电针足三里穴抗大鼠应激性胃黏膜损伤作用与NTS内受体的关系

目的:探讨(EA)足三里穴抗大鼠应激性胃黏膜损伤作用与NTS(NTS)内受体关系．方法:健康♂SD大白鼠56只随机分为8组:应激模型组、EA-应激组、生理盐水(NS)-EA-应激组、哌唑嗪-EA-应激组、育亨宾-EA-应激组、心得安-EA-应激组、阿托品-EA-应激组、纳络酮-EA-应激组．采用束缚-冷方法制备大鼠应激性胃溃疡模型,观察NTS内微量注入不同受体阻断剂,胃溃疡指数(UI)的变化．结果:NS-EA-应激组、EA-应激组大鼠胃黏膜损伤明显减轻,UI分别为26．3±3．5,25．4±3．1,与应激模型组37．5±4．2比较有显著性差异(t= 5．42,t=6．13,P<0．01)．哌唑嗪-EA-应激组UI为34．6±3．4明显高于NS-EA-应激组(t=4．50, P<0．01)．育亨宾-EA-应激组和心得安-EA-应激组分别与NS-EA-应激组比较,UI无显著性差异．阿托品-EA-应激组大鼠UI为33．1±3．7明显高于NS-EA-应激组(t=3．53,P<0．01),纳络酮-EA-应激组与NS-EA-应激组比较,UI无显著性意义．结论:EA对大鼠应激性胃黏膜损伤的保护作用部分是通过NTS内α1,M受体介导的,而与α2,β和阿片肽受体无明显关系．     

大鼠孤束核微量注射γ-氨基丁酸对电针抗应激性胃黏膜损伤的影响

[目的]探讨孤束核内γ-氨基丁酸(GABA)对电针(EA)抗应激性胃黏膜损伤的影响及机制。[方法]70只健康SD大鼠随机分为5组:单纯应激组、EA+应激组、0.85%氯化钠+EA+应激组、GABA+EA+应激组、荷苞牡丹碱+EA+应激组,每组14只。采用冷束缚法制备大鼠应激性胃溃疡模型,通过脑立体定位仪进行孤束核微量注射GABA和荷苞牡丹碱,测定各组大鼠胃黏膜溃疡指数(UI)、胃黏膜血流量(GMBF)、胃液酸度的变化。[结果]EA+应激组大鼠胃黏膜UI、胃液酸度降低,GMBF增加,与单纯应激组比较差异有统计学意义(P0.01)。预先孤束核给予GABA处理,可减弱EA抗胃黏膜损伤的作用,胃黏膜UI、胃液酸度增高,GMBF减少,与NS+EA+应激组比较差异有统计学意义(P0.01)。荷苞牡丹碱则明显加强EA对胃黏膜损伤的保护作用,胃黏膜UI、胃液酸度降低,GMBF增加,与NS+EA+应激组比较差异有统计学意义(P0.05)。[结论]GABA能削弱EA抗应激性胃黏膜损伤作用,其作用部分是通过孤束核内GABAA受体介导的。     

精氨酸加压素参与电针对大鼠应激性胃黏膜损伤的保护作用

目的：探讨精氨酸加压素(AVP)参与电针(EA)对应激性大鼠胃黏膜损伤保护作用及机制.方法：健康SD大鼠98只,随机分为模型组、电针组、生理盐水对照组、AVP 100ng组、AVP 200ng组、AVP 300ng组和AVP-V_1受体阻断剂组.采用束缚冷应激胃黏膜损伤大鼠模型,观察孤束核微量注射AVP,AVP-V_1受体阻断剂,大鼠胃黏膜血流量(GMBF)、溃疡指数(UI)、胃液酸度的变化.结果：与模型组比较,电针组大鼠UI减少(t= 7.5201,P＜0.01),GMBF(mv)增加(t=2.9606,P＜0.05),胃液酸度降低(t=4.2090,P＜0.01). AVP 100,200,300ng组分别与生理盐水对照组比较,UI明显减少(t=2.2718,t=4.9082,t =6.0413：P＜0.05-0.01),GMBF明显增加(t= 2.6845,t=3.8269,t=4.8795；P＜0.05-P＜0.01),胃液酸度明显降低(t=3.0526,t=3.8565,t= 5.6251；P＜0.05-P＜0.01),并且表现明显的剂量-效应依赖关系(r=0.9978,r=0.9980,r= 0.9829；P＜0.05).AVP-V_1受体阻断剂组与生理盐水对照组比较UI增大(t=5.6815,P＜0.01),GMBF减少(t=2.3750,P＜0.05),胃液酸度增高(t=2.2046,P＜0.05).结论：孤束核内AVP参与了电针对大鼠应激性胃黏膜损伤保护作用过程.     

