花生油灌胃对大鼠浸水应激性胃溃疡和胃运动的影响

采用束缚-浸水应激法建立大鼠应激性胃溃疡模型,观察花生油对胃粘膜损伤程度和胃运动的影响.结果表明,花生油可以明显减轻胃粘膜损伤,明显抑制胃运动,但对胃粘膜血流量无影响.提示抑制胃运动可能是花生油保护大鼠浸水应激性胃粘膜损伤的机制之一.     

花生油灌胃对大鼠浸水应激性胃溃疡和胃运动的影响

采用束缚－浸水应激法建立大鼠应激性胃溃疡模型,观察花生油对胃粘膜损伤程度和胃运动的影响。结果表明,花生油可以明显减轻胃粘膜损伤,明显抑制胃运动,但对胃粘膜血流量无影响。提示抑制胃运动可能是花生油保护大鼠浸水应激性胃粘膜膜损伤的机制之一。     

大鼠侧脑室注射GABA对束缚-浸水应激性胃溃疡的影响

为探索脑内γ-氨基丁酸(GABA)对应激性胃溃疡的影响及其机制,采用大鼠束缚-浸水应激性胃溃疡模型,观察了侧脑室注射γ-氨基丁酸及其A型受体的激动剂和拮抗剂对大鼠应激性胃溃疡的影响。结果表明:与侧脑室注射生理盐水组比较:(1)侧脑室注射γ-氨基丁酸,大鼠束缚-浸水应激性胃溃疡程度显著减轻(P<0.01);(2)侧脑室注射戊巴比妥钠(GABAA型受体激动剂),胃溃疡程度也显著减轻(P<0.05);(3)侧脑室注射荷包牡丹碱(GABAA型受体拮抗剂),胃溃疡程度明显加重(P<0.05)。这些结果表明:外源性γ-氨基丁酸对大鼠束缚-浸水应激性胃溃疡的形成有抑制作用,这种抑制作用是通过脑内GABAA型受体介导的;在应激过程中,脑内也有内源性γ-氨基丁酸的释放并通过其A型受体的活动,减轻胃溃疡的形成。     

束缚-浸水应激大鼠下丘脑前部、延髓内脏带突触可塑性的变化

目的:研究束缚-浸水应激不同时间段(0,1,2和4 h)雄性Wistar大鼠下丘脑前部(主要是室旁核和视上核)、延髓内脏带(主要是迷走复合体)中突触膨体素和突触蛋白I表达量的变化情况,以期探讨在束缚-浸水应激致胃粘膜损伤过程中上述部位的突触可塑性是否发生了改变。方法:随机将雄性Wistar大鼠分为4组:束缚-浸水应激0,1,2和4 h组,利用免疫组织化学和Western Blot两种方法统计各组下丘脑前部、延髓内脏带中突触膨体素和突触蛋白I的分布和含量变化情况。结果:在束缚-浸水应激0 h到4 h过程中,下丘脑前部中突触膨体素表达在不同应激时间段差异均无统计学意义,但突触蛋白I,尤其是突触蛋白I b的含量发生了显著性变化(P<0.05);迷走复合体中的突触膨体素和突触蛋白I的表达均发生了显著性变化(P<0.05)。结论:这些结果提示,下丘脑前部、延髓内脏带在束缚-浸水应激致胃粘膜损伤的中枢调控过程中均发生了突触可塑性的变化。     

束缚浸水应激对大鼠脑组织中游离氨基酸含量的影响

为探讨脑中神经递质与动物应激反应之间的关系,本研究运用双向上行层析法,测定了大鼠束缚浸水应激5 h后,脑组织中几种游离氨基酸的含量。结果表明:大鼠5 h束缚浸水应激后,脑中天冬氨酸(Asp)、谷氨酸(Glu)、谷氨酰胺(Gln)3种兴奋性氨基酸的含量,较对照组分别增加了69.19%(P<0.05)、77.42%(P<0.01)、136.84%(P<0.01)。但抑制性氨基酸γ-氨基丁酸(GABA)的含量变化不显著(P>0.05)。     

