 1 ) ,IR、TFL无统计学意义 (P>0 0 5)。运动前及运动后吸入NO后较吸入前 ,对照组均无统计学差异 (P >0 0 5) ;吸入NO组运动前吸入后较吸入前ηb、ηp、IR降低

0 0 5)。结论 :吸入低浓度NO对运动机体可发挥有效的保护作用