Nesfatin-1对大鼠胃酸分泌的影响

目的:探讨Nesfatin-1对大鼠胃酸分泌的影响.方法:♂SD大鼠36只,随机分为6组,分别在侧脑室注射Nesfatin-1(0.05g/只)、Nesfatin-1(0.5g/只)及等量的注射灭菌水(5L/只),外周静脉注射Nesfatin-1(10g/kg)、Nesfatin-1(50g/kg)及等量的灭菌水(150L/只),每组6只.采用幽门结扎法收集胃液,3h后处死大鼠分别测定胃液胃酸分泌量,H+-K+-ATPase表达量.结果:侧脑室注射Nesfatin-1(0.05g/只及0.5g/只)后大鼠3h胃液的分泌量分别为2.4mL/3h±0.3mL/3h、2.5mL/3h±0.3mL/3h,与对照组(3.3mL/3h±0.3mL/3h)相比,其分泌量明显减少,差异具有统计学意义(P<0.05,n=6).侧脑室注射Nesfatin-1(0.05g/只及0.5g/只)后大鼠3h胃酸的分泌量分别为373.6mol/3h±61.5mol/3h、380.0mol/3h±55.8mol/3h,与对照组(582.7mol/3h±59.3mol/3h)相比,其分泌量明显减少,差异具有统计学意义(P<0.05,n=6).外周静脉注射Nesfatin-1(10g/kg及50g/kg)后大鼠胃液分泌量分别为3.3mL/3h±0.4mL/3h、3.8mL/3h±0.5mL/3h与对照组(3.7mL/3h±0.7mL/3h)相比差异无统计学意义(P>0.05,n=6).外周静脉注射Nesfatin-1(2g/只及10g/只)后大鼠胃酸分泌量分别为573.8mol/3h±97.4mol/3h、594.4mol/3h±121.0mol/3h与对照组(647.6mol/3h±102.8mol/3h)相比差异无统计学意义(P>0.05,n=6).侧脑室注射Nesfatin-1(0.05g/只及0.5g/只)后3h大鼠胃H+-K+-ATPasemRNA表达明显下调(P<0.05).外周静脉注射Nesfatin-1(10g/kg及50g/kg)后3h大鼠胃H+-K+-ATPasemRNA表达与对照组相比差异无统计学意义(P>0.05).结论:Nesfatin-1通过中枢注射可以明显抑制大鼠胃酸的分泌.     

电针对LPS干预大鼠延髓NOS神经元的影响

目的探讨细菌脂多糖（LPs）对大鼠延髓一氧化氮合酶（NOS）神经元的影响，进一步观察电针足三里穴对这种影响的作用，并探讨其与胃排空功能的关系。方法。先行电针刺激大鼠足三里穴或非经非穴5天，之后予LPS2．5ms／kg腹腔注射，与不行电针单纯LPs处理组作对照；以免疫组化（ABC法）检测大鼠延髓神经元型NOS（nNOS）、诱导型NOS（iNOS）阳性神经元分布及数日，结果正常大鼠延髓各核团未观察到nNOS阳性神经元，延髓迷走神经背运动核（DMV）及孤束核（NTS）可见极少数iNOS阳性神经元分布。LPs腹腔注射7．5h后，延髓DMV中nNOS、iNOS阳性神经元的数目均明显增多；若先予以电针足三里穴5天，则可明届抑制LPS引起的此种反应（P＜0．01），而非经非穴点电针效果不明显。大鼠腹腔注射LPs后，延髓DMV中nNOS及iNOS阳性细胞数日明显增加，电针足三里穴可使之明显减少。结论电针对胃运动的作用可能与其对DMV中NO合成神经元的作用有关。     

辣椒素对胃酸分泌的影响及机制

辣椒素(capsaicin,CAP)对胃酸分泌有一定影响,多数研究显示小剂量抑制胃酸分泌,大剂量则可能促进胃酸分泌,甚至报道有些剂量的CAP对胃酸分泌没有影响.CAP对胃酸分泌影响的差异可能与其药理特性有关,不同剂量、不同时期及给药的不同途径对胃酸分泌的影响不同.CAP可能通过直接刺激中枢、外周辣椒素-敏感感觉神经(capsaicin-sensitive sensoryneurons,CSSN)及壁细胞等的辣椒素受体,引起降钙素基因相关肽、P物质、神经激肽A、血管活性肠肽等神经递质的释放,参与胃酸分泌的调节.     

