妊娠早期小鼠卵巢、输卵管及子宫内诱导型一氧化氮合酶的分布

目的　了解胚泡着床前后妊娠昆明系小鼠卵巢、输卵管及子宫内诱导型一氧化氮合酶 (inducible ni-tric oxide synthase,i NOS)的分布。　方法　免疫细胞化学 L SAB法。　结果　妊娠 2～ 5 d小鼠的卵巢内 ,黄体细胞上有 i NOS的阳性表达 ;输卵管粘膜上有 i NOS的分布 ,肌层则为阴性 ;妊娠 2、3d的小鼠子宫内 ,阳性标记主要出现在子宫内膜上皮以及子宫内膜中的子宫腺上皮 ,内膜基质细胞为阴性 ;妊娠 4d的子宫内 ,子宫腺及蜕膜部分均有 i-NOS的分布 ,妊娠 5 d时 ,在小鼠胚泡的表面也检测到了 i NOS的存在。　结论　小鼠胚泡着床前后 ,在其卵巢、输卵管及子宫内均有 i NOS的存在 ,提示 i NOS在小鼠胚胎早期发育及着床过程中起作用。     

SA-30诱导的小鼠子宫内诱导型一氧化氮合酶的变化

目的　检测精子膜抗原 SA- 30对小鼠子宫内诱导型一氧化氮合酶 (i NOS)含量及分布的影响 ,从而了解 SA - 30的抗生育机制。　方法　 SA- 30免疫雌性昆明小鼠后 ,应用免疫组织化学方法 ,对子宫内的 i NOS进行了检测。结果　 SA - 30免疫后对间情期小鼠子宫内的 i NOS没有明显影响 ,无论是免疫组还是对照组 ,在子宫内膜基质中均有大量阳性细胞分布 ,两者无明显差异 ;在妊娠第 3d时 ,对照组的小鼠子宫中有较多 i NOS表达 ,阳性标记主要集中在内膜上皮及固有膜中的子宫腺上 ,经 SA- 30免疫的小鼠子宫中 ,i NOS表达则显著减少 ,整个内膜标记极弱 ,只在子宫肌层内有少量 i NOS阳性细胞分布。　结论　 SA - 30可能通过使妊娠早期小鼠子宫内 i NOS表达显著减少 ,而影响小鼠胚胎植入及早期胚胎的发育     

一氧化氮合酶在大鼠附睾内的表达及其可能的作用

目的　为了阐明一氧化氮合酶 (NOS)在附睾内的表达 ,同时探讨NO在男性生殖功能中的作用。方法　本研究采用正常大鼠附睾组织 ,用免疫组织化学ABC法研究两种NOS(iNOS、eNOS)的表达。结果　在附睾上皮细胞内eNOS及iNOS均为免疫反应阳性 ,其中eNOS表达强 ,iNOS表达较强 ,血管内皮及平滑肌细胞内仅为eNOS免疫反应阳性 ,附睾间质中仅iNOS为免疫反应阳性。结论　两种NOS在附睾内均有不同程度的表达 ,各有特定的分布区域 ,提示NOS与附睾的功能密切相关     

妊娠早期小鼠卵巢,输卵管及子宫内诱导型一氧化氮合酶的分析

目的 了解胚泡着床前后妊娠昆明系小鼠卵巢、输卵管及子宫内诱导型一氧化氮合酶（ｉｎｄｕｃｉｂｌｅ ｎｉｔｒｉｃ ｏｘｉｄｅ ｓｙｎｔｈａｓｅ,ｉＮＯＳ）的分布。方法 免疫细胞化学ＬＳＡＢ法。结果 妊娠２～５ｄ小鼠的卵巢内,黄体细胞上有ｉＮＯＳ的阳性表达;输卵管粘膜上有ｉＮＯＳ的分布,肌层则为阴性;妊娠２、３ｄ的小鼠子宫内,阳性标记主要出现在子宫内膜上皮以及子宫内膜中的了宫腺上皮,内膜基质细胞为阴性;妊娠４ｄ的子宫内,子宫腺及蜕膜部分均有ｉＮＯＳ的分布,妊娠５ｄ时,在小鼠胚泡的表面也检测到了ｉＮＯＳ的存在。结论 小鼠胚泡着床前后,在其卵巢、输卵管及子宫内均有ｉＮＯＳ的存在,提示ｉＮＯＳ在小鼠胚胎早期发育及着床过程中起作用。     

