Distribution of nitric oxide synthase in stomach myenteric plexus of rats

AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus. METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique. RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus.The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62+/-38 cells mm(2) (antrum), 43+/-32 cells/mm(2) (body), and 32+/-28 cells mm(2) (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels. CONCLUSION: Nitric oxide might be involved in the modulation of motility, secretion and blood circulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach.

Distribution of constitutive nitric oxide synthase in the jejunum of adult rat

AIM: To study the distribution of the constitutive nitric oxide synthase (NOS) in the jejunum of adult rat. METHODS: The distribution of endothelial NOS (eNOS) was detected by immunohistochemistry. Immunofluorescence histochemical dual staining technique were used for studying the distribution of neuronal NOS (nNOS) and eNOS. The dual stained slides were observed under a confocal laser scanning microscope. RESULTS: Positive neuronal NOS (nNOS) and endothelial NOS (eNOS) cells were found to be distributed in lamina propria of villi, and the epithelial cell was not stained. eNOS was mainly located in submucosal vascular endothelia, while nNOS was mainly situated in myenteric plexus. Some cells in the villi had both nNOS and eNOS. More than 80% of the cells were positive for both nNOS and eNOS, the rest cells were positive either for nNOS or for eNOS. CONCLUSION: The two constitutive nitric oxide synthases are distributed differently in the jejunum of rat. nNOS distributed in myenteric plexus is a neurotransmitter in the non-adrenergic non-cholinergic (NANC) inhibitory nerves. eNOS distributed in endothelial and smooth muscle cells of blood vessels plays vasodilator role. eNOS and nNOS are coexpressed in some cells of lamina propria of villi. NO generated by those NOS is very important in the physiological and pathological process of small intestine.

Effect of diabetes and insulin treatment on nitric oxide synthase content in rat corpus cavemosum

Aim: To study the effect of diabetes mellitus and insulin treatment on rat penile nitric oxide synthase content.Methods: Male Wistar rats were divided at random into two groups: the Control (n = 8) and the Diabetic (n =17). Diabetes mellitus was induced by intraperitoneal injection of streptozotocin. The diabetic animals were then ran-domly divided into two subgroups; diabetic rats without insulin treatment (n = 7) and diabetic rats with insulin treat-ment (n = 10). The neuronal nitric oxide synthase (nNOS) in the penile corpus cavernosum were assayed by immumo-histochemical staining with specific antibody to nNOS and the nNOS-positive nerve fibers were counted semiquantita-tively under a high power microscope. Results: The nNOS- positive nerve fibres in diabetic rats with treatment washigher than that in diabetic rats without treatment ( P < 0.05) and lower than that in the controls ( P < 0.01). ThenNOS-positive nerve fibres in diabetic rat without treatment were also lower than that in the controls ( P < 0.01). Con-clusion; In streptozotocin-induced diabetic rats, the nNOS content in the penile corpus cavernosum was significantlydecreased. Insulin treatment at the dose level employed partially restores the penile nNOS content in these rats.

EFFECT OF RADIX SALVIAE MILTIORRHIZAE ON THE GENE EXPRESSION OF NITRIC OXIDE SYNTHASE IN ISCHEMIC RAT BRAINS

The effect of Radix Salviae Miltiorrhizae (RSM) on the gene expression of nitric oxide synthase (NOS) in rat brains during ischemia was studied with in situ hybridization and the results were analyzed with IBAS 2000 Image Analysis System. It was found that NOS gene expression of cerebral cortex and caudate-putamen was markedly increased in 24 hours in ischemia group (P

Effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats

AIM: To investigate the effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats. METHODS: Rats with cirrhosis induced by carbon tetrachloride were randomly divided into two groups, one n =13 receiving 0.5mg.kg(-1) per day of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, for 10 days, whereas the other group (n =13) and control (n =10) rats were administrated the same volume of 9g.L(-1) saline. Half gastric emptying time and 2h residual rate were measured by SPECT, using (99m)Tc-DTPA-labeled barium sulfate as test meal. Gastrointestinal transition time was recorded simultaneously. Serum concentration of nitric oxide (NO) was determined by the kinetic cadmium reduction and colorimetric methods. Immunohistochemical SABC method was used to observe the expression and distribution of three types of nitric oxide synthase (NOS) isoforms in the rat gastrointestinal tract. Western blot was used to detect expression of gastrointestinal NOS isoforms. RESULTS: Half gastric emptying time and trans-gastrointestinal time were significantly prolonged(124.0 +/- 26.4 min; 33.7 +/- 8.9 min; 72.1 +/- 15.3 min; P【0.01), (12.4 +/- 0.5h; 9.5 +/- 0.3h; 8.2 +/- 0.8h; P【0.01), 2h residual rate was raised in cirrhotic rats than in controls and cirrhotic rats treated with L-NAME (54.9 +/- 7.6%,13.7 +/- 3.2%, 34.9 +/- 10.3%, P【0.01). Serum concentration of NO was significantly increased in cirrhotic rats than in the other groups (8.20 +/- 2.48) micromol.L(-1), (5.94 +/-1.07) micromol.L(-1) and control (5.66 +/- 1.60 micromol.L(-1), P【0.01. NOS staining intensities which were mainly located in the gastrointestinal tissues were markedly lower in cirrhotic rats than in the controls and cirrhotic rats after treated with L-NAME. CONCLUSION: Gastrointestinal motility was remarkably inhibited in cirrhotic rats, which could be alleviated by L-NAME. Nitric oxide may play an important role in the inhibition of gastrointestinal motility in cirrhotic rats.

Effects of endogenous nitric oxide induced by 5-fluorouracil and L-Arg on liver carcinoma in nude mice

AIM： To study the effects of endogeous nitric oxide induced by 5-fluorouracil （5-FU） and L-arginine （L-Arg） on the human liver carcinoma model in nude mice. METHODS： The human liver carcinoma model in nude mice was established with BEL-7402 cells and normal saline （NS）, 5-FU and 5-FU ＋ L-Arg injected intraperitoneally. The tumor size was measured. The necrotic degree and range were observed under microscope. The apoptosis of cancer cell was detected by turmina deoxynucleotidyl transferanse mediated dUTP nick end labeling （TUNEL） method. Immunohistochemical method was performed to determine the expression of iNOS, P16, BAX. The chemical colorimetry was used to test the activity and nitrate reductase method was adopted to test the concentration of nitric oxide （NO） in the tumor tissue. The BI2000 pathological image analyzer was used to analyze the result of immunohistochemistry. RESULTS： 5-FU combined with L-Arg could inhibit the tumor growth apparently. In NS, 5-FU and 5-FU＋L- Arg groups, the changes of tumor volumes were 257.978 ± 59.0, 172.232 ± 66.0 and 91.523 ± 26.7 mm3, respectively （P 〈 0.05 5-FU vs 5-FU ± L-Arg group;P 〈 0.05 NS ys 5-FU ± L-Arg group; P 〈 0.05, NS ys 5-FU group）. The necrotic range and apoptosis index were significantly increased after the drug injection. The necrotic range was biggest in 5-FU ＋ L-Arg group （X^2= 15.963, P 〈 0.05）. The apoptosis indexes were as follows： NS, 17.4% ± 6.19%; 5-FU, 31.3% ± 12.3%; and 5-FU ± L-Arg, 46% ± 15.24% （P 〈 0.05, 5-FU ys 5-FU ± L-Arg; P 〈 0.05, NS ys 5-FU ± L-Arg; P 〈 0.05, NS ys 5-FU）. The expression and activity of iNOS were increased in the tumor tissue. The concentration of NO was also increased. F of opticaldensity of iNOS, iNOS activity and NO concentration are 31.693, 21.949, and 33.909, respectively, P 〈 0.05. The concentration of NO was related to the expression of PI6 and BAX. The correlation coefficient was 0.764 and 0.554. CONCLUSION： 5-FU combined with L-Arg can inhibit the growth of tumor in nude mice. The effect may be related to inducing the synthesis and increasing the activity of iNOS. The production of NO is increased, and it can enhance the expression of apoptosis-related gene and antioncogene.