幽门螺杆菌对胃酸分泌的影响

阐述急性及慢性Hp感染对胃酸分泌的影响并探讨Hp感染与胃酸分泌之间的相互作用在十二指肠溃疡发病中的地位及其机制。     

性激素对大鼠实验性十二指肠溃疡愈合与胃酸分泌的影响

目的 研究性激素对十二指肠溃疡（ＤＵ）的愈合及对胃酸分泌的影响。方法 用冰醋酸局部涂抹的方法建立大鼠ＤＵ模型，第４天起隔日分别注射雌二醇、孕酮、丙酸睾酮，对照组注射生理盐水。术后第２３天测定溃疡面积、胃液量和胃酸等。结果 术后７２小时各例大鼠都形成了穿通性溃疡，雌雄大鼠溃疡面积无显著差异。术后第２３天，雌性对照组、雄性雌二醇组、雄性孕酮组溃疡面积显著小于雄性对照组；雌性对照组、雄性雌二醇组胃液量和     

氨对胆囊收缩素抑制大鼠胃酸分泌的影响

目的旨在观察氨对胆囊收缩素（ＣＣＫ）抑制大鼠胃酸分泌的影响及其可能机制。方法３０只Ｗｉｓｔａｒ大鼠随机分为对照组（１５只）和实验组（１５Ｒ），后者给予０．１％氨水处理的饲料和含０．０１％氨的饮用水。２个月后采用胃内连续灌注引流法观察ＣＣＫ－８Ｓ及ＣＣＫ－８Ｓ合用ｌｏｘ（特异性ＣＣＫ－Ａ受体拮抗剂）对五肽胃泌素刺激的大鼠胃酸分泌变化，同时测定血浆生长抑素（ＳＳＴ）水平和胃Ｄ细胞数量变化。结果实验组大鼠的胃氨水平（８．００±１．８８ｕｇ／ｇ）明显高于对照组（１．２９±０．５６ｕｇ／ｇ，Ｐ＜０．００１），但其胃Ｄ细胞数（２．７８±０．４个／高倍镜）与对照组（２．５８±０．３８个／高倍镜）比较，差异无显著性（Ｐ＞０．０５）。ＣＣＫ－８Ｓ可使对照组大鼠血浆ＳＳＴ水平升高并部分抑制五肽胃泌素刺激的胃酸分泌，这种作用可被ｌｏｘ所拮抗；然而，ＣＣＫ－８Ｓ虽可使实验组大鼠血浆ＳＳＴ水平升高，但不抑制其胃酸分泌，施予ｌｏｘ对酸分泌也无进一步的影响。结论上述结果表明，ＣＣＫ抑制胄酸分泌主要是经过ＳＳＴ介导的，氨干扰ＣＣＫ－ＳＳＴ的抑酸效应可能是氨影响了靶细胞对ＳＳＴ的敏感性。     

电针足三里穴对胃酸分泌的影响及与促胃液素、表皮生长因子的关系

目的探讨电针足阳明胃经原穴足三里穴对胃酸分泌的调节作用及机制.方法采用完全随机方法分组.在清醒状态下电针大鼠足三里穴,并与空白对照组及非经非穴组相对比,在针剌不同时间点测胃酸分泌及取血,放免法检测胃液及血浆促胃液素(GAS)和表皮生长因子(EGF)浓度.结果电针足三里穴后空腹胃液量显著减少(P＜0.01)pH值上升(P＜0.05),酸度变化不大.足三里穴组胃液及血浆GAS浓度均降低,分别为239 ng/L±61 ng/L vs 294 ng/L±32ng/L(P＜0.05)和81 ng/L±22ng/L vs 102ng/L±30 ng/L(P＜0.01).胃液EGF浓度显著升高3.16μg/L±1.05 μg/L vs 1.65μg/L±0.35μg/L(P＜0.01).血浆EGF浓度显著降低0.25μg/L±0.01μg/L vs 0.54 μg/L±0.11μg/L(P＜0.01).其他组无显著变化.结论电针足三里穴明显抑制胃酸分泌并使胃液pH升高,与血浆、胃液GAS下降有关;电针足三里穴诱导上消化道EGF分泌增加,EGF参与抑制胃酸分泌,具有重要意义.     