褪黑素减轻浸水-束缚应激大鼠胃黏膜损伤

目的探讨褪黑素(MT)对大鼠应激性胃溃疡的保护作用及对胃黏膜MMP-9、MMP-2和TIMP-2表达的影响。方法用浸水-束缚应激(WIRS)建立大鼠应激性溃疡模型。应激前30 min,分别腹腔注射褪黑素10、20、40和60 mg/kg。应激3 h后,观察大鼠胃黏膜病变,对溃疡指数(UI)进行评分;组织学观察胃出血;用real-time PCR及Western blot检测胃黏膜MMP-9、MMP-2和TIMP-2的mRNA及蛋白表达。结果 WIRS应激3 h能成功诱导大鼠应激性胃溃疡。预先注射MT可明显降低应激性胃溃疡大鼠的UI(P0.01),明显降低黏膜层炎性细胞浸润数(P0.01)。WIRS诱导大鼠胃黏膜MMP-9和MMP-2 mRNA和蛋白表达上调(P0.01),TIMP-2则下降;MT预处理后,MMP-2/MMP-9明显下降(P0.05或P0.01);而TIMP-2的mRNA及蛋白表达增加(P0.05或P0.01)。结论MT可能通过下调MMP-9和MMP-2表达,及增加TIMP-2表达,减轻WIRS诱导的大鼠应激性胃溃疡。     

半胱氨酸对大鼠浸水应激性胃溃疡的影响

目的；研究半胱氨酸对大鼠胃溃疡的影响及其作用机制，方法：利用大鼠浸水应激性胃溃疡模型，观察腹注盐酸半胱氨酸对胃溃疡指数、胃粘膜谷胱甘肽（ＧＳＨ）含量１胃酸分泌和胃粘液分泌的影响。结果：半胱氨酸能抑制大鼠胃溃疡的形成；浸水应激可使大鼠胃粘膜ＧＳＨ含量明显降低，半胱氨酸对ＧＳＨ含量的降低无影响；事先给予Ｎ－乙酰马来酰氨或消炎痛对半胱氨酸的抗溃疡作用无影响；半胱氨酸能抑制浸水应激大鼠胃酸的分泌，但对胃粘     

神经降压素在大鼠应激性胃溃疡中的作用

选健康雄性Ｗｉｓｔａｒ大鼠１２２只，用脑室微量注射和放射免疫等分析方法，观察了中枢内、外源性神经降压素（ＮＴ）在大鼠束缚加水浸诱导的应激性胃溃疡中的作用。结果表明：（１）在大鼠应激性胃溃疡产生的同时，其血浆内神经降压素样免疫活性物（ＮＴＬＩ）的含量明显减少（Ｐ〈０．０５），而下丘脑、中脑、脑桥、延脑和垂体中ＮＴ－ＩＲ含量则明显升高（Ｐ〈０．０１）；（２）侧脑室注射抗ＮＴ血清中，大鼠应激性胃溃疡的产     

十五味黑药丸对大鼠应激性胃溃疡的影响

目的:观察十五味黑药丸对大鼠应激性胃溃疡的治疗效果。方法:SD大鼠分为五组,即十五味黑药丸0.5 g.kg-1、1.0 g.kg-12、.0 g.kg-1剂量组,甲氰咪胍阳性对照组(0.1 g.kg-1),阴性对照组(生理盐水);各组连续给药7天,末次给药后水浴法造成大鼠应激性溃疡,20小时后放血处死动物;检查胃病变情况,由此观察十五味黑药丸对溃疡的治疗作用。结果:十五味黑药丸组大鼠溃疡面积和溃疡指数均明显小于对照组,其中以2.0 g.kg-1组作用最为显著(P<0.01)。结论:十五味黑药丸对大鼠应激性胃溃疡具有明显的防治作用。     

束缚应激对大鼠血小板-氧化氮释放的影响

目的 观察急性应激对大鼠血小板一氧化氮(NO)释放的影响及其机制.方法 大鼠浸水-束缚应激(WRS)2、4和8 h,以胃溃疡指数(UI)作为应激损伤的标识,采用Greiss法测定血小板孵育液中亚硝酸盐(NO2-)含量;同位素法测其一氧化氮合酶(NOS)活性和L精氨酸(L-Arg)转运量.结果 WRS 2 h血小板L-Arg转运量、NOS活性和孵育液NO2-含量较对照组显著增加,但随应激时间延长,其呈下降趋势,应激8 h时均显著低于对照组,胃溃疡逐渐加重.结论 WRS应激早期阶段可上调血小板L-Arg/NO通路,促进血小板NO生成;长时间应激下调L-Arg/NO通路,减少NO释放.     