Effects of aminoguanidine on nitric oxide production induced by inflammatory cytokines and endotoxin in cultured rat hepatocytes

AIM: To study the effects of aminoguanidine (AG) and two L-arginine analogues N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-nitro-L-arginine (L-NNA) on nitric oxide (NO) production induced by cytokines (TNF-alpha, IL-1 beta, and IFN-gamma) and bacterial lipopolysaccharide (LPS) mixture (CM) in the cultured rat hepatocytes, and examine their mechanisms action. METHODS: Rat hepatocytes were incubated with AG, L-NAME, L-NNA, Actinomycin D (ActD) and dexamethasone in a medium containing CM (LPS plus TNF-alpha, IL-1 beta, and IFN-gamma) for 24h. NO production in the cultured supernatant was measured with the Griess reaction. Intracellular cGMP level was detected with radioimmunoassy. RESULTS: NO production was markedly blocked by AG and L-NAME in a dose-dependent manner under inflammatory stimuli condition triggered by CM in vitro. The rate of the maximum inhibitory effects of L-NAME (38.9%) was less potent than that obtained with AG(53.7%, P 【 0.05). There was no significant difference between the inhibitory effects of AG and two L-arginine analogues on intracellular cGMP accumulation in rat cultured hepatocytes. Non-specific NOS expression inhibitor dexamethasone (DEX)and iNOS mRNA transcriptional inhibitor ActD also significantly inhibited CM-induced NO production. AG(0.1 mmol x L(-1)) and ActD (0.2 ng x L(-1)) were equipotent in decreasing NO production induced by inflammatory stimuli in vitro, and both effects were more potent than that induced by non-selectivity NOS activity inhibitor L-NAME (0.1 mmol x L(-1)) under similar stimuli conditions (P【0.01). CONCLUSION: AG is a potent selective inhibitor of inducible isoform of NOS,and the mechanism of action may be not only competitive inhibition in the substrate level, but also the gene expression level in rat hepatocytes.

Nitric oxide synthase gene expression in injured spinal cord tissue

OBJECTIVE: To investigate gene expression of three nitric oxide synthase isozymes in injured spinal cord tissue. METHODS: Thirty-six adult SD rats were randomly divided into six groups: a normal group and five injury groups, with six per each group. Animals in the injury groups were sacrificed at 2, 6, 12, 24, 48 h after injury. A compression injury model on the spinal cord was made according to Nystrom B et al and gene expression of the three NOS isozymes were examined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Gene expression of nNOS and eNOS were detectable in the normal group and were up-regulated quickly after injury, reaching a maximum at 6 h: (0.633 +/- 0.012) and (1.236 +/- 0.207). Gene expression of iNOS was detectable only in the injury groups and it was gradually up-regulated after injury, reaching a maximum at 24 h: (1.043 +/- 0.049). CONCLUSION: Injury to the spinal cord leads to early up-regulation of cNOS and late up-regulation of iNOS. Different NOS isozymes may play different roles in secondary spinal cord injury.

柴术理胃饮对功能性消化不良大鼠脑-肠轴功能及胃肠动力的影响

目的观察柴术理胃饮对功能性消化不良(FD)大鼠脑-肠轴功能及胃肠动力的影响。方法通过矿场实验选取SPF级雄性Sprague-Dawley大鼠60只,其中50只采用郭氏夹尾刺激法+慢性疲劳+饮食失节的多重因素造模方法制备FD肝郁脾虚模型。造模成功后随机分为模型组、柴术理胃饮低、中、高剂量组和多潘立酮组,每组10只,并给予不同治疗方案,持续21 d。实验结束后观察并计算FD大鼠进食量、糖水消耗量、体质量变化,胃排空率、小肠推进率的变化,并检测大鼠血清5-羟色胺(5-HT)、一氧化氮(NO)及一氧化氮合酶(NOS)水平。最后取胃窦组织,经苏木素-伊红(HE)染色法观察各组大鼠胃窦组织病理学改变。结果造模之初大鼠均未见异常,随着造模程序的推进,除正常组大鼠外,其余各组大鼠情绪由稳定变为烦躁、易怒、易惊,最后转化为情绪低落,并逐渐在夹尾时叫声微弱;大鼠毛发由润泽变为枯黄毛躁并散乱易掉落;大鼠饮水量、进食量、糖水消耗均减少,体质量逐渐减轻;活动量减少,嗜睡少动,扎堆,不活跃,弓背蜷缩,对外界声音不敏感;大便稀溏不成形。在3周的治疗后,各治疗组一般情况逐渐恢复造模前的状态。造模后,与正常组比较,模型组大鼠进食量、体质量及糖水消耗量均降低(P<0.05)。治疗后,与模型组比较,多潘立酮组和柴术理胃饮低、中、高剂量组大鼠体质量、进食量、糖水消耗量均升高(P<0.05);柴术理胃饮高剂量组大鼠体质量、进食量、糖水消耗量均高于柴术理胃饮低剂量组(P<0.05)。与正常组比较,模型组大鼠胃排空率及小肠推进率均降低(P<0.05);与模型组比较,多潘立酮组和柴术理胃饮低、中、高剂量组大鼠胃排空率及小肠推进率均有不同程度提高(P<0.05);柴术理胃饮高剂量组胃排空率及小肠推进率均高于柴术理胃饮低剂量组(P<0.05)。与正常组比较,模型组大鼠血清NO、NOS含量均升高(P<0.05),5-HT含量降低(P<0.05);与模型组比较,多潘立酮组和柴术理胃饮低、中、高剂量组大鼠血清NO、NOS含量均降低(P<0.05),5-HT含量均升高(P<0.05);柴术理胃饮高剂量组大鼠血清NO、NOS含量均低于柴术理胃饮低剂量组(P<0.05),5-HT含量高于柴术理胃饮低剂量组(P<0.05)。正常组无炎症细胞浸润,模型组可见上皮细胞肿胀,以及大量炎症细胞浸润,柴术理胃饮各剂量组和多潘立酮组与模型组相比,胃窦黏膜层均可见轻微充血和少量淋巴细胞及中性粒细胞浸润。结论柴术理胃可以明显改善大鼠的焦虑、烦躁、紧张等不良精神状态,增强大鼠体质,显著增加或下调大鼠脑肠肽5-HT、NO、NOS水平,最终显著缓解FD症状。

