针刺大鼠耳胃穴对幽门结扎型胃溃疡模型影响

通过针刺大鼠耳胃穴、针刺大鼠耳类心穴、空白对照三种方法处理１４天后，采用幽门结扎的方法制备大鼠胃溃疡模型，１８ｈ后处死大鼠，比较观察三种方法对模型大鼠胃液量、胃液ｐＨ值、胃蛋白酶活性及溃疡发生率、溃疡等级的影响，结果证实，针刺耳胃穴在提高胃液ｐＨ值及降低胃蛋白酶活性、溃疡发生率、溃疡等级等方面优于针刺耳类心穴及空白对照（Ｐ＜０．０５～０．０１）．３种处理方法对胃液量影响不大（Ｐ＞０．０５）。提示针刺耳胃穴对胃溃疡有一定的治疗作用。     

止血愈疡颗粒对幽门结扎型胃溃疡大鼠氧自由基参数的影响

目的：观察止血愈疡颗粒（ZY）对幽门结扎型胃溃疡大鼠组织，血中氧自由基参数的影响。方法：将动物随机分成正常组，假手术组，空白对照组，甲氰咪胍（CI）组，ZY组，后3组采用幽门结扎法建立胃溃疡模型，观察胃溃疡组织，血中氧自由基参数变化及与溃疡积分之间的关系。结果：幽门结扎型胃溃疡大鼠血中超氧化物歧化酶（SOD）活性降低，丙二醛（MDA）含量增加，胃溃疡组织SOD，谷胱甘肽过氧化酶（GSHpx)活性降低，MDA含量增加与溃疡积分之间存在显著正相关，ZY能提高组织中SOD，GSHpx活性及血中SOD活性，降低组织中MDA含量，结论：ZY有抗氧自由基损伤，减少溃疡形成的作用。     

养胃宁片治疗胃溃疡病的药理研究

目的：探讨养胃宁片治疗胃溃疡的作用机制。方法：用消炎痛、阿司匹林、冰乙酸(HAC)和幽门结扎所致4种大鼠溃疡模型，观察养胃宁的治疗作用，并测定对胃液分泌及胃酸、胃蛋白酶的影响。对小鼠用0．6％HAC致扭体法和电刺激法测定其镇痛作用。结果：养胃宁能显著使溃疡面积缩小，抑制胃液分泌，降低其酸度，保护胃粘膜免受损害，对小鼠有镇痛作用。结论：养胃宁抗溃疡作用与抑制胃酸分泌、阻止胃粘膜受损、增加血流量有关。     

牛磺酸对大鼠肝纤维化形成的影响

目的 :观察牛磺酸对实验性大鼠肝纤维化的作用。方法 :用四氯化碳诱导大鼠肝纤维化模型 ,实验分4组 :正常对照组 ,模型对照组 ,牛磺酸高、低剂量组 ,观察大鼠血清丙氨酸氨基转移酶 (ALT)、白蛋白 (Alb)、总胆红素 (TBil)、透明质酸 (HA)、Ⅲ型前胶原 (PCⅢ )、层粘蛋白 (LN)及肝组织中超氧化物歧化酶 (SOD)活性、丙二醛(MDA)含量 ,并观察肝组织病理变化。结果 :牛磺酸治疗组血清ALT、TBil、HA、PCⅢ、LN及肝组织MDA水平显著降低 ,血清Alb及肝组织中SOD活性明显升高 ,肝纤维化程度减轻。结论 :牛磺酸具有抗肝纤维化作用 ,其机制可能与抗脂质过氧化有关     

深入开展幽门螺杆菌与胃癌关系的研究

幽门螺杆菌 (Ｈｐ)与胃癌的关系首先是建立在一个合理的生物学假说上。Ｃｏｒｒｅａ提出的从慢性胃炎到胃癌发病的序列学说 ,即慢性胃炎→萎缩→肠化→异型增生→胃癌。在Ｈｐ发现之前 ,便有大量流行病学证据支持序列学说并得到普遍接受。而Ｈｐ是慢性胃炎的最重要病因亦已得到确认。近 10多年来 ,对Ｈｐ与胃癌关系进行了大量流行病学研究 ,其中最有说服力的证据来自前瞻性的队列研究 ,多数研究证明Ｈｐ感染增加胃癌危险性。通过综合分析发现 ,差异主要在于随访时间不同 ,延长随访时间 ,Ｈｐ感染者胃癌危险性的ＯＲ值 (优势比 )显著增大。Ｈ…     