胆囊收缩素对胃蛋白酶原和胃酸分泌的影响

胆囊收缩素(CCK)广泛分布于胃肠道和神经系统,对胃蛋白酶原(PG)和胃酸分泌具有双重影响。体外研究表明CCK由主细胞、壁细胞上相应受体介导促进PG和胃酸的分泌;在体内CCK通过某种途径(如刺激D细胞释放生长抑素)间接抑制PG和胃酸的分泌。CCK对PG和胃酸分泌具有生理性调节作用。十二指肠溃疡患者CCK抑酸机制可能有缺陷。     

胆囊收缩素对胃蛋白酶原和胃酸分泌的影响

胆囊收缩素广泛分布于胃肠道和神经系统，对胃蛋白酶原和胃酸分泌具有双重影响。体外研究表明ＣＣＫ由主细胞、壁细胞上相应受体介导促进ＰＧ和胃酸的分泌；在体内ＣＣＫ通过某种途径间接抑制ＰＧ和胃酸的分泌。     

大鼠胃扩张致胃酸分泌中NO对胃粘膜血流量的影响

胃酸分泌时,来自胃腺壁细胞的信号到达粘膜下层引起胃粘膜血流增加[1],但给予5肽促胃液素促进胃酸分泌时并不能使血流增加呈平行反应[2-4],表明在一定条件下胃酸分泌和胃粘膜血流之间的变化可以相互分离.近年来内皮来源的舒血管物质NO在调节胃粘膜微循环中起重要生理作用[5-7],但关于胃内生理性刺激因素胃扩张引起胃酸分泌过程中NO对胃粘膜 血流影响的作用如何尚不清楚.我们以氢气清除法测定胃粘膜血流量,观察静脉注射NO合酶抑制剂L-NAME对胃粘膜血流量的影响,探讨NO在胃扩张引起胃酸分泌作用中对胃粘膜血流量的影响以及胃扩张过程中胃酸分泌和胃粘膜血流变化之间的关系.     

膈下迷走神经切断术对腹腔注射乙酸致内脏痛大鼠孤束核及胸髓中Fos蛋白表达的影响

目的 探讨迷走神经在内脏痛觉信息传入通路中的作用。方法 将SD大鼠随机分为5组：空白对照组，腹腔注射乙酸刺激组（内脏痛组）、腹腔注射牛理盐水组、迷走神经切断术后＋内脏痛组和假手术后＋内脏痛组（每组6只）。应用免疫组化染色方法，观察各组动物Fos在巾枢延髓孤束核及胸髓的表达。结果 免疫组化染色发现：腹腔注射乙酸刺激组较空白对照组和腹腔注射生理盐水组Fos阳性反应数日在中枢延髓孤束核及胸髓背角浅层表达明显增高；迷走神经切断术后内脏痛组Fos反应数目在孤束核的表达明显减少，而在胸髓背角浅层表达有所增加；假手术后＋内脏痛组与内脏痛组之间Fos表达无明显差异。结论 大鼠腹腔注射乙酸诱发内脏伤害性刺激信息主要是由迷走神经向延髓孤束核传递的，起主导作用；胸髓亦参与了该内脏伤害性刺激的信息传递。     

碘过量对成年大鼠海马胶质原纤维酸性蛋白的影响

目的研究碘过量对Wistar成年大鼠海马星形胶质细胞的影响。方法断乳一个月Wistar大鼠，雌雄各半，随机分为4组：适碘组（NI），10倍碘组（10HI），50倍碘组（50HI）和100倍碘组（100HI）。给予不同浓度碘酸钾水喂养6个月后，处死，取大脑，应用免疫组织化学技术观察海马CA，区星形胶质细胞，并对胶质原纤维酸性蛋白GFAP反应阳性细胞进行形态计量学分析。结果各碘过量组海马GFAP阳性细胞的Vv，NA和细胞质的平均灰度值与NI组比较均无明显差异（P〉0．05）。结论碘过量不会造成Wistar成年大鼠海马神经元的明显损伤，其星形胶质细胞Vv，NA和细胞质的平均灰度值无明显改变。     