硝普钠对大鼠应激性胃粘膜损伤的保护作用

采用浸水束缚应激法建立大鼠应激性胃溃疡模型，观察一氧化氮供体硝普钠对大鼠胃粘膜损伤的保护作用。结果表明，硝普钠可以明显减轻浸水应激引起的胃粘膜损伤，抑制胃运动亢进，同时增加胃粘膜血流量以及血浆和胃粘膜中NO和SOD含量，降低MDA和ET含量。提示硝普钠对浸水应激性胃粘膜损伤的保护作用可能是通过增加胃粘膜血流量和抑制胃运动亢进共同实现的。     

c-Fos expression in the supraoptic nucleus is the most intense during different durations of restraint water-immersion stress in the rat

Restraint water-immersion stress (RWIS) can induce anxiety, hypothermia, and severe vagally-mediated gastric dysfunction. The present work explored the effects of different durations of RWIS on neuronal activities of the forebrain by c-Fos expression in conscious rats exposed to RWIS for 0, 30, 60, 120, or 180 min. The peak of c-Fos induction was distinct for different forebrain regions. The most intense c-Fos induction was always observed in the supraoptic nucleus (SON), and then in the hypothalamic paraventricular nucleus (PVN), posterior cortical amygdaloid nucleus (PCoA), central amygdaloid nucleus (CeA), and medial prefrontal cortex (mPFC). Moreover, body temperature was reduced to the lowest degree after 60 min of RWIS, and the gastric lesions tended to gradually worsen with the prolonging of RWIS duration. These data strongly suggest that these nuclei participate in the organismal response to RWIS to different degrees, and may be involved in the hypothermia and gastric lesions induced by RWIS.     

Effect of Restraint Stress Duration on Humoral Immune Response in Albino Rats: Modulation by Chlordiazepoxide

We evaluated the effect of restraint stress (1hr/day) for 6, 10, 14 and 21 days on antibody response against sheep RBC (SRBC) and modulation by chlordiazepoxide (CDP) pretreatment (10 mg/kg/day) in albino rats. Anti-SRBC titer was significantly decreased with increase in number of days of restraint stress exposure. CDP pretreatment significantly reversed the effects of 6, 10 and 14 (but not of 21) days of restraint stress. CDP treatment for 21 days per se suppressed immune response, but no additive effect was observed. CDP was not effective in chronic stress (i.e., 21 days of stress). Hence, the rationale behind benzodiazepines therapy in chronic stress needs to be evaluated.     

Facilitation and inhibition of gastric pathology after lesions in the amygdala of rats

Bilateral lesions in the dorsomedial amygdala attenuated the effects of physical restraint on stomach pathology in rats. Posterolateral lesions increased the incidence and severity of gastric ulcers and hemorrhages. Combined lesions in these two amygdaloid areas also attenuated the restraint-induced pathology. It was concluded that the dorsomedial amygdala is excitatory, whereas the posterolateral area is inhibitory during restraint stress.     

The effects of food deprivation on restraint induced gastric lesions in the rat

The effects of pre-restraint fasting on subsequent development of stomach lesions was examined in each of two experiments. In Experiment 1, rats were food deprived for 0, 12, 24, 48 or 72 hours prior to 3 hours of supine cold-restraint. The extent of glandular lesion induction was significantly greater for animals fasted for 12 hours as compared to the stomach conditions of rats assigned to the other pre-restraint treatment conditions. The effects of extended fasting intervals and restraint induction of rumenal stomach lesions was investigated in Experiment 2. Rats were food deprived for 48, 72 or 96 hours and immobilized. Restraint-stress was found to potentiate the severity of rumenal lesions for animals receiving 96 hours of prior fasting when compared to control rats similarly food deprived but not restrained. These findings suggest that the rat stomach is differentially susceptible to restraint-induced lesion formation. Shorter fasting intervals are related to lesions in the corpus of the stomach, while protracted periods of fasting will intensify rumenal pathology.     