幽门螺杆菌诱导大鼠胃黏膜细胞胃蛋白酶原

本研究应用新的大鼠胃黏膜细胞系 (ＯＵＭＳ 3 7) ,研究幽门螺杆菌 (Ｈｐ)提取物对胃蛋白酶原合成与分泌的影响[1] 。材料与方法一、Ｈｐ菌株及细胞提取物Ｈｐ菌株ＳｙｄｎｅｙＳＳ 1由日本冈山大学医学部细菌科横田副教授惠赠 ,Ｈｅｌａ细胞空泡试验证实为ＶａｃＡ阳性。Ｈｐ在布氏培养液中增菌培养 7ｄ收获 ,以 60 0 0ｒ/ｍｉｎ离心 3 0ｍｉｎ ,弃上清 ,用 2 0ｍｌ冰ＰＢＳ(ｐＨ7.4 )洗涤细菌 2次 ,将其置超声粉碎仪中破碎细菌 2 0ｍｉｎ ,4°Ｃ 2 0 0 0 0ｒ/ｍｉｎ离心 2 0ｍｉｎ ,收集上清 ,0 .4 μｍ滤纸过滤 ,- 70°Ｃ冰冻。二、大鼠…     

牛磺酸对大鼠胰岛素抵抗高血压的影响

目的探讨牛磺酸对胰岛素抵抗高血压大鼠的影响。方法在输注胰岛素和葡萄糖引起动物胰岛素抵抗高血压模型上，测量平均动脉压、心率、血糖，放射免疫法测定血浆胰岛素和内皮素及主动脉组织内皮素，用２－脱氧葡萄糖摄取评估骨骼肌葡萄糖转运活性，用乙醇沉淀法测定肌糖原合成，测定肝胰岛素清除。结果胰岛素抵抗高血压大鼠血压升高，心率加快，血糖和血浆胰岛素含量增加（Ｐ＜０．０１）。牛磺酸治疗可明显改善上述指标，并增加骨骼肌葡萄糖转运活性，促进肌糖原合成和肝胰岛素清除，同时减轻血浆和主动脉内皮素含量。结论牛磺酸治疗胰岛素抵抗高血压大鼠是有效的。     

牛磺酸对重度颅脑创伤大鼠脑组织AQP4/牛磺酸转运体基因的影响

目的研究牛磺酸（Tau）对重度颅脑创伤（TBI）大鼠脑组织的脑组织含水量、水通道蛋白-4（AQP-4）/Tau转运体（TAUT）基因表达的影响。方法按随机数字表法将84只雄性SD大鼠分为7组：假手术组（Sham组）、脑外伤组（TBI组）、Tau治疗组（Tau组）,Tau预防组（Pre-Tau组）、β-丙氨酸组（β-Ala组）、维生素C组（Vc组）、叶酸组（Fa组）,每组12只。后6组均采用液压打击制作重度TBI模型。造模成功后即刻尾静脉给药200 mg/kg。Sham组和TBI组给予相同量等渗盐水,24 h后取脑。采用HE染色法观察TBI后各组脑组织形态学变化、测定脑组织含水量,用荧光定量RT-PCR方法检测AQP-4/TAUT基因表达。结果形态学检查：TBI 24 h后,神经细胞肿胀,细胞丢失,细胞核固缩,突起短小消失,坏死灶边缘可见炎性细胞浸润,β-Ala组同TBI组。但与TBI组比较,Tau组、Vc组、Fa组、Pre-Tau组形态上无显著改善;脑组织含水量：与Sham组相比,TBI组、β-Ala组伤后24 h显著升高（P〈0.05）。而Tau组、Vc组、Fa组明显降低,与Sham组无统计学差异;Pre-Tau组显著低于Sham组（P〈0.05）。基因表达：与Sham组相比,TBI组脑组织AQP-4 mRNA表达量显著升高（P〈0.05）,Fa组TAUT mRNA表达量显著升高（P〈0.05）。结论 Tau、Vc、Fa及Tau预防性治疗均可以显著降低脑水肿和AQP-4基因表达,对TBI后脑水肿有较好的治疗作用,但Tau、Vc对TBI早期的TAUT无调节作用,其对脑组织含水量的有效性并不是通过调节TAUT实现的。     

牛磺酸对血脂的影响

目的研究牛磺酸对大鼠实验性高脂血症的影响。方法预先给予β－丙氨酸造成牛磺酸缺乏。建立正常与牛磺酸缺乏大鼠高脂血症动物模型。观察外源性补充牛磺酸对高脂血症大鼠血中总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、低密度脂蛋白胆固醇（ＬＤＬＣ）、高密度脂蛋白胆固醇（ＨＤＬＣ）的影响。结果（１）饲养法可诱发大鼠的实验性高脂血症，体内缺乏牛磺酸时，可加重高脂血症并出现明显动脉粥样硬化的病理改变；（２）每日口服牛磺酸（２ｇ／ｋｇ）能预防大鼠血中ＴＣ、ＴＧ升高或降低大鼠血中ＴＣ和ＴＧ水平，并能降低ＬＤＬＣ水平、升高ＨＤＬＣ水平。结论（１）内源性牛磺酸不足易导致血脂异常升高和动脉粥样硬化性病变；（２）牛磺酸对实验性高脂血症有良好降脂作用。     