电针足三里穴抗大鼠应激性胃黏膜损伤的作用途径

[目的]探讨电针（EA）足三里穴抗大鼠应激性胃黏膜损伤的作用途径。[方法]采用束缚-冷应激方法制备大鼠应激性胃溃疡模型，观察切断膈下迷走神经或切除腹腔交感神经节及注射受体阻断剂对EA抗应激性胃黏膜损伤的影响。[结果]EA-模型组胃黏膜损伤明显减轻，溃疡指数（UI）与模型组比较差异有统计学意义（P〈0．01）。切断双侧膈下迷走神经或切断腹腔交感神经节，大鼠UI减小，分别与腹部假手术组比较差异有统计学意义（P〈0．01）。静脉给予β受体阻断剂普萘洛尔，可部分削弱EA对胃黏膜损伤的保护作用，与0．85％氯化钠组比较P〈0．01；而给予M受体阻断剂阿托品、α受体阻断剂酚妥拉明对EA保护胃黏膜损伤作用无明显影响（P〉0．05）。[结论]迷走神经和交感神经参与了电针对应激性胃黏膜损伤的调控作用，其作用部分是由β受体介导实现的。     

艾灸足三里穴对孤束核损毁术后大鼠胃黏膜损伤修复作用的影响

目的:观察艾灸"足三里"穴对胃黏膜损伤大鼠内源性保护因子白介素(interleukin,IL)-4、前列腺素E2(prostaglandin E2,PGE2)含量的影响,探讨孤束核在艾灸对胃黏膜损伤神经通路修复机制中的作用.方法:将48只SD大鼠随机分为4组(n=12):正常组(A组);模型组(B组);艾灸+模型组(C组);艾灸+模型+孤束核损毁组(D组).先将D组大鼠双侧孤束核损毁,护理3 d;继之将B、C、D组大鼠无水乙醇及阿司匹林混悬液灌胃造模3 d(A组生理盐水灌胃对照);再之C、D组大鼠进行艾灸捆绑处理(A、B组只绑不灸),2次/d,连续3 d.最后取全胃计算胃黏膜溃疡指数(ulcer index,UI),并检测血清及胃组织IL-4及PGE2含量.结果:B组胃黏膜损伤明显(P0.01),说明造模成功;C组UI较B组低(P0.01);与B组比较,C组大鼠组织及血清IL-4、P G E2含量显著升高(P0.01),而D组升高不明显,并且D组大鼠IL-4、PGE2含量明显低于C组(P0.05,P0.01),说明孤束核损毁后,艾灸对胃黏膜的修护作用受到影响.结论:艾灸足三里穴对胃黏膜损伤有明显修复作用,其修复作用可能与升高血清及胃组织IL-4及PGE2含量有关,而孤束核损毁能明显抑制其修复效应,证明孤束核可能是艾灸足三里穴产生胃黏膜修复效应信号传导通路中的重要调节部位.     

应激大鼠胃黏膜氧化应激指标受褪黑素影响的研究

目的探讨褪黑素干预应激大鼠胃黏膜氧化应激指标影响的研究.方法采用浸水-束缚(WIR)应激实验复制大鼠应激性溃疡模型.应激前30 min,MT(melatonin)5、20mg·kg-1和应激组大鼠分别腹腔注射MT 5、20mg·kg-1和等体积生理盐水.应激6h后,观察各组大鼠胃黏膜病变情况,对溃疡指数(UI)进行评分,同时检测各组大鼠胃黏膜内丙二醛(MDA)含量、胃黏膜超氧化物歧化酶(SOD)活性和还原型谷胱甘肽(GSH)水平.结果WIR应激6h后,应激组大鼠胃黏膜MDA水平显著高于对照组(P＜0.01).MT 5、20mg·kg-1组较应激组MDA水平显著下降(P＜0.01),且MT 20mg·kg-1组显著低于MT 5mg·kg-1组(P＜0.01).应激组大鼠SOD、GSH活性较对照组明显降低(P＜0.01),MT 5、20mg·kg-1组较应激组SOD、GSH活性有升高趋势.比较各组UI发现,MT 5、20mg·kg-1组UI显著低于应激组(P＜0.01),其中MT 20mg·kg-1组UI显著低于MT 5mg·kg-1组(P＜0.05).结论褪黑素通过其抗氧化的作用对应激大鼠胃黏膜损伤起保护作用.     