Ascorbic Acid Protects Against Restraint Stress-Induced Memory Deficits in Wistar Rats

OBJECTIVE:

Chronic stress has been shown to cause oxidative damage in the central nervous system. Although stress-induced impairments in learning and memory have been studied extensively, very few studies have investigated possible ways to prevent their ill effects. The present work was designed to study the protective effects of ascorbic acid in memory loss induced by chronic restraint stress.

METHODS:

Adult male Wistar rats were designated into the following groups: (i) Normal control, (ii) Ascorbic acid treatment, (iii) Vehicle control, (iv) Restraint stress, (v) Restraint stress + vehicle, and (vi) Restraint stress + ascorbic acid treatment. At the end of 21 days, animals of all groups were subjected to memory tests using Morris water maze and passive avoidance apparatus. Then, the results obtained were compared between the experimental groups.

RESULTS:

Rats exposed to restraint stress alone and those pretreated with vehicle solution before restrained stress showed deficits in learning and impaired memory retention in the memory tests when compared to animals in other experimental groups. Animals pretreated with ascorbic acid before restraining showed significant improvement in memory retention in the same memory tests.

CONCLUSIONS:

Results of this study suggest the possibility of using ascorbic acid as a dietary supplement to prevent stress-induced memory impairments.     

Effects of Nabumetone and Dipyrone on Experimentally Induced Gastric Ulcers in Rats

Nabumetone and dipyrone are non-acidic, nonsteroidal anti-inflammatory drugs. Both of them are known to have weak inhibitory effects of cyclooxygenases. Gastric side effects represent the most common adverse drug effects of the widely used nonsteroidal anti-inflammatory drugs. The gastric effects of these drugs may be comparable in experimental ulcer models. In the present study, the gastric ulcerogenic activity of nabumetone and dipyrone were investigated on stress- and diethyldithiocarbamate-induced experimental ulcer models by determining the ulcer index and gastric mucus secretion in rats. It was found that diethyldithiocarbamate increased both ulcer index and mucus secretion. Nabumetone inhibited dose-dependently the increase of diethyldithiocarbamate-induced mucus secretion. Dipyrone inhibited both stress- and diethyldithiocarbamate-induced ulcer index and mucus secretion. Nabumetone inhibited stress-induced ulcer index at 25-mg/kg dose but stimulated dose-dependently mucus secretion. These effects may be attributed to their non-acidic structures and weak inhibitory effects on gastric mucosal cyclooxygenases.     

急性实验性应激状态下大鼠胃粘膜NOS变化及与胃粘膜损伤的关系

目的：探讨躯体性心理性应激状态下大鼠胃粘膜ＮＯＳ变化及与胃粘膜损伤发生的关系。方法：采用高压恒流脉冲刺激器复制胃粘膜损伤模型,将９６只雄性ＳＤ大鼠随机分为３组：对照组（Ｃ）,规则光组（Ｒ）及不规则光组（Ｉ）,分光光度法检测ＮＯＳ活性和Ｎｉｌｓ Ｌａｍｂｅｃｔｈ法测定胃粘膜损伤指数,使用兔源大鼠ＮＯＳⅠ,ＮＯＳⅡ,ＮＯＳⅢ多抗,采用免疫组化方法研究ＮＯＳ的分布规律。结果：正常情况下ＮＯＳ活性平稳,心理性应激后,大鼠胃粘膜ＮＯＳ活性明显升高（Ｐ〈０．０５）;与对照组比较,Ｒ,Ｉ组胃粘膜损伤指数均较高,且Ｉ组较Ｒ组变化显著（Ｐ〈０．０５）;ＮＯＳⅠ,ＮＯＳⅢ在３组中均有表达,而ＮＯＳⅡ只在Ｒ,Ｉ组中表达,且其表达无明显差异（Ｐ〉０．０５）。结论：心理性应激程度愈高胃粘膜损伤愈严重,胃粘膜损伤程度及ＮＯＳ活性变化与心理