荆花胃康胶丸对阿司匹林致小鼠胃黏膜损伤的修复作用

目的:探讨中药荆花胃康胶丸对阿司匹林所致小鼠胃黏膜损伤的修复作用.方法:建立阿司匹林所致小鼠急性胃黏膜损伤模型,观察中药荆花胃康胶丸(30mg·kg-1,ig)与胶体果胶铋胶囊(130mg·kg-1,ig)对胃黏膜损伤的修复作用,计算溃疡指数和溃疡抑制率.结果:中药荆花胃康胶丸能明显缩小阿司匹林烧灼引起的溃疡面积,溃疡指数较单纯损伤组显著降低(P＜0.05);与胶体果胶铋组比较,胃黏膜溃疡指数和溃疡抑制率无明显差异,保护作用相当.结论:中药荆花胃康胶丸对阿司匹林所致的小鼠胃黏膜损伤有较好的修复作用.     

壳聚糖对乙醇急性损伤时大鼠胃壁细胞的影响

胃酸是胃黏膜最常见的内源性损伤因子,在胃黏膜损伤过程中起着重要作用.壁细胞的主要功能是分泌胃酸,其超微结构与泌酸关系密切.壳聚糖是少见的带正电荷的天然高分子聚合物,有研究发现壳聚糖有促进溃疡愈合和黏膜保护作用.     

吉法酯对阿司匹林致大鼠急性胃黏膜损伤的保护作用

目的:研究吉法酯等胃黏膜保护剂对阿司匹林致大鼠急性胃黏膜损伤的保护作用及其机制.方法:60只健康雄性Wistar大鼠随机分为6组:空白对照组、单纯损伤组、400mg·kg-1吉法酯保护组、80mg·kg-1枸橼酸铋钾保护组、0.1mg·kg-1米索前列醇保护组和0.5g·kg-1硫糖铝保护组;每组各10只.各保护组动物分别用相应的药物提前给予灌胃处理,然后用阿司匹林行腹腔注射致大鼠急性胃黏膜损伤,分别测定各组的胃黏膜溃疡指数、胃黏膜血流、胃黏膜氨基己糖含量等指标,并在显微镜下观察组织学变化,以评价损伤程度及预防保护效果.结果:各预防保护组与单纯损伤组比较,胃黏膜损伤指数明显下降(P<0.001),胃黏膜血流明显增加(P<0.001),胃黏膜氨基己糖含量亦明显增加(P<0.001).组织学切片亦显示各预防保护组的损伤程度及炎症反应均较单纯损伤组明显减轻.结论:吉法酯对阿司匹林所致大鼠急性胃黏膜损伤具有明显的预防保护作用,与枸橼酸铋钾和米索前列醇的保护作用相当,优于硫糖铝.     

兰索拉唑对乙醇诱导大鼠胃黏膜损伤的保护作用及其机制

目的　研究兰索拉唑 (LP)对乙醇诱导大鼠胃黏膜损伤的保护作用 ,探讨胃泌素受体和环氧化酶 2 (COX 2 )表达在此过程中的作用。方法　大鼠ig给予LP 0 5、5、5 0mg·kg-1·d-1,或ig联合给予LP 5 0mg·kg-1·d-1和胃泌素受体拮抗剂AG 0 4 1R 3、10、30mg·kg-1·d-1,对照组ig给予羧甲基纤维素 (CMC) 2 5mg·kg-1·d-1,连续 14d。末次给药后 8h各组大鼠ig给予无水乙醇 1ml,观察胃损伤指数 (LI)及光镜下的胃黏膜病理学改变。酶免疫方法测定胃黏膜前列腺素E2 (PGE2 )水平 ,WesternBlot和免疫组化检测胃黏膜COX 2表达。评价特异性COX 2抑制剂NS 398对LP诱导的PGE2 合成及胃黏膜保护作用的影响。结果　在 0 5、5、5 0mg·kg-1LP组 ,LI分别为 (2 5 3± 0 33) %、(1 84±0 2 9) %和 (0 83± 0 12 ) % ,小于对照组 (3 6 5± 0 19) % (P<0 0 5 ) ;胃黏膜PGE2 含量分别为 (42 7± 32 ) ,(483± 12 1)和 (6 14± 82 ) pg·g-1wwt ,高于对照组 (2 6 6± 81) pg·g-1wwt(P <0 0 5 )。LP剂量依赖性地增加大鼠胃黏膜COX 2表达。然而 ,同时给予AG 0 4 1R阻断了LP诱导的胃黏膜保护作用、COX 2表达和PGE2 合成。NS 398抑制LP诱导的PGE2 合成及胃黏膜保护作用。结论　LP的胃黏膜保护作用与内源性胃泌素激活胃泌素受     