电针抗应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶的变化

观察应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶（NOS）活性的变化．并对电外足三里穴和阳陵泉穴NOS的变化及与胃粘膜损伤的关系作了比较。结果发现,应激性胃溃疡大鼠脑组织和胃粘膜NOS均增高，尤其是胃粘膜NOS增高非常显著（P＜0.01）；电针足三里使脑和胃NOS回降，应激前先电针更为明显，使胃溃疡损伤指数显著下降（P＜0.01）；而电针阳陵泉．与应激组相比虽也下降，但无统计学意义。提示NOS参与了电针对应激所致胃粘膜损伤的保护．这种保护作用可能与中枢和肠神经系统对胃功能的双重调节有关，同时NOS的变化与电针胃经足三里穴位特异性有一定的联系。     

艾灸足三里和梁门穴诱导热休克蛋白70抗大鼠胃黏膜氧化损伤作用

目的:观察艾灸足三里和梁门穴对应激性溃疡大鼠胃黏膜热休克蛋白70(HSP70)表达的影响,探讨艾灸足阳明经穴抗胃黏膜氧化损伤的作用机制.方法:将SD大鼠60只完全随机平均分为空白组、模型组、艾灸足三里等穴组和艾灸非穴对照点组,采用水浸-束缚应激法制备应激性溃疡模型.按Guth法计算胃黏膜损伤指数(UI),用激光多普勒血流仪测定胃黏膜血流量(GMBF),用免疫组织化学法和硫代巴比妥酸染色法对处理后大鼠检测其胃黏膜HSP70的表达和丙二醛(MDA)的含量.结果:与模型组和艾灸非穴组比较,艾灸足三里等穴可使应激性溃疡大鼠胃黏膜损伤指数明显下降(14.100±5.425vs26.800±9.807,26.200±7.729,P<0.01),HSP70表达上调(0.133±0.035vs0.077±0.057,0.059±0.038,P<0.01)、血流量增高(279.827±172.862mL/minvs139.489±33.133,141.512±58.450mL/min,P<0.05)、MDA含量减少(2.586±0.252μmol/Lvs3.906±0.768,3.464±1.502μmol/L,P<0.05).结论:艾灸足三里和梁门穴能诱导胃黏膜HSP70高表达并降低MDA含量,以达到其抗氧化损伤作用,并有相对的穴位特异性.     

大鼠运动应激性胃溃疡模型的建立以及苦苣总黄酮的预防作用

背景:近年运动应激性胃溃疡受到广泛关注,有研究证实苦苣总黄酮有抗炎、抗氧化作用。目的:建立快速、稳定、可重复的大鼠运动应激性胃溃疡模型,并探讨苦苣总黄酮对运动应激性胃溃疡的干预作用。方法:100只Wistar大鼠随机分为安静对照组、1 h无负荷运动组、1 h负荷运动组、2 h无负荷运动组和2 h负荷运动组,每组20只,雌雄各半。采用游泳方式建立大鼠运动应激性胃溃疡模型,观察胃黏膜溃疡指数(UI)和病理学改变。40只雄性Wistar大鼠随机分空白对照组、1 h负荷运动模型组、大剂量苦苣总黄酮组(生药3.2 g/kg)和小剂量苦苣总黄酮组(生药1.6 g/kg),观察胃黏膜病理学改变,检测胃黏膜SOD以及胃黏膜和血清MDA含量。结果:与1 h负荷运动组相比,1 h无负荷运动组UI显著降低(P<0.01),2 h负荷运动组显著升高(P<0.01),2 h无负荷运动组无明显差异(P>0.05)。1 h、2 h无负荷运动组和1 h负荷运动组雄性大鼠UI明显高于雌性大鼠(P<0.05)。与空白对照组相比,1 h负荷运动后大鼠胃黏膜SOD含量明显降低(P<0.01),胃黏膜和血清中MDA含量明显上升(P<0.05),大剂量苦苣总黄酮可明显改善上述指标(P<0.05)。结论:1 h负荷游泳运动可有效快速地建立大鼠运动应激性胃溃疡模型。大剂量苦苣总黄酮对运动引起的大鼠应激性胃溃疡有明显预防作用。     

