牛磺酸对大鼠幽门结扎型胃溃疡的影响

目的:探讨牛磺酸对大鼠幽门结扎型胃溃疡的影响及其机制.方法:采用结扎大鼠幽门的方法建立大鼠胃溃疡模型.45只Wistar大鼠随机分为三组,即正常对照组、溃疡模型组和牛磺酸处理组.经6 h后各组大鼠处死,检测三组大鼠胃黏膜溃疡指数(UI)、胃液总酸度、胃蛋白酶活性和壁细胞H~ ,K~ -ATP酶活性.结果:与正常对照组相比,溃疡模型组大鼠UI值(35.3±3.7 vs,P<0.01)和胃液总酸度增大(28.56±3.81 mmol/L vs 20.34±4.40 mmol/L,P<0.01),同时胃液胃蛋白酶活性[7.58±1.58μg/(mL·min)vs 5.83±1.22μg/(mL·min),P<0.01]和壁细胞H~ ,K~ -ATP酶活性升高(8.86±1.50 U/mg vs 6.95±1.03 U/mg,P<0.01);而应用牛磺酸则减轻了大鼠应激性胃黏膜损伤,UI值(15.4±3.6 vs 35.3±3.7,P<0.01)和胃液总酸度减小(19.58±3.68 mmol/L vs 28.56±3.81 mmol/L,P<0.01),胃液胃蛋白酶活性[6.36±1.45μg/(mL·min)vs 7.58±1.58μg/(mL·min),P<0.05]和壁细胞H~ ,K~ -ATP酶活性(7.62±1.46 U/mg vs 8.86±1.50 U/mg,P<0.05)降低.结论:牛磺酸具有抗大鼠幽门结扎型胃溃疡的作用,其机制可能与抑制胃酸及胃蛋白酶分泌有关.     

应激状态下大鼠胃黏膜组织中内皮素-1A受体mRNA的表达及其意义

应激性溃疡(SU)是危重疾病的常见严重并发症,其发生机制尚不清楚。研究表明内源性缩血管因子内皮素(ET)-1与SU密切相关,而关于其受体表达在SU发生中作用的研究尚少。目的:探讨ET-1A受体(ETAR)mRNA表达在SU发生中的作用和意义。方法:以冷束缚应激(CRS)制备大鼠胃溃疡模型,应激前和应激1 h、3 h、6 h、9 h、12 h后分别采用放射免疫测定、逆转录聚合酶链反应(RT-PCR)和斑点杂交等方法,动态检测血浆和胃黏膜组织中的ET-1和胃黏膜组织中的ETAR mRNA水平,同时检测胃黏膜血流量(GMBF)和溃疡指数(UI)等指标的变化情况。结果:与正常对照组相比,各应激组大鼠血浆和胃黏膜组织中的ET-1水平均显著升高(P<0.05),GMBF显著下降(P<0.01),UI显著增加(P<0.01);胃黏膜组织中的ET-1水平与UI呈显著正相关(r=0.98,P<0.01),与GMBF呈显著负相关(r=-0.89,P<0.05),而血浆ET-1水平与GMBF、UI相关性不显著(r=-0.61,0.43,P>0.05)。GMBF与UI呈显著负相关(r=-0.98,P<0.01)。RT-PCR和斑点杂交显示各应激组大鼠胃黏膜组织中ETAR mRNA的表达水平较正常对照组显著升高(P<0.01),并与胃黏膜组织中的ET-1水平和UI呈显著正相关(r=0.93,0.95,P<0.01)。结论:在CRS诱发大鼠急性胃黏膜损伤的过程中,胃黏膜组织可显著增加ET-1的合成分泌和ETAR mRNA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.     

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.     

不同抗溃疡药物对应激性溃疡发生、发展过程中细胞凋亡的影响

背景：研究不同抗溃疡药物在防治应激性溃疡(SU)时，其对胃黏膜细胞学行为的作用是否有助于SU的防治。目的：观察抗溃疡药物奥美拉陛、米索前列醇和铝碳酸镁对SU的疗效，及其对细胞凋亡和与凋亡相关的细胞因子一氧化氮合酶(NOS)表达的影响。方法：水浸—束缚应激(WRS)结束后2h，计算胃黏膜损伤的溃疡指数(UI)；原位末端标记(TUNEL)法检测胃黏膜细胞凋亡；免疫组化法检测神经型NOS(nNOS)和诱导型NOS(iNOS)表达的变化。结果：奥美拉陛(0)组、米索前列醇(M)组和铝碳酸镁(H)组胃黏膜损伤均较生理盐水组显著减轻(P＜0．01)，胃黏膜细胞凋亡发生率均显著降低(P＜0．01)，但0组和M组的效果优于H组。与生理盐水组比较，3组用药组的nNOS表达均显著增加(P＜0．01)，iNOS表达均显著降低(P＜0．01)，M组和H组的nNOS表达升高较0组更为显著(P＜0．05)。结论：奥美拉唑、米索前列醇和铝碳酸镁作用于SU发生的不同环节，可显著抑制细胞凋亡的发生，对SU均有明显防治作用。寻找对细胞有直接保护作用的药物以提高细胞的抗应激能力可能是防治SU的最终途径。     