葛根汤与桂枝汤对兔颈椎间盘组织IL-1β、iNOS、TNFα、TGFβ mRNA表达的调节作用

目的 检测兔动物模型风寒湿颈椎病组、低头位颈椎病组、风寒湿加低头位颈椎病组的颈椎间盘组织中白细胞介素1β(interleukin 1β ,IL 1β)、诱导型氮氧化物合酶 (induciblenitric oxidesynthase,iNOS)、肿瘤坏死因子α(tumornecrosisfactor al pha ,TNFα)、转化生长因子 β(transforminggrowthfactor beta ,TGFβ)的mRNA的表达 ,并检测葛根汤、桂枝汤对兔风寒湿颈椎病组颈椎间盘组织中上述细胞因子mRNA的调节作用。方法 36只大白兔随机分为正常对照组、风寒湿颈椎病组、低头位颈椎病组、风寒湿加低头位颈椎病组、葛根汤治疗组、桂枝汤治疗组。葛根汤、桂枝汤治疗组均以风寒湿颈椎病模型为基础。采用逆转录聚合酶链反应法检测颈椎间盘组织中上述细胞因子mRNA的表达。结果 各模型组与正常对照组比较IL 1βmRNA、iNOSmRNA表达上调 (P <0 .0 1) ;葛根汤、桂枝汤治疗组与风寒湿颈椎病组比较 ,IL 1βmRNA、iNOSmRNA表达均下调 (P <0 .0 5或 <0 .0 1) ;低头位加风寒湿颈椎病组TNFαmRNA表达上调 ,与风寒湿及低头位颈椎病组比较 (P <0 .0 1) ;葛根汤下调TNFαmRNA表达 ,与风寒湿颈椎病组比较 (P <0 .0 1) ;各模型组同正常对照组比较 ,TGFβmRNA表达均下调(P <0 .0 1) ;与风寒湿颈椎病组比较 。

噪声对大鼠学习记忆中海马区NOS阳性神经元表达的影响

目的 :拟在白噪声下观察对大鼠学习记忆的影响及海马区NOS的变化 ,探讨噪声所致大鼠学习记忆下降的机制。方法 :44只SD大鼠 ,其中 2 0只随机分两组 ,分别在持续 80dB (A)白噪声和无噪声的环境下 ,在Y -迷宫中进行空间辨别学习记忆训练 ,了解噪声对大鼠学习记忆的影响 ,另 2 4只大鼠随机分三组 :噪声训练组、正常训练组和噪声观察组 ,以同样的方法训练 ,用免疫组化的方法观察持续噪声对海马区NOS阳性神经元表达变化。结果 :噪声能降低大鼠学习记忆能力 ,而且海马区NOS阳性神经元较正常对照组的数量及染色强度显著降低。结论 :噪声降低海马区神经元活性 ,NOS的合成减少 ,抑制海马习得性长时程突触增强 ,影响记忆的获得与保持 。