Gastric mucosal blood flow in ethanol-induced mucosal damage in the rat

Gastric mucosal blood flow in ethanol-induced mucosal damage was studied in urethane-anaesthetised rats by reference to ¹⁴C-aminopyrine clearance in the gastric mucosa. Irrigation of the stomach with 30% ethanol in acid saline (100 mM HCl plus 50 mM NaCl) for 40 min broke the gastric mucosal barrier, as indicated by an increased outflow of Na⁺ and K⁺ ions and back-diffusion of H⁺ ions. Gastric mucosal blood flow also increased about 2-fold, decreasing after cessation of ethanol irrigation along with the net ion fluxes. The increase in gastric mucosal blood flow occasioned by 10, 20 and 30% ethanol in acid saline was directly proportional to the net fluxes of H⁺, Na⁺ and K⁺ ions. When the stomach was irrigated with 30% ethanol in a less acid medium (10 mM HCl, 90 mM choline chloride plus 50 mM NaCl) there was still a significant increase in the outflow of Na⁺ and K⁺ ions, but only a slight back-diffusion of H⁺ ions. During this low rate of acid back-diffusion 30% ethanol reduced gastric mucosal blood flow by about 50%. The results suggest that ethanol-induced mucosal damage in the rat is associated with an increase in gastric mucosal blood flow only if combined with back-diffusion of H⁺ ions.     

阿司匹林与幽门螺杆菌对胃酸分泌的影响

目的:探讨阿司匹林与幽门螺杆菌对胃酸分泌的影响。方法:用醋酸诱导大鼠胃溃疡,然后分为A组(生理盐水+生理盐水)、B组(幽门螺杆菌+生理盐水)、C组(阿司匹林+生理盐水)、D组(幽门螺杆菌+阿司匹林)。观察了环氧化酶-1、环氧化酶-2和胃泌素在胃黏膜中的表达,测定了胃黏膜前列腺素E2的含量和胃液的pH。结果:阿司匹林通过抑制环氧化酶的活性进而减少前列腺素E2生成来增加胃酸分泌,阿司匹林也通过增加胃泌素来增加胃酸分泌。幽门螺杆菌通过增加胃泌素来增加胃酸分泌。结论:阿司匹林与幽门螺杆菌对胃酸分泌有协同作用。     

Possible biochemical effects following inhibition of ethanol-induced gastric mucosa damage by Gymnema sylvestre in male Wistar albino rats

Context: Gymnema sylvestre (GS) R. Br. (Gymnema) (Asclepiadaceae) has been used from ancient times as a folk medicine for the treatment of diabetes, obesity, urinary disorder, and stomach stimulation.

Objective: The present study was designed to investigate the effects of G. sylvestre leaves ethanol extract on gastric mucosal injury in rats.

Materials and methods: Gastric mucosal damage was induced by 80% ethanol in 36?h fasted rats. The effect of G. sylvestre on gastric secretions induced in Shay rats was estimated. In stomach, wall mucus, non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), total proteins and nucleic acids levels were estimated. Histopathological changes were observed.

Results: G. sylvestre pretreatment at doses of 100, 200 and 400?mg/kg provided 27, 49, and 63% protection against the ulcerogenic effect of ethanol, respectively. Pylorus ligation accumulated 10.24?mL gastric secretions with 66.56 mEq of acidity in control rats. Pretreatment with G. sylvestre significantly inhibited the secretions volume and acidity in dose-dependent manner. Ethanol caused significant depletion in stomach-wall mucus (p < 0.001), total proteins (p < 0.01), nucleic acids (p < 0.001), and NP-SH (p < 0.001) levels. Pretreatment with G. sylvestre showed protection against these depleted levels in dose-dependent manner. The MDA levels increased from 19.02 to 29.22 nmol/g by ethanol ingestion and decreased with G. sylvestre pretreatments in dose-dependent manner.