阿魏酸钠对大鼠脑白质胶质纤维酸性蛋白表达的影响

目的探讨阿魏酸钠对大鼠前脑缺血再灌注（I/R）后白质胶质纤维酸性蛋白表达的影响。方法双侧颈总动脉夹闭法制备大鼠前脑I/R模型。雄性Wistar大鼠45只，随机分为假手术组（n=15），I/R组（n=15），I/R阿魏酸钠治疗组（n=15），每组按I/R2、4、6w3个时间点再分为3组（n=5）。模型制备免疫组化法检测I/R后2、4、6w胼胝体、内囊和脑室周围GFAP的表达。结果I/R后胼胝体、内囊和脑室周围GFAP的表达随时间延长逐渐增多，阿魏酸钠治疗组GFAP的表达较假手术组多，较缺血再灌注组减少，6w差异最显著（P〈0.05）。结论大鼠前脑缺血再灌注后白质GFAP表达增多，阿魏酸钠对脑白质缺血性损伤具有保护作用，其机制可能与调节星形胶质细胞活化状态，减轻内皮素对血管损伤有关。     

GFAP promoter directs lacZ expression specifically in a rat hepatic stellate cell line

AIM: The GFAP was traditionally considered to be a biomarker for neural glia (mainly astrocytes and non-myelinating Schwann cells). Genetically, a 2.2-kb human GFAP promoter has been successfully used to target astrocytes in vitro and in vivo. More recently, GFAP was also established as one of the several makers for identifying hepatic stellate cells (HSC). In this project, possible application of the same 2.2-kb human GFAP promoter for targeting HSC was investigated. METHODS: The GFAP-lacZ transgene was transfected into various cell lines (HSC, hepatocyte, and other non-HSC cell types). The transgene expression specificity was determined by X-gal staining of the beta-galactosidase activity. And the responsiveness of the transgene was tested with a typical pro-fibrotic cytokine TGF-beta1. The expression of endogenous GFAP gene was assessed by real-time RT-PCR, providing a reference for the transgene expression. RESULTS: The results demonstrated for the first time that the 2.2 kb hGFAP promoter was not only capable of directing HSC-specific expression, but also responding to a known pro-fibrogenic cytokine TGF-beta1 by upregulation in a dose- and time-dependent manner, similar to the endogenous GFAP. CONCLUSION: In conclusion, these findings suggested novel utilities for using the GFAP promoter to specifically manipulate HSC for therapeutic purpose.     

Effects of omeprazole on gastric mucosal microcirculation and acid secretion in the rat

Omeprazole, a potent long-acting inhibitor of gastric acid secretion that exerts its inhibitory action by direct blocking of the H+, K+-adenosine triphosphatase in the parietal cells, was either applied topically to the solution bathing the exposed mucosa of the test rats or administered intravenously as a bolus injection. The superficial mucosal vessels were monitored on a television screen through a microscope and videorecorded for off-line analysis of red cell velocities and vessel diameters, from which blood flow was calculated. Intravenous omeprazole (5 or 10 mumol/kg) totally abolished the basal secretion 15-25 min after injection, with a parallel decrease in blood flow of approximately 25% for both doses. Omeprazole, 5 mumol/kg, given intravenously to rats stimulated with pentagastrin (20 micrograms/kg X h) significantly inhibited the stimulated acid output, but the blood flow was not significantly decreased. Topical application of omeprazole (2.5 mM in 6 ml) significantly increased blood flow (approximately 15%) while in contact with the mucosa both in the resting and in the pentagastrin (20 micrograms/kg X h)-stimulated situations. However, 10-20 min after the application period, blood flow was restored to the values before application of omeprazole and the acid output was significantly decreased. The results indicate that omeprazole exerts only minor influences on the gastric mucosal microcirculation in spite of its potent acid-inhibitory effect.     

大鼠结肠慢性炎性刺激诱导腰骶髓和延髓Fos的表达及其意义

目的　探讨实验性大鼠结肠慢性炎性刺激诱导腰骶髓和延髓中Fos的表达及其意义。方法　成年雄性SD大鼠 ,实验组 (n =1 6 )予三硝基苯磺酸 (TNBS)灌肠诱导结肠炎 ,实验对照组 (n =8)予生理盐水灌肠 ,空白对照组 (n =2 )不予任何刺激 ;分别在灌肠后 3、7、1 4和 2 8d ,采用免疫组化法观察实验组大鼠腰骶髓和延髓中Fos阳性神经元的数量和分布 ,并与对照组进行比较。结果　TNBS灌肠诱导Fos表达多数分布在脊髓背角深层 (Ⅲ～Ⅳ和Ⅴ～Ⅵ层 )和由孤束核、腹外侧区及网状结构形成的延髓内脏带中。TNBS灌肠后 3d ,脊髓和延髓中Fos表达无明显增多。灌肠后 7和 1 4d ,脊髓和延髓中Fos表达明显多于实验对照组 (P <0 .0 5 )。灌肠后 2 8d ,延髓中Fos表达下降 ,与对照组无明显差异 ,部分大鼠脊髓中Fos阳性神经元数 (5 4 .1± 1 6 .3)仍明显多于对照组 (1 2 .2± 2 .6 ,P <0 .0 5 )。结论　脊髓Fos阳性神经元可能在结肠慢性炎性刺激引起的内脏高敏感性中起作用 ,而延髓可能不是内脏高敏感性形成的主要部位。     