滋阴益气活血法对糖尿病合并脑缺血大鼠内皮素、一氧化氮及一氧化氮合酶含量的影响

目的:研究滋阴益气活血中药抗糖尿病脑缺血作用及与ET、NO和NOS的关系。方法:采用STZ所致糖尿病大鼠及结扎双颈总动脉的糖尿病合并不完全性脑缺血模型,于缺血2h,再灌注48h后测定ET、NO、NOS。结果:糖尿病合并脑缺血血浆ET及脑组织中NO均显著增高,血浆NO、NOS有降低趋势,脑组织中NOS有增高趋势。滋阴益气活血中药方及西药均可防止糖尿病脑缺血后血浆ET及脑组织NO的升高,降低脑组织NOS活性。结论:糖尿病合并脑缺血损伤与ET、NO及NOS的作用有一定的关系,滋阴益气活血方可能通过降低血浆ET及脑组织中NO的生成而发挥抗糖尿病脑缺血作用。

结构型与诱生型一氧化氮合酶在大鼠胃溃疡模型中的表达和活性变化

目的研究结构和诱生型一氧化氮合酶(iNOS和eNOS)在大鼠胃溃疡模型中的表达和活性变化,以探讨它们在溃疡病理中的表达规律及所起的作用.方法采用乙酸胃腔内注射方法制备大鼠胃溃疡模型,采集溃疡诱导后1 h～15 d的溃疡基底、边缘和正常胃组织标本,采用RT-PCR方法和Westernblot方法测定组织中iNOS和eNOS的nRNA表达及蛋白水平,采用测定组织匀浆液转化L[3H]-精氨酸成L-[3H]一瓜氨酸的能力的方法检测标本的总NOS和iNOS活性.结果乙酸诱导的大鼠胃溃疡模型溃疡基底在1 d～3 d出现自限性的iNOS的高表达和活性,这一时间与炎症高峰出现时间相一致,正常胃组织检测不到iNOS的表达,溃疡愈合期的iNOS表达和活性较低.eNOS的表达和活性水平在整个过程中相对稳定.结论机体在损伤后能够自限性诱导和调节iNOS的表达,而主要来源于iNOS活性的NO在胃溃疡的损伤和炎症到愈合的病理过程中起到重要作用.

扶正化痰方对哮喘豚鼠肺组织NO、NOS浓度的影响

目的:观察扶正化痰方对哮喘豚鼠肺组织中一氧化氯(NO)、一氧化氮合酶(NOS)浓度的影响,探讨扶正化痰法防治哮喘的机理。方法:40只健康豚鼠随机分为正常组、造模组、中药组、西药组,以卵蛋白致敏豚鼠并诱喘成功后,予中药扶正化疲方、西药酮替芬等治疗后,测定各组豚鼠肺组织中NO、NOS水平。结果:造模组豚鼠血清NO、NOS水平较正常组豚鼠显著升高(P<0.01),中药组豚鼠肺组织NO、NOS较造模组显著降低(p<0.01)。结论:扶正化痰方可降低哮喘豚鼠肺组织NO、NOS水平,对哮喘有一定的防治作用。

银杏叶提取物联合盐酸文拉法辛对抑郁大鼠海马nNOS蛋白表达及NO水平的影响

目的 :探讨抑郁症脑损伤的机制 ,研究银杏叶提取物 (EGb)及合成抗抑郁药盐酸文拉法辛(Venlafaxine)对抑郁大鼠的抗脑损伤及神经元保护作用。方法 :慢性应激建立大鼠抑郁模型。将 84只雄性大鼠分为正常对照组、抑郁模型组和不同治疗组。快速断头法处死 ,取海马后一侧进行免疫组化反应 ,观察海马CA3区nNOS蛋白的表达 ;另一侧检测NO含量 ;同时测定血清中NO含量。结果 :抑郁模型组海马nNOS表达增加 ,海马及血清中NO含量增加 ,P <0 0 1;联合用药组海马nNOS表达下降 ,海马及血清中NO含量减少 ,P <0 0 1。结论 :慢性应激增加海马nNOS表达 ;EGb有减轻神经元损伤 ,保护神经元的作用 ,其与Venlafaxine合用可能会达到对抑郁进行多靶点、多层次的治疗 ,弥补单一用药的不足。