细胞凋亡和增殖在大鼠应激性溃疡发病中的作用

目的　从生化及形态学角度研究应激性溃疡 (SU)发生发展过程中胃黏膜细胞的死亡形式及增殖功能的变化。方法　原位末端标记 (TUNEL)法检测水浸 束缚应激 (WRS)结束前后不同时间点细胞凋亡的发生 ;透射电镜下观察细胞形态的变化 ;免疫组化ABC法原位检测增殖细胞核抗原(PCNA)蛋白的表达。结果　正常大鼠胃黏膜上皮散在TUNEL阳性细胞 ,PCNA蛋白主要在胃腺颈部近胃小凹处呈中等阳性表达。WRS 2h～WRS结束后 5hTUNEL阳性细胞较对照组明显增多 (P <0 .0 1)并逐渐达高峰 ,而PCNA表达较正常对照组显著减少 (P <0 .0 1) ;WRS后 8～ 12hTUNEL阳性细胞逐渐减少 ,而PCNA表达达高峰 ;WRS后 2 4hTUNEL阳性细胞仍高于正常水平 (P <0 .0 5 ) ,PCNA表达基本恢复至正常水平 (P >0 .0 5 )。透射电镜下可见正常胃黏膜细胞形态规则 ,核形规整 ;而发生凋亡的细胞形态各异。结论　应激期胃黏膜细胞凋亡明显增加 ,增殖能力下降 ,它们之间的失衡是溃疡发生的重要原因 ;在应激性损伤恢复的早期阶段 ,大量细胞发生凋亡可能是启动细胞增殖的必要条件。     

欣胃颗粒对慢性萎缩性胃炎大鼠胃黏膜病理形态学及胃液pH影响的研究

[目的]探讨欣胃颗粒治疗慢性萎缩性胃炎(CAG)的疗效及其机制.[方法]采用100 μg/ml甲基硝基亚硝基胍(MNNG)自由饮用,0.3 g/kg雷尼替丁喂养,配合饥饱失常等综合方法进行造模,3个月制成大鼠CAG模型.设正常、模型、维酶素组及欣胃颗粒高、中、低剂量治疗组,观察大鼠胃黏膜病理形态学及胃液pH变化.[结果]各药物治疗组大鼠胃黏膜均有不同程度改善,欣胃颗粒高、中、低剂量组与模型组、维酶素组比较,pH值明显降低(P＜0.05,或＜0.01).[结论]欣胃颗粒通过改善胃黏膜的病理形态,从而促进胃酸分泌治疗CAG.     

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.     

健胃消胀片对胃肠系统药理作用研究

[目的]研究健胃消胀片对胃肠系统的药理作用。[方法]建立盐酸乙醇致大鼠胃黏膜损伤模型和幽门结扎大鼠模型,测定小鼠小肠对碳末的推进率和小鼠胃对酚红液的排空率,观察健胃消胀片对胃黏膜保护、胃液分泌、小肠推进及胃排空的作用。[结果]健胃消胀片对盐酸乙醇所致大鼠胃黏膜损伤有保护作用,对幽门结扎大鼠有抑制胃酸分泌作用,对正常小鼠小肠推进有促进作用,与阳性对照组比较差异无统计学意义(P0.05),但显著高于正常对照组(P0.01或0.05);健胃消胀片对胃排空无明显影响(P0.05)。[结论]健胃消胀片能保护胃黏膜、抑制胃酸分泌、促进小肠运动。     

血管紧张素Ⅱ拮抗剂在大鼠应激性溃疡中的作用

目的:探讨血管紧张素Ⅱ拮抗剂在大鼠应激性溃疡(SU)中的作用.方法:水浸束缚应激后,肉眼计算胃黏膜溃疡指数(UI);取动脉血和胃液做血气分析计算胃黏膜内pH值;采用放射免疫方法检测血栓素B2(TXB2)和6-酮前列腺素F1α(6-K);观察胃组织病理形态学变化.结果:管紧张素Ⅱ拮抗剂组与阴性对照组比较,pH值、6-K水平显著升高(4.82±0.31vs4.53±0.11,P=0.026;974.95±109.11ng/Lvs654.50±221.31ng/L,P<0.01),而TXB2,UI显著降低(48.53±8.26ng/Lvs98.18±39.24ng/L,P<0.01;36.13±6.49vs69.00±33.27,P<0.01).病理形态学观察,血栓形成减少.血管紧张素Ⅱ拮抗剂组与奥美拉唑组比较,除6-K(974.95±109.11ng/Lvs737.61±96.10ng/L,P<0.05)外,其他数据无统计学差异.结论:血管紧张素Ⅱ拮抗剂通过舒张血管,增加胃黏膜血流量起到保护胃黏膜的作用,其机制可能是减轻肾上腺髓质对应激的反应,抑制由应激引起的儿茶酚胺的合成和释放,促进前列腺素的分泌.     