雌孕激素与子宫内膜的一氧化氮合酶

NO(NitricOxide) /NOS(NitricOxideSynthase)在雌性生殖生理功能方面如卵泡发育、激素分泌、胚胎着床、维持妊娠、促进分娩及内膜周期性变化、细胞凋亡等方面都具有重要作用。有关子宫内膜NOS的表达及调控机制仍存在异议。三种NOS神经型NOS(neuronalNOS ,nNOS)、内皮型NOS(endothelialNOS ,eNOS)和诱导型NOS(inducibleNOS ,iNOS)在内膜不同部位和时期呈强弱不等的表达 ,生理作用也不尽相同 ,且与雌孕激素对内膜的调节 ,内膜周期性变化关系密切。本文就NOS在子宫内膜的活性表达及其与雌孕激素关系的研究进行综述。     

肝癌组织中诱导型一氧化氮合酶的表达及其与血管形成、bcl-2和细胞增生的关系

一氧化氮合酶 (NOS)是NO合成的关键限速酶 ,它的生物学活性直接决定着NO的合成量。NOS有两个异构体 ,即结构型NOS(cNOS)和诱导型NOS(iNOS)。通常iNOS与肿瘤的免疫相关 ,且产生NO的能力较cNOS高出 10 0～ 10 0 0倍。NOS活性的增高与肿瘤血管形成关系密切[1] 。另有研究显示 ,iNOS产生的NO可通过bcl 2介导途径抑制细胞凋亡并有利于生长停止的肿瘤细胞的存活[2 ] 。我们采用免疫组织化学法检测肝细胞性肝癌中iNOS、血管内皮生长因子(VEGF)、CD34标记的微血管密度 (MVD)及凋亡相关蛋白bcl 2和p5 3蛋白的表达。同时应用流式…     

睾丸一氧化氮合酶与雄性生殖

一氧化氮合酶 (nitricoxidesynthase ,NOS)在NADPH(还原型辅酶Ⅱ )存在下催化L -精氨酸分解生成一氧化氮(nitricoxide,NO)。NOS有以下几种形式 :神经型NOS(nNOS) ,诱导型NOS(iNOS) ,内皮型NOS(eNOS)。NO是目前研究最多的体内信息分子和效应分子 ,广泛存在于人体的心血管系统、神经系统、消化系统、免疫系统、生殖系统等。NOS和NO对生殖活动的作用已被广泛研究 ,如对睾丸微循环的调解 ,参与睾酮分泌 ,调解精子活动等。本文对睾丸NOS/NO与雄性哺乳动物生殖关系的研究进展作一概述。     

内源性一氧化氮在急性高原病中的研究进展

1一氧化氮(nitric oxide,NO)与内源性一氧化氮(endogenous NO,eNO) NO是具有调节血管张力、血流等众多生物学作用的脂溶性气体信号分子,eNO是由L-精氨酸(L-arginine,L-Arg)经过体内一氧化氮合酶[nitric oxide synthase,NOS;主要有神经源型(neuronal NOS,nNOS)、诱导型(inducible NOS,iNOS)和内皮源型(endothelial NOS,eNOS)3种]催化合成的,广泛存在于全身组织[1].NO通过一些生物分子和细胞间相互作用参与机体的保护、调节及逆转等生理过程[2].近年来的研究发现NO在调节血管张力、抑制炎症以及抗动脉粥样硬化中发挥关键作用[1-2].     

兔急性上颌窦炎早期一氧化氮合酶的表达及意义

目的 :探讨一氧化氮合酶 (NOS)在兔急性上颌窦炎 (AMS)窦粘膜中的表达及其意义。方法 :健康新西兰白兔 36只 ,分为空白、阴性对照组和AMS组。通过阻塞窦口并注入 1.0ml的肺炎链球菌悬液 (10 9CFU)建立AMS模型 ,观察时间点为自手术第 5、10天。应用黄递酶———NADPH组织化学技术 ,以NADPH脱氢酶特异性测定NOS在空白、阴性对照组和AMS组兔上颌窦粘膜中的分布及不同时间点AMS组NOS活性表达。结果 :正常和急性上颌窦炎兔窦粘膜酶化学染色均有反应 ,主要分布于粘膜上皮、血管内皮和腺体细胞 (染色程度与正常组相比 ,P<0 .0 5或P <0 .0 1)。结论 :正常兔上颌窦粘膜存在NOS ,一氧化氮 (NO)与上颌窦急性炎症有关 ,炎症时NOS活性明显增高 ,过多的NO会对组织或细胞产生损伤 ,提示NO在AMS发病机制中有重要意义     