艾灸足三里、梁门穴对应激性溃疡大鼠胃黏膜细胞凋亡的干预作用

目的:探讨艾灸足三里、梁门穴对应激性溃疡胃黏膜细胞凋亡的影响,分析其与血浆多巴胺(DA)、胃黏膜内皮素(ET)的关系,揭示艾灸足三里、梁门穴对抗应激性损伤,进而保护胃黏膜的机制.方法:SD大鼠60只随机分为4组,即束缚对照组、模型组、艾灸足三里和梁门穴组、艾灸非穴点对照组,每组15只.束缚水浸应激法造模,免疫组化方法测定细胞凋亡指数(×10-6个/μm2).采用生物信号分析仪检测胃黏膜血流量(GMBF),高效液相色谱法测定血浆DA含量,放射免疫法测定胃黏膜ET含量.结果:预先艾灸足三里、梁门穴可显著降低随后的应激性胃黏膜损伤指数,降低胃黏膜ET和血浆DA含量,增加胃黏膜血流量,降低胃黏膜细胞凋亡指数.造模后,B组UI值(26.80±9.81vs12.00±5.94,P<0.01)、血浆DA(9.97±3.69μg/Lvs4.54±2.61μg/L,P<0.01)、胃黏膜ET(361.469±98.080ng/Lvs149.205±94.1425ng/L,P<0.01)以及凋亡指数(9.65±4.19vs4.36±2.60,P<0.01)显著高于A组,而GMBF低于A组(139.489±33.133mL/minvs377.090±85.840mL/min,P<0.01);C组UI值、凋亡指数显著低于B组和D组(UI:14.10±5.42vs26.80±9.81,26.20±7.23,P<0.01;凋亡指数:3.00±1.58vs9.65±4.19,8.20±5.17,P<0.01),而GMBF高于B组和D组(316.552±85.469mL/minvs139.489±33.133,141.512±58.450mL/min,P<0.01);C组血浆DA含量及胃黏膜ET显著低于B组(DA:4.41±2.48μg/Lvs9.97±3.69μg/L,P<0.01;148.271±69.113ng/Lvs361.469±98.080ng/L,P<0.01),但与D组比较无显著性差异(P>0.05).结论:艾灸足三里、梁门穴预处理可减轻束缚水浸应激所造成大鼠胃黏膜的损伤程度,这一作用可能是通过降低血浆DA和胃黏膜ET含量,增加胃黏膜血流量,抑制细胞凋亡实现的.     

艾灸预处理对应激性溃疡大鼠胃黏膜HSP70蛋白及mRNA表达的影响

目的:观察艾灸足三里和梁门穴预处理对应激性溃疡大鼠胃黏膜热休克蛋白70(HSP70)及其基因表达的影响,探讨艾灸足阳明经穴保护胃黏膜的作用机制.方法:将60只大鼠完全随机分为空白组(A)、模型组(B)、艾灸足三里等穴组(C)和对照组(D)4组,采用水浸-束缚应激法(WRS)制备应激性溃疡模型.按Guth法计算胃黏膜损伤指数(UI),用免疫组织化学法、逆转录聚合酶链式反应(RT-PCR)法和放射免疫法分别检测处理后大鼠胃黏膜HSP70,HSP70mRNA的表达和内皮素(ET)、前列腺素E2(PGE2)的含量.结果:SU大鼠胃黏膜损伤指数B组与A、C组(P=0.000,P=0.001),D组与A、C组(P=0.001)有显著性差异,艾灸足三里等穴可使SU大鼠胃黏膜损伤指数明显下降.胃黏膜PGE2含量A组与B、D组比较差异显著(P=0.011,P=0.028),C组与B、D组比较差异显著(P=0.020,P=0.048),经艾灸预处理的大鼠胃黏膜PGE2含量均有不同程度升高.ET含量B组与A组之间有显著差异(P=0.040),经艾灸预处理的大鼠ET含量下降显著,B组与C组相比差异显著(P=0.020).造模后胃黏膜的HSP70蛋白和mRNA表达均有不同程度的增强,B组与A组相比有显著性差异(P=0.039,P=0.008);经艾灸预处理后HSP70蛋白和mRNA显著增强,C组与B、D组比较有统计学意义(蛋白:P=0.003,P=0.035;mRNA:P=0.000,P=0.001).结论:艾灸足三里、梁门穴能通过增强HSP70的蛋白和基因表达,达到对胃黏膜的保护作用,并有一定的穴位特异性.     

Dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress in rats

AIM: To investigate the dynamic functional and ultrastructural changes of gastric parietal cells induced by water immersion-restraint stress (WRS) in rats. METHODS: WRS model of Sprague-Dawley (SD) rats was established. Fifty-six male SD rats were randomly divided into control group, stress group and post-stress group. The stress group was divided into 1, 2 and 4 h stress subgroups. The post-stress group was divided into 24, 48 and 72 h subgroups. The pH value of gastric juice, ulcer index (UI) of gastric mucosa and H , K -ATPase activity of gastric parietal cells were measured. Ultrastructural change of parietal cells was observed under transmission electron microscope (TEM). RESULTS: The pH value of gastric juice decreased time-dependently in stress group and increased in post-stress group. The H , K -ATPase activity of gastric parietal cells and the UI of gastric mucosa increased time-dependently in stress group and decreased in post-stress group. Compared to control group, the pH value decreased remarkably (P = 0.0001), the UI and H , K -ATPase activity increased significantly (P = 0.0001, P = 0.0174) in 4 h stress subgroup. UI was positively related with stress time (r = 0.9876, P < 0.01) but negatively with pH value (r = -0.8724, P < 0.05). The parietal cells became active in stress group, especially in 4 h stress subgroup, in which plenty of intracellular canalicular and mitochondria were observed under TEM. In post-stress group, the parietal cells recovered to resting state. CONCOUSION: The acid secretion of parietal cells is consistent with their ultrastructural changes during the development and healing of stress ulcer induced by WRS and the degree of gastric mucosal lesions, suggesting gastric acid play an important role in the development of stress ulcer and is closely related with the recovery of gastric mucosal lesions induced by WRS.     

Effect of pre-moxibustion on apoptosis and proliferation of gastric mucosa cells

AIM： TO observe the effects of pre-moxibustion on apoptosis and proliferation of gastric mucosal cell in rats with stress-induced ulcer, and to analyze the relationship between those effects and the expression of heat-shock protein 70 （HSP70）.
METHODS： Sixty healthy Sprague Dawley rats were randomly assigned into four groups, namely group A, B, C and D. The animal model of stress ulcer was established by water immersion and restraint stress. The rats in group A, B, and D served as the restraint, model, and non-acupoint controls, respectively, while those in group C received moxibustion at Zusanli and Uangmen points. Immunohistochemical methodology was used to detect the expression of HSP70, apoptosis index （AI, × 10^-6/μm^2） and proliferation index （PCNA-LI, × 10^-6/μm^2）. The mucosal expression of transforming growth factor α （TGF-α） was detected by radioimmunoassay.
RESULTS： IVloxibustion at Zusanli and Liangmen points significantly decreased the gastric injury and the apoptosis of gastric mucosal cells, while markedly increased the mucosal expression of TGF-α and HSP70 as well as the proliferation of gastric mucosal cells. Compared with group A, ulcer index （UI） （26.8 ± 9.8 vs 12.0 ± 5.9, P 〈 0.01）, AI （9.6 ± 4.2 vs 4.4 ± 2.6, P 〈 0.05） and expression of HSP70 （9.6 ± 4.2 vs 4.4 ± 2.6, P 〈 0.05） were significantly increased, but the content of TGF-α （104.7 ± 51.2 pg/mL vs 254.0 ± 86.9 pg/mL, P 〈 0.01） and PCNA-LI （6.9 ± 4.7 vs 14.9 ± 4.6, P 〈 0.05） were significantly decreased in group B. However, ulcer index values （UI） and AI were obviously lower in group C compared to groups B and D （14.1 ± 5.4 vs 26.8 ± 9.8 and 26.2 ± 7.7, P 〈 0.01, 3.0 ± 1.6 vs 9.6 ± 4.2 and 8.2 ± 5.2, P 〈0.05, respectively）, but content of TGF-α （237.0 ± 72.6 pg/mL vs 104.7 ± 51.2 pg/mL and 154.1 ± 61.3 pg/mL, P 〈0.01） and expression of HSP70 （0.13 ± 0.03 vs 0.08 ± 0.06 and 0.06 ± 0.04, P 〈 0.05） were higher in group C. Furth     