三叶因子2基因治疗对实验性大鼠胃溃疡愈合影响的研究

目的探讨三叶因子2(TFF2)基因治疗对实验性大鼠胃溃疡的疗效及其机制。方法2005-06-10—2006-03-15南方医科大学南方医院消化病研究所将48只雄性Wistar大鼠随机分为2组,治疗组24只,对照组24只。治疗组每只应用pcDNA3.1g TFF2100μg,对照组每只应用等容积pcDNA3.1g TFF2100μg,均在造模时经胃壁浆膜下注入。用药后分别在第3、7、14天处死动物,测量大鼠胃溃疡指数、胃总酸度及黏液糖蛋白量的变化。结果在应用pcDNA3.1g TFF2的第3天,治疗组和对照组比较,各项指标差异无统计学意义(P>0.05);第7天,治疗组的黏液糖蛋白量显著增加,与对照组比较差异有统计学意义(P<0.01)。第14天,治疗组的溃疡面积显著缩小,与对照组比较差异有统计学意义(P<0.01);治疗组黏液糖蛋白量有所下降,不过与对照组比较差异也有统计学意义(P<0.05);而治疗组的胃总酸度变化不大,与对照组比较差异无统计学意义(P>0.05)。结论TFF2基因治疗对实验性大鼠胃溃疡愈合有促进作用,增加胃黏液糖蛋白的分泌是其促进溃疡愈合的机制之一,而与抑制胃酸分泌无关。     

三叶因子2基因治疗对实验性大鼠胃溃疡愈合影响的研究

目的 探讨三叶因子2（TFF2）基因治疗对实验性大鼠胃溃疡的疗效及其机制。方法2005—06-10-2006—03—15南方医科大学南方医院消化病研究所将48只雄性Wistar大鼠随机分为2组，治疗组24只，对照组24只。治疗组每只应用pcDNA3．1g＋TFF2 100μg，对照组每只应用等容积pcDNA3．1g＋TFF2 100μg，均在造模时经胃壁浆膜下注入。用药后分别在第3、7、14天处死动物，测量大鼠胃溃疡指数、胃总酸度及黏液糖蛋白量的变化。结果在应用pcDNA3．1g＋TFF2的第3天，治疗组和对照组比较，各项指标差异无统计学意义（P〉0．05）；第7天，治疗组的黏液糖蛋白量显著增加，与对照组比较差异有统计学意义（P〈0．01）。第14天，治疗组的溃疡面积显著缩小，与对照组比较差异有统计学意义（P〈0．01）；治疗组黏液糖蛋白量有所下降，不过与对照组比较差异也有统计学意义（P〈0．05）；而治疗组的胃总酸度变化不大，与对照组比较差异无统计学意义（P〉0.05）。结论 TFF2基因治疗对实验性大鼠胃溃疡愈合有促进作用，增加胃黏液糖蛋白的分泌是其促进溃疡愈合的机制之一，而与抑制胃酸分泌无关。     

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.     

苯妥英钠对大鼠实验性胃溃疡的保护作用

目的观察苯妥英钠对大鼠实验性胃溃疡的保护作用。方法采用水应激法、冰醋酸烧灼法建立大鼠动物实验两种溃疡模型随机分为苯妥英钠（PHT）大剂量组、小剂量组、雷尼替丁组和生理盐水组、连续给药14d，处死动物后观察实验结果。结果苯妥英钠大、小剂量组均显示出保护作用（P〈0.05），但大剂量组的保护作用不如小剂量组明显。结论苯妥英钠对大鼠实验性胃溃疡的胃黏膜有一定的保护作用，且保护作用与剂量成负相关，小剂量的保护作用要好干大剂量。     

Sex-specific effects of Eugenia punicifolia extract on gastric ulcer healing in rats

AIM To evaluate the sex-specific effects of a hydroalcoholic extract from Eugenia punicifolia(HEEP) leaves on gastric ulcer healing.METHODS In this rat study involving males, intact(cycling) females, and ovariectomized females, gastric ulcers were induced using acetic acid. A vehicle, lansoprazole, or HEEP was administered for 14 d after ulcer induction. Body weight was monitored throughout the treatment period. At the end of treatment, the rats were euthanized and the following in vivo and in vitro investigations were performed: macroscopic examination of the lesion area and organ weights, biochemical analysis, zymography, and evaluation of protein expression levels. Additionally, the concentration-dependent effect of HEEP was evaluated in terms of subacute toxicity and cytotoxicity.RESULTS Compared to the vehicle, HEEP demonstrated a great healing capacity by substantially reducing the ulcerative lesion area in males(52.44%), intact females(85.22%), and ovariectomized females(65.47%), confirming that HEEP accelerates the healing of acetic acidinduced gastric lesions and suggesting that this effect is modulated by female sex hormones. The antiulcer effect of HEEP was mediated by prostaglandin E2 only in male rats. Overall, the beneficial effect of HEEP was the highest in intact females. Notably, HEEP promoted the expression of vascular endothelial growth factor(intact vs ovariectomized females) and decreased the expression of Caspase-8 and Bcl-2(intact female vs male or ovariectomized female). Additionally, HEEP enhanced fibroblast proliferation and migration into a wounded area in vitro, confirming its healing effect. Finally, no sign of subacute toxicity or cytotoxicity of HEEP was observed.CONCLUSION In gastric ulcers, HEEP-induced healing(modulated by female sex hormones; in males, mediated by prostaglandin) involves extracellular matrix remodeling, with gastric mucosa cell proliferation and migration.     