败血症休克大鼠血管L-精氨酸/一氧化氮途径的变化

目的:观察败血症休克大鼠主动脉内膜、中膜和外膜一氧化氮合成途径的改变。方法:雄性Wistar大鼠盲肠结扎并穿孔复制败血症休克模型,分别测定假手术组、早期休克组和晚期休克组大鼠主动脉内膜、中膜和外膜的亚硝酸盐(NO^-₂)含量、一氧化氮合酶(NOS)活性及L-精氨酸(L-Arg)转运;免疫组化染色检测诱导型一氧化氮合酶(iNOS)在主动脉各层的分布。结果:早期及晚期败血症休克大鼠主动脉内膜产生的NO^-₂含量、NOS活性及L-Arg转运速率均低于假手术组,而中膜和外膜的NO^-₂、NOS活性及L-Arg转运速率则显著高于假手术组,外膜增加的程度尤为显著。免疫组织化学染色显示,败血症休克时血管中膜和外膜尤其是外膜iNOS阳性染色明显较强。结论:败血症休克时血管内膜NO合成受到抑制,而中膜和外膜NO合成显著增强,这一改变与休克状态下血管中L-Arg转运、iNOS表达及其活性的变化有关。     

Role of nitric oxide in implantation and menstruation

Nitric oxide (NO) is a major paracrine mediator of various biological processes, including vascular functions and inflammation. In blood vessels, NO is produced by the low-input constitutive endothelial NO synthase (eNOS) and is a potent vasodilator and platelet aggregation inhibitor. The inducible NOS isoform (iNOS) is capable of producing NO at high concentrations which have pro-inflammatory properties. Immunohistochemical and molecular studies of endometrial NOS expression, as well as animal experiments with NOS inhibitors, indicate that NO plays an important role in endometrial functions such as endometrial receptivity, implantation and menstruation. In rodents, both iNOS and eNOS are highly up-regulated in the implantation sites, and NOS inhibitors show synergistic effects with antiprogestins in inhibiting the establishment of pregnancy. In the human endometrium, eNOS have been localized in the glandular epithelium and in endometrial microvascular endothelium, primarily during the luteal phase. iNOS has been found in the endometrial epithelium during menstruation, in immunocompetent endometrial cells, and in decidualized stromal cells. In primates, NO may be involved in the initiation and maintenance of menstrual bleeding by inducing tissue breakdown and vascular relaxation as well as by inhibiting platelet aggregation. Endometrium-derived NO may also play a role in myometrial relaxation during menstruation. These studies open up new applications for NO-donating and -inhibiting agents in uterine disorders. NO donors may be useful in the treatment of dysmenorrhoea and for promoting fertility. Antiprogestins, progesterone receptor modulators and iNOS inhibitors may find applications in the treatment and prevention of abnormal uterine bleeding.     

Nitric Oxide Synthase in Human Parathyroid Glands and Parathyroid Adenomas

Nitric oxide (NO) is a novel gaseous intercellular transmitter thought to play important physiological roles in the regulation of blood flow and hormone secretion in, for example, the pituitary, the thyroid, and the endocrine pancreas. Whether nitric oxide synthase (NOS) is present in the human parathyroid glands has not yet been demonstrated. In the present study, histologically normal, but functionally suppressed human parathyroid glands and parathyroid adenomas from patients with primary hyperparathyroidism were investigated by immunocytochemistry with antibodies against neuronal NOS and by reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry. We also used H&E to identify the NOS-immunoreactive cells. Immunocytochemistry demonstrated the presence of neuronal-type NOS in a subpopulation of glandular cells, identified as oxyphilic cells, in both normal parathyroid glands and adenomas. NADPH-diaphorase staining visualized NOS in the endothelium of blood vessels and in glandular cells, corresponding to those containing immunoreactive NOS. In addition, we found NADPH-diaphorase staining in many chief cells. Our results indicate that both glandular cells and vascular endothelium in human parathyroid glands and adenomas express NOS. There is thus a morphological substrate for locally produced NO that may be involved in the regulation of parathyroid blood flow and hormone secretion.     

Cell-specific expression and immunolocalization of nitric oxide synthase isoforms and soluble guanylyl cyclase α and β subunits in postnatal porcine uteri

The aim of the present study was to investigate the cellular expression and immunolocalization of nitric oxide synthase (NOS) isoforms and soluble guanylyl cyclase (sGC) subunits in postnatal porcine uteri. Immunohistochemical experiments showed that three isoforms of NOS were mainly localized in the uterine luminal and glandular epithelium and myometrium, and the intensity of immunostaining for iNOS and eNOS was increased gradually with temporal development of the postnatal uterus. In addition, sGC subunits, sGCα1 and β, were present in the uterine luminal and glandular epithelium, myometrium and stromal cells. The uterine NOS activity data showed that the total NOS and iNOS activities were significantly increased at postnatal days 21 and 35. Although constitutive NOS activity was increased at postnatal day 21, it decreased subsequently at postnatal day 35. Immunoblot analysis revealed that iNOS protein expression was significantly increased at postnatal days 21 and 35. Furthermore, sGCα1 protein expression was not significantly changed throughout days 7 to 35. Collectively, our findings suggest that NO/cGMP signaling is involved in the process of postnatal porcine uterine development.     