电针刺激内关穴对模拟失重大鼠心脑血管氧化应激的影响

目的 探讨电针刺激内关穴对模拟失重大鼠心脑血管氧化应激水平的影响。 方法 30只雄性SD大鼠随机分为尾吊组、穴位刺激尾悬吊组和对照组,尾吊组和穴位刺激尾吊组大鼠均头低位-30°尾吊7 d,穴位刺激尾吊组大鼠需进行每天30 min的电针刺激内关穴,对照组不做任何处理。三组均在7 d后测量血清、心脏组织、脑组织、颈动脉及股动脉的超氧化物歧化酶（SOD）和丙二醛（MDA）含量。 结果 尾悬吊后大鼠血清及各血管组织中SOD含量显著低于对照组,MDA含量则显著高于对照组（P<0.05）。给予电针刺激后,穴位刺激尾悬吊组大鼠SOD和MDA含量与对照组相比无显著差异。 结论 电针刺激大鼠内关穴可减轻7 d尾悬吊模拟失重效应所产生的心脑血管氧化应激。     

结肠途径治疗对高温中暑狗肝脏的保护作用

目的:探讨结肠途径治疗对高温中暑狗肝脏的保护作用.方法:建立高温中暑狗的动物模型,将狗随机分为两组(肠疗组、常规组),比较两组的降温时间,测定两组中暑前、中暑后6,24,48 h的血谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化酶歧化酶(SOD)水平.中暑后48 h处死狗,测定肝脏MDA和SOD含量,并行肝脏光镜和电镜病理学检查.结果:与常规组相比,肠疗组降温时间明显缩短(t=5.39,P＜0.01);血ALT,AST,MDA在中暑后24 h (t=3.46,P＜0.01;t=3.74,P＜0.01;t=2.43,P＜0.05)和48 h(t=3.33,P＜0.01;t=2.97,P＜0.05;t=3.32,P＜0.01)均明显降低,血SOD在中暑后24 h (t=2.44,P＜0.05)和48 h (t=4.34,P＜0.01)明显增高;肝脏MDA明显下降(t=4.08,P＜0.01),SOD明显升高(t=6.52,P＜0.01).两组血LDH各时间点均无显著性差异.病理学检查光镜下可见肠疗组肝细胞淤胆、脂肪变性、坏死等损害较常规组明显减轻,肝窦充血减轻,炎细胞浸润较少.电镜下见肠疗组线粒体嵴融合及粗面内质网脱颗粒现象较常规组减轻.结论:结肠途径治疗可加快高温中暑狗降温速度,促进血清酶恢复,减轻肝脏脂质过氧化损伤和病理损害,对高温中暑狗肝脏具有保护作用.     

Effects of electro-needling at Zusanli on stress gastric ulcer in rats: Changes in nitric oxide and catecholamine

AIM: To investigate the effects of electro-needling at Zusanli (ST36) on changes of nitric oxide (NO), dopamine (DA) and norepinephrine (NE) in rats with stress gastric ulcer. METHODS: By biochemical methods the changes in contents of NO, DA and NE in gastric antral mucosa, corporal ventriculi mucosa and in blood after electro-needling (EN) were analysed. For observation all animals were randomly divided into four groups: stress group, EP after stress group, stress after EP group and control group. RESULTS: NO content in serum of stress gastric ulcer rats (5.78 ± 1.49 μmol/L) was significantly decreased, as compared with the control group (13.30 ± 2.75 μmol/L; P < 0.01). DA content in gastric antral mucosa was markedly decreased (3.31 ± 0.67 ng/mg vs 6.78 ± 4.65 ng/mg, P < 0.05). DA in corporal ventriculi mucosa showed a tendency to increase. EN at Zusanli made NO level recover in stress gastric ulcer rats (7.91 ± 1.11 μmol/L), as compared with the stress group (P < 0.01). EN regulated DA and NE contents in antrum and corpora ventriculi mucosa bi-directionally, i.e., the contents were decreased when they formerly rose, and increased when formerly fell, respectively, as compared with the stress group (P < 0.01). CONCLUSION: EN has a protective effect on the gastric mucosa. EN bi-directionally regulates DA and NE, and the vascular relaxation partially brought about by NO regulates the gastric mucosal blood flow, and strengthens the defensive function of the gastric mucosa.     