阿司匹林对大鼠胃溃疡愈合的影响和机制

目的 探讨阿司匹林对胃溃疡愈合的影响和机制.方法 用乙酸诱导大鼠胃溃疡,8 d后随机分为模型组、盐水组、阿司匹林组.用组织学方法检测溃疡形态、肉芽组织中毛细血管数;用氢气清除法检测溃疡边缘胃黏膜血流;用免疫组化方法检测表皮生长因子(EGF)、血管内皮生长因子(VEGF)在胃黏膜中的表达并检测其积分光密度.结果 阿司匹林组的溃疡面积高于模型和盐水对照组(P<0.05);阿司匹林组的毛细血管数和胃黏膜血流低于模型和盐水组(P<0.01);阿司匹林组的EGF和VEGF积分光密度低于模型和盐水组(P<0.01).结论 阿司匹林通过抑制EGF和VEGF的表达抑制溃疡愈合.     

Effect of faeces trogopterorum extract B1 on the experimental gastric ulcer and gastric secretion in rats

AIM: To study the effects of extracts B1, B2, and B3 from faeces trogopterorum on the experimental gastric ulcer in rats.METHODS: Two different animal models of gastric ulcers were used in this experiment: Shay''s model (n = 72) and the reserpine-induced ulcer model (n = 76). The total volume and the pH of the gastric juices were recorded. The lesion scores of gastric mucosa were also recorded.RESULTS: The lesion scores of gastric mucosa in the Shay’s model of animals in the WLZ-B₁ groups treated with either 40 g/kg or 80 g/kg were 8.6 ± 10.8 and 1.6 ± 1.9 respectively, which were lower than that of the 0.9% NaCl control group (47.0 ± 31.4, P < 0.05, P < 0.01). The lesion scores for the 80 g/kg group was lower compared to those of the Ran group (20.5 ± 16.4, P < 0.01). The pH of the gastric juices of the 80 g/kg group (3.425 ± 0.143) was higher than that of the 0.9% NaCl group (2.836 ± 0.632, P < 0.05). In the reserpine model, the lesion score of the 40 g/kg group of the WLZ-B₁ (20.7 ± 16.5) was also lower than that of the 0.9% NaCl control group (76.3 ± 50.6, P < 0.05).CONCLUSION: B₁ is the most effective of the three sections in inhibiting gastric secretion, protecting gastric mucosa and preventing experimental ulceration.     

Importance of pepsin and stomach distension in morphological alterations of stress-induced gastric lesions in pylorus-ligated rats

Pylorus ligation changed the morphology and location of gastric lesions induced by water-immersion stress (WI stress) in rats; linear lesions in the corpus mucosa disappeared, and punctate lesions appeared in both the corpus and antrum, in association with the loss of H⁺ and the gain of Na⁺ in the gastric contents. Oral administration of antipeptic drugs such as amylopectin sulfate and sulfated glyptide or porcine pepsin significantly prevented or aggravated the lesions, respectively, although another type of elongated lesion appeared in response to high doses of antipeptic drugs. These antipeptic drugs or exogenous pepsin significantly reduced or increased pepsin activity, respectively, without effect on the acid output. Similar punctate lesions were produced in the atropinized rats (10 mg/kg) by instillation of acid solution (100 mM HCl plus 54 mM NaCl) with pepsin into the pylorus-ligated stomach and subjecting to WI stress. On the other hand, when the gastric contents were drained through a fistula to prevent accumulation of gastric juice in the pylorus-ligated stomach, WI stress again induced linear lesions only in the corpus mucosa. Acid hypersecretion in these rats induced by intravenous infusion of histamine, tetragastrin, or carbachol significantly aggravated the severity of lesions but did not change their morphology. These results suggest that pepsin in the presence of acid is prerequisite for development of gastric lesions in pylorusligated rats induced by WI stress. The morphological alterations may be accounted for by the distensions of the stomach due to accumulation of gastric juice in the lumen caused by pylorus ligation, but not due to acid hypersecretion.