Nitric oxide in the endometrium

Nitric oxide (NO) is an important mediator of paracrine interactions, especially within the vascular system. It is a powerful inhibitor of platelet aggregation and a potent vasodilator. NO is also a neurotransmitter and it plays a role in cell-mediated cytotoxicity. NO-generating enzymes (nitric oxide synthases, NOS) have been described in the endometrium of a number of species, suggesting that NO might be involved in endometrial function. In human endometrium, endothelial NOS and inducible NOS have been localized to glandular epithelium in the non-pregnant uterus. Weak inducible NOS immunoreactivity has been observed in decidualized stromal cells. NO might participate in the initiation and control of menstrual bleeding. Furthermore, it may play a part in the inhibition of platelet aggregation within the endometrium, where menstrual haemostasis is thought to occur primarily by vasoconstriction rather than clot organization. Endometrially derived NO could also suppress myometrial contractility. Recent attention has focused on the part that NO might play in maintaining myometrial quiescence during pregnancy. NO also appears to relax the non-pregnant myometrium, an action which could be exploited for the medical treatment of primary dysmenorrhoea.     

一氧化氮、一氧化氮合酶和心脏功能

一氧化氮合酶(nitric　oxide synthase,NOS)催化L-精氨酸的氧化反应生成L-胍氨酸和一氧化氮(nitric oxide,NO)。其产物NO可通过依赖cGMP(环磷酸鸟苷)途径与非依赖cGMP途径发挥其复杂的生理学功能,如在心血管系统具有维持血管张力、调节血压,抑制血管平滑肌细胞迁移、增生,抑制血小板聚集与白细胞对血管壁的粘附以及调节影响心肌收缩与舒张功能的作用,并参与心率变异调节功能。本文就3种NOS同工酶的基因及其基因表达调节及影响因素进行简要综述。着重介绍nNOS1的心脏自主神经调节机制,iNOS对心脏收缩抑制以及心脏保护与损伤的双重作用,并对eNOS参与心功能调节的机制及其它生理、病理学等方面研究进展进行综述。     

大鼠主动脉内膜球囊剥脱后再生内皮细胞表型改变的研究

目的 探索大鼠主动脉内膜球囊剥脱后,内皮修复过程中再生内皮细胞结构和功能的改变,方法 大鼠主动脉内膜球囊剥脱２周和６周对内膜进行形态学观察,同时测定血管反应性,亚硝酸盐量和ＮＯＳ的活性,结果：剥脱２周和６周后,再生内皮细胞不仅结构与正常内皮细胞不同,而且血管再生内皮依赖性舒张反应９减弱,ＮＯ的释放减少,血管组织ｉＮＯＳ和ｃＮＯＳ活性均比正常降低,剥脱６周后的ｉＮＯＳ比剥脱２周时有所增加,但ｃＮＯＳ     

The expression and activity of renal nitric oxide synthase and circulating nitric oxide in polycystic kidney disease rats

Nitric oxide (NO) influences tubular fluid and electrolyte transport, and hence possibly also fluid accumulation in renal cysts. The expression and activity of intrarenal constitutive NO synthase (cNOS) [neuronal NOS, nNOS and endothelial NOS, eNOS] and inducible NOS (iNOS) and plasma nitrite/nitrate (PNOx) concentration were assessed in homozygous Han:SPRD polycystic kidney disease (PKD) rats (cy/cy), heterozygous Han:SPRD PKD rats (cy/+), homozygous normal Han:SPRD littermates (+/+) and Sprague Dawley rats (sd). The results showed: 1) nNOS expression was decreased in proximal tubules and thick ascending limbs of the loop of Henle in cy/cy and cy/+ rats compared to +/+ and sd rats (p<0.05). nNOS was weakly expressed in the epithelium of small cysts and unexpressed in epithelium of large cysts. 2) iNOS expression was increased in proximal tubular epithelial cells in cy/+ rats compared to +/+ rats and sd rats (p<0.01). iNOS expression in cyst epithelium was decreased in cy/+ rats (p<0.05) and absent in cy/cy rats. 3) eNOS expression was similar in the endothelium of intrarenal arteries in all groups. 4) The activity of renal cNOS was decreased in cy/cy and cy/+ rats; the activity of iNOS was decreased only in cy/cy rats, with no significant difference among the other three groups. 5) PNOx concentration was higher in cy/cy rats than in the other three groups, and correlated positively with plasma creatinine and urea. In conclusion, NOS expression and activity decreased as cysts developed, suggesting that NO downregulation is involved in the pathogenesis of PKD.