Protective role of metallothionein in stress-induced gastric ulcer in rats

AIM: To illustrate the pathophysiological role of metallothionein (MT) in gastric ulcer induced by stress. METHODS: Wistar rats underwent water-immersionrestraint (WIR) stress, ZnSO_4 (an MT inducer) treatment, WIR+ZnSO_4 or WIR+MT, and the ulcer index (UI) was estimated in excised stomach and liver tissues. The mRNA level of gastric MT was determined by semi-quantitative RT-PCR. The MT content in gastric and hepatic tissues was determined by Cd/hemoglobin affinity assay. The lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CD) were estimated by use of thiobarbituric acid reactive species and ultraviolet spectrophotometry. RESULTS: WIR stress induced severe gastric mucosal lesions in rats. Compared with control rats, stressed rats had increased lipid peroxide content in serum and stomach and liver tissues. MDA content was increased by 34%, 21% and 29% and CD level by 270%, 83% and 28%, respectively. MT content in the stomach and liver was increased by 0.74- and 1.8-fold, and the MT-mRNA level in the stomach was increased by 26%. Pretreatment with ZnSO_4 prevented gastric lesion development (the UI was 87% lower than that without pretreatment), and the MDA and CD content in serum and tissues was lower. The MT content in the liver was double in rats that were not pretreated, and the MT mRNA level in the stomach was 35% higher. MT administration 1 h before the WIR stress prevented gastric lesion development (the UI decreased by 47% compared with that in rats not pretreated), and the MDA and CD content in serum and tissues was significantly lower. CONCLUSION: In WIR-stressed rats, the MT level was increased in serum and in stomach and liver tissues. Pre-administration of exogenous MT or pre-induction of endogenous MT can protect the gastric mucosa against stress-induced ulcers and inhibits the formation of stressinduced lipid peroxide. MT could have a gastroprotective effect and might be a new interventive and therapeutic target in stress-induced gastric ulcers.     

水浸束缚应激大鼠胃壁细胞形态和泌酸功能的研究

背景:应激性溃疡(SU)是临床危重疾病的常见并发症,通常认为胃黏膜缺血是SU的主要发病机制,而胃酸则在此基础上起重要作用,但胃酸在SU发病中的确切作用尚未完全阐明.目的:研究水浸束缚应激(WRS)大鼠胃壁细胞形态和泌酸功能的变化,以进一步阐明胃酸在SU发病中的作用.方法:将15只Sprague-Dawley大鼠随机分为WRS2 h组、WRS 4 h组和正常对照组,予相应处理后测定胃液pH值,处死大鼠,评估胃黏膜溃疡指数(UI),以免疫荧光技术标记H /K -ATP酶后用激光共聚焦扫描显微镜观察壁细胞形态并进行分类和计数.分析胃液pH值与胃黏膜UI和分泌期壁细胞数之间的关系.结果:WRS 2 h组和WRS 4 h组的胃液pH值均较正常对照组显著降低(P＜0.01),两组WRS组之间则无显著差异.WRS 2 h组和WRS 4 h组的胃黏膜UI和分泌期壁细胞(网格样细胞)数均显著高于正常对照组(P＜0.01),其中WRS 4 h组显著高于WRS 2 h组(P＜0.01).正常对照组的胃液pH值与分泌期壁细胞数呈负相关(r＝-0.81,P＜0.05),WRS组的胃液pH值与胃黏膜UI和分泌期壁细胞数均呈负相关(r=-0.85,P＜0.05;r=-0.89,P＜0.05).结论:WRS大鼠的胃酸分泌与胃黏膜UI和分泌期壁细胞数呈正相关,从细胞学水平证明胃酸增高在SU的形成中起重要作用.