顺铂对耳蜗螺旋神经节细胞毒性作用及机制

目的通过透射电镜及免疫组化法观察顺铂对耳蜗螺旋神经节细胞的毒性作用。方法16只豚鼠随机均分为2组。顺铂组连续5天腹腔注射顺铂2mg/kg/d;对照组连续5天腹腔注射生理盐水2mg/kg/d;用药前后测试听力,处死动物后制作耳蜗标本,透射电镜观察及免疫组化法测定诱导型一氧化氮合酶(induciblenitricoxidesynthase,iNOS)的表达。结果ABR:顺铂组听力下降明显,阈值显著升高(P<0.01)。透射电镜观察:顺铂组螺旋神经节细胞的细胞器损伤严重,核变形,线粒体肿胀,大量空泡样变,粗面内质网增多,有髓神经纤维的髓鞘增厚;对照组螺旋神经节细胞核无变形,核仁基本居中,线粒体结构正常。免疫组织化学显示:顺铂组螺旋神经节有iNOS阳性反应显色,灰度值降低,iNOS活性升高,与对照组比较,有显著性差异(P<0.01)。结论顺铂可致耳蜗螺旋神经节细胞损伤并呈iNOS阳性表达,导致听力下降。

诱导型一氧化氮合酶与动物疾病

一氧化氮 ( nitric oxide,NO)是近年来引起人们特别注意的无机气体自由基 ,有独特的理化性质和生物学活性 ,几乎对全身各个系统都有影响 ,其中诱导型一氧化氮合酶及其催化产生的 NO在动物疾病的发生、发展过程中都起着重要的作用。

一氧化氮与大鼠肠缺血再灌注损伤关系的研究

目的了解一氧化氮(NO)与大鼠肠缺血再灌注损伤之间存在的关系。方法制作肠缺血再灌注损伤的动物模型,设立对照组、缺血组、再灌注45min和90min组,检测不同时点血浆NO浓度、肠组织一氧化氮合酶(iNOS)免疫组化染色光密度及肠管病理损伤程度。结果伴随肠缺血再灌注进程,各组大鼠Chiu病理评分及iNOS免疫组化染色光密度值依次升高,且组间均有显著性差异。F值分别为287.13,62.484,P均小于0.01。而血浆NO含量则是在再灌注后才呈现渐增趋势,F=38.667,P<0.01。结论肠组织中iNOS表达在缺血期即被激活,由iNOS催化合成的NO在大鼠肠缺血再灌注过程中基本以致损作用为主。

牛珀至宝微丸对内毒素休克大鼠脑神经型一氧化氮合酶表达的影响

目的:探讨牛珀至宝微丸对内毒素休克大鼠脑神经型一氧化氮合酶(neuronalnitricoxide synthase,nNOS)表达的影响。方法:将SD大鼠随机分成正常对照组、模型组、牛珀至宝微丸组。模型组静 脉注射内毒素脂多糖(lipopolysaccharide,LPS)1.5mg/kg、腹腔注射D 氨基半乳糖(D galactosamine, D GalN)100mg/kg造成内毒素休克模型,牛珀至宝微丸组用药7d后再作以上处理。用免疫组织化学方法 检测各组nNOS在不同脑区的表达。结果:nNOS阳性细胞广泛分布于大脑皮质Ⅱ、Ⅲ、Ⅳ层,海马分子层, 齿状回多形层,脑干网状结构,小脑分子层、颗粒层和普尔基涅细胞层。在大脑皮质、海马、脑干及小脑各部 位,牛珀至宝微丸组的nNOS阳性细胞数略高于正常对照组,但明显低于模型组(P<0.05)。结论:牛珀至 宝微丸有部分下调内毒素休克所致广泛脑区nNOS过度表达的作用。

左旋精氨酸对离体培养SHR大鼠主动脉内皮细胞一氧化氮合成酶活性的影响

目的探讨左旋精氨酸对离体培养SHR大鼠主动脉内皮细胞一氧化氮合成酶(nitricoxidativesynthase,NOS)活性的影响。方法6周龄雄性SHR大鼠,取其主动脉,采用贴块法进行体外内皮细胞培养,传代6～8代,将细胞分成实验组和对照组,实验组在生长液中加入1mol/L左旋精氨酸,对照组不施干预措施,分别在加入左旋精氨酸后1/2、1、2、4小时取二组细胞,反复冻融三次使细胞破裂,用分光光度法测定细胞内NOS活性。结果内皮细胞对左旋精氨酸较敏感,实验组加入左旋精氨酸1/2小时后,NOS活性即上升,1小时达最高,随后下降,至4小时恢复正常。结论左旋精氨酸可增强离体SHR大鼠主动脉内皮细胞NOS活性。