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.     

雷贝拉唑抑制大鼠胃壁细胞泌酸功能的机制研究

目的 探讨质子泵抑制剂雷贝拉唑对大鼠胃壁细胞泌酸功能的抑制作用.方法 将72只SD大鼠分成对照组(0.9%氯化钠溶液)、雷贝拉唑低剂量组(10 mg/kg)和雷贝拉唑高剂量组(20 mg/kg),每组24只.分别在1、2、4、6、12和24 h每组各处理4只大鼠.用氢氧化钠滴定法测定大鼠胃内pH值,比色法测定胃壁细胞内H+-K+-ATP酶活性,电镜下观察胃壁细胞超微结构的改变.结果 与对照组(1.97±0.30)相比,雷贝拉唑低剂量组(3.37±0.97)和高剂量组(5.96±0.26)在给药后1 h内胃液pH值显著升高(P<0.01),壁细胞H+-K+-ATP酶活性明显抑制(3.28±0.41比1.47±0.27和0.92±0.07,P<0.05).而且在给药12 h的差异仍有统计学意义(P<0.01).电镜下胃壁细胞超微形态改变与胃液pH值和壁细胞H+-K+-ATP酶活性变化相符.雷贝拉唑低剂量组与高剂量组在抑酸作用和起效时间方面差异有统计学意义(P<0.01).结论 壁细胞超微结构的变化和H+-K+-ATP酶活性能准确反映壁细胞的泌酸情况,雷贝拉唑能迅速强效抑制大鼠壁细胞的泌酸功能,且与剂量有关.     

左旋精氨酸甲酯及左旋精氨酸对应激状态下胃黏膜耐受性细胞保护作用的影响

目的：探讨内源性一氧化氮（NO）在应激状态下胃黏膜耐受性细胞保护中的作用及其可能的机制。方法：以重复浸水束缚应激（WRS）制作动物模型,以左旋精氨酸甲酯（L－NAME）或左旋精氨酸（L－Arg）抑制或促进内源性NO的合成,动态检测胃黏膜血流量（GMBF）、溃疡指数（UI）、黏膜一化氮含量的变化。结果：重复应激后,实验对照组大鼠UI明显下降,同时GMBF上升,黏膜内NO含量增高;L－NAME使WWRS引起的胃黏膜损伤加重,消除了GMBF的递增趋势,黏膜NO含量下降;而L－Arg可减轻WRS造成的黏膜损伤,GMBF、黏膜NO含量增相应增加;GMBF、UI、黏膜NO含量变化之间有相关关系。结论：内源性NO通过调节GMBF而介导耐受性细胞保护作用,L－NAME抑制其合成,延缓这一作用,L－Arg增加其合成,促进该作用。     

Influence of NG‐nitro‐L‐arginine methyl ester and L‐arginine on gastric mucosal tolerant cytoprotection under stress

OBJECTIVE : To determine the role of endogenous nitric oxide (NO) in gastric mucosal tolerant cytoprotection under stress and its possible mechanism. METHODS : Sprague–Dawley rats were exposed to repeated water immersion and restraint stress (WRS), during which N^G‐nitro‐L ‐arginine methyl ester (L ‐NAME), a non‐selective NO synthase inhibitor, and L ‐arginine (L ‐Arg), a substrate for NO synthesis, were administered to inhibit or promote the synthesis of endogenous NO, respectively. Gastric mucosal blood flow (GMBF) was measured with an LDF‐3 Flowmeter (Electronic Instrument Factory of Nankai University, Tianjin, China), the NO level in the gastric mucosa was monitored by the Griess reaction and gastric mucosal lesions were evaluated using the ulcer index (UI). The relationships between changes in GMBF, UI and NO content in the gastric mucosa were analyzed by linear correlation analysis. RESULTS : Repeated WRS induced gastric mucosal tolerant cytoprotection and this was accompanied by increased GMBF and NO levels in the gastric mucosa. Inhibition of endogenous NO synthesis by L ‐NAME worsened mucosal lesions induced by single WRS and, after repeated WRS, the adaptive incremence in GMBF was abolished and the NO content in the gastric mucosa was significantly reduced. In contrast, enhancement of endogenous NO synthesis by L ‐Arg attenuated mucosal erosions caused by single WRS. After repeated WRS, GMBF and the NO content in the mucosa increased gradually. Mucosal lesions were negligible after rats were exposed to the fourth WRS. CONCLUSIONS : During the tolerant cytoprotection, GMBF, UI and the NO content showed regular changes and there were good relationships between them. L ‐NAME and L ‐Arg changed the levels of endogenous NO, which, accordingly, affected GMBF and the gastric tolerance. By regulating GMBF, endogenous NO may play an important role in the gastric mucosal tolerant cytoprotection under stress. Inhibition of the synthesis of NO delayed the induction of tolerant cytoprotection, whereas increased NO synthesis promoted cytoprotection.     