Conclusion: The protective effect of G. sylvestre observed in the present study is attributed to its effect on mucus production, increase in nucleic acid and NP-SH levels, which appears to be mediated through its free radical scavenging ability and/or possible cytoprotective properties.     

Effect of acid secretion blockade on acute gastric mucosal lesions induced by Tityus serrulatus scorpion toxin in anaesthetized rats

Scorpion venom (TX) promotes gastric acid and pepsin secretion leading to acute gastric mucosal lesions (AGML), when injected in animals.The goal of the present study was to observe the effects of acid gastric secretion blockers over the incidence of TX-induced AGML in vivo. To verify this model, we used male albino rats, fasted 18-20 h (n=122) and anaesthetized with urethane (1.4 g/kg, i.p.). Their trachea and left femoral vein were both cannulated; the first to avoid airway obstructions during scorpion intoxication and the second for administration of saline, TX and acid blockers. Following the surgical procedure, the animals were divided in 10 groups of at least 10 animals each. Control groups were injected with NaCl 0.9% 1 ml/kg (n=10) or TX 375 μg/kg (n=32). Test groups (n=10, each) received atropine 5 mg/kg, cimetidine 10 mg/kg, ranitidine 2.5 mg/kg, ranitidine 5 mg/kg, omeprazol 1 mg/kg, omeprazol 4 mg/kg, octreotide 80 and octreotide 100 μg/kg 10 min before the TX was injected. After 1 h of intoxication, the stomach was resected for macroscopic study and the gastric secretion was collected for volume, pH and acid output assessment. We observed that all blockers were able to completely or partially prevent the TX-induced acid secretion as well as the AGML (p<0.05). Our data suggest the TX-induced AGML can be prevented by different class of acid blockers injected before the intoxication.     

Calcium and ethanol-induced gastric mucosal damage in rats

The effects of graded doses of ethanol on stomach mucosal damage and calcium levels were studied in rats. The influence of verapamil and/or calcium chloride on these changes was also investigated. Orally administered ethanol (20, 50 or 80% v/v) markedly decreased gastric glandular tissue calcium and it concentration dependently produced mucosal lesions. Pretreatment with verapamil (2.5 or 5 mg/kg, i.p.) dose dependently lessened glandular wall calcium levels and worsened ethanol-induced mucosal damage. Calcium chloride (50 mg/kg, i.p.) significantly prevented ethanol-induced gastric calcium depletion; it also dose dependently antagonized the damaging effect of ethanol as well as the lesion-intensifying action of verapamil. The findings that verapamil potentiated, whereas calcium chloride prevented, ethanol-induced glandular mucosal damage and tissue calcium changes indeed suggest that altered gastric cell calcium levels could be closely related to the mucosal lesions produced by ethanol in rats.     

栀子总苷对小剂量阿司匹林致胃黏膜损伤大鼠的保护作用

目的研究栀子总苷（TGZ）对小剂量阿司匹林所致胃黏膜损伤的保护作用。方法采用TGZ（140,70,35 mg.kg^-1）与小剂量阿司匹林（5.0 mg.kg^-1）连续ig给药14 d,观察栀子总苷140、70、35 mg.kg^-1 3个剂量组和对照组的胃黏膜损伤指数,并同时检测血清一氧化氮（NO）含量和一氧化氮合酶（NOS）的活性,以及胃组织中细胞间黏附分子（ICAM-1）的表达。结果TGZ用药组的胃黏膜损伤指数较模型对照组显著降低;与模型组比较,NO含量与NOS活性增加。免疫组化结果显示ICAM-1在模型组表达明显高于正常对照组,TGZ预防给药组可减少ICAM-1在胃组织中的表达。结论栀子总苷对小剂量阿司匹林所致胃黏膜损伤有明显的保护作用。     

水黄皮根乙酸乙酯萃取物对大鼠乙醇型胃黏膜损伤的保护作用(英文)

目的研究水黄皮根乙酸乙酯萃取物(PREA)对乙醇致胃黏膜损伤