GFAP and Fos immunoreactivity in lumbo-sacral spinal cord and medulla oblongata after chronic colonic inflammation in rats

AIM: To investigate the response of astrocytes and neurons in rat lumbo-sacral spinal cord and medulla oblongata induced by chronic colonic inflammation, and the relationship between them. METHODS: Thirty-three male Sprague-Dawley rats were randomly divided into two groups: experimental group (n = 17), colonic inflammation was induced by intra-luminal administration of trinitrobenzenesulfonic acid (TNBS); control group (n = 16), saline was administered intra-luminally. After 3, 7, 14, and 28 d of administration, the lumbo-sacral spinal cord and medulla oblongata were removed and processed for anti-glial fibrillary acidic protein (GFAP), Fos and GFAP/Fos immunohistochemistry. RESULTS: Activated astrocytes positive for GFAP were mainly distributed in the superficial laminae (laminae Ⅰ-Ⅱ) of dorsal horn, intermediolateral nucleus (laminae Ⅴ), posterior commissural nucleus (laminae Ⅹ) and anterolateral nucleus (laminae Ⅸ). Fos-IR (Fos-immunoreactive) neurons were mainly distributed in the deeper laminae of the spinal cord (laminae Ⅲ-Ⅳ, Ⅴ-Ⅵ). In the medulla oblongata, both GFAP-IR astrocytes and Fos-IR neurons were mainly distributed in the medullary visceral zone (MVZ). The density of GFAP in the spinal cord of experimental rats was significantly higher after 3, 7, and 14 d of TNBS administration compared with the controls (50.4±16.8, 29.2±6.5, 24.1±5.6, P<0.05). The density of GFAP in MVZ was significantly higher after 3 d of TNBS administration (34.3±2.5, P<0.05). After 28 d of TNBS administration, the density of GFAP in the spinal cord and MVZ decreased and became comparable to that of the controls (18.0±4.9, 14.6±6.4,P>0.05). CONCLUSION: Astrocytes in spinal cord and medulla oblongata can be activated by colonic inflammation. The activated astrocytes are closely related to Fos-IR neurons. With the recovery of colonic inflammation, the activity of astrocytes in the spinal cord and medulla oblongata is reduced.     

幽门螺杆菌感染相关的炎症反应和胃酸分泌

全球超过50％的人感染Helicobecter pylori，但感染造成的结局却各不相同。多数感染者表现为慢性胃炎，仅少数人发展为更严重的疾病：消化性溃疡、胃癌及胃MALT淋巴瘤。导致不同结局的因素可能为：①H.pylori菌株毒力的不同；②宿主对H.pylori感染反应的差异；③环境因素；④处于H.pylori感染的不同     

碘过量对仔鼠海马GFAP阳性星形胶质细胞的影响

目的探讨碘过量与甲状腺激素对仔一代Wistar大鼠大脑海马星形胶质细胞的形态学影响。方法将断乳后1个月Wistar大鼠随机分为5组(NI、5HI、10HI、50HI、100HI),饮用不同浓度的KIO3碘水,饲养3个月后雌雄合笼,取60日龄仔鼠大脑,应用免疫组织化学技术观察海马CA1、CA2、CA3、CA4区星形胶质细胞,并进行形态计量学分析。结果与NI组比较,50HI、100HI组的海马各区GFAP阳性星形胶质细胞面数密度、平均灰度值和阳性细胞的强阳性率均明显降低。结论长期严重碘过量会影响仔鼠甲状腺激素水平,阻碍其大脑海马星形胶质细胞发育,其机理可能与碘过量所致的甲状腺功能低下有关,但大鼠对碘过量有极强的耐受力,当碘摄入量为正常摄入量的50倍以内时,不会影响仔鼠大脑海马星形胶质细胞的发育。