Structure and function of rat parietal cells during treatment with omeprazole, SCH 28080, SCH 32651, or ranitidine

For 2 weeks four groups of adult female rats were given daily peroral doses of 400 mumols/kg of one of the following inhibitors of gastric acid secretion: omeprazole, SCH 28080, SCH 32651, or ranitidine; additional control rats were given vehicle only. Six rats in each group were killed 2 h after the last dose and another six in each group at 48 h. Samples of the gastric corpus wall were processed for light and electron microscopy. The maximal reduction of stimulated acid secretion in parallel gastric fistula rats was 100%, 90%, 40%, and 85%, respectively. Forty-eight hours after the last dose only SCH 28080 produced significant inhibition of acid secretion. 'Vacuolation' of parietal cells was occasionally observed in paraffin sections. Such 'vacuoles', which were not found in plastic sections, probably represent dilated secretory canaliculi. A small number of lucid parietal cells--presumably in the process of desquamation--were seen in all groups of rats; their proportion was significantly higher 2 h after the last dose of ranitidine, SCH 28080, or SCH 32651 than in the controls. Forty-eight hours after the last dose the proportion of such degenerating parietal cells was about the same in all groups.     

不同鼠龄大鼠胃内pH值与胃内细菌和肺部感染的关系

目的 研究不同鼠龄大鼠胃内pH值的变化与胃和肺部细菌数量变化的关系,以及胃内细菌的生长是否能引起大鼠肺部的炎性反应.方法 Wister大鼠30只,分为非老龄组、非老龄奥美拉唑组和老龄组.2周后检测大鼠胃内pH值,取大鼠胃和肺组织进行细菌培养,并行肺组织病理切片.结果 老龄组与非老龄组比较,大鼠胃内pH值(2.450±1.344和2.010±0.507,t=101.50)、胃内细菌数量[(5.579±4,316)cfu/g和(1.505±3.259)efu/g,t=80.003及肺部细菌数量[(1.617±3.509)cfu/g和(0.475±1.503)cfu/g,t=99.00],差异均无统计学意义(均为P>0.05);非老龄奥美拉唑组胃内pH(5.560±1.007,t=9.96)、胃内细菌数量[(9.942±1.663)cfu/g,t=57.003及肺内细菌数量[(6.272±3,830)cfu/g,t=66.00],与非老龄组比较,差异均有统计学意义(均为P<0.01).非老龄组与老龄组肺组织均有轻度淋巴细胞浸润,非老龄奥美拉唑组中30%的大鼠肺部炎症稍重.结论 随胃内pH值升高,大鼠胃及肺部细菌数量增加,组织学上可见肺部炎性反应增加.老龄鼠胃及肺部细菌数量增加不明显,组织学未见明显的肺部炎性反应.     

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.     

汉防己甲素对肝硬化门脉高压大鼠胃粘膜及肝脏的影响

为探讨汉防己甲素对门脉高压性胃粘膜病变的治疗作用，观察了汉防己甲素对门脉高压大鼠门脉压力、胃粘膜屏障功能、肝脏组织学和肝功能的影响，并与普萘洛尔进行了对比。结果表明，汉防己甲素和普萘洛尔均可使门脉高压大鼠的ＰＶＰ下降，胃粘膜ＰＧＥ２含量、ＧＭＢＦ和ＧＡＭ增加。但普萘洛尔使肝细胞坏死增加，ＡＬＴ和ＳＴＢ不能降低，ＡＬＰ反有升高。而汉防己甲素则使肝细胞损害减轻，肝内纤维组织减少，ＡＬＴ、ＡＬＰ和ＳＴＢ降至正常水平。提示，普萘洛尔虽可使ＰＨＴ性ＧＭＬ改善，却可加重肝损害。而汉防己甲素不仅可改善胃粘膜屏障功能，而且还能改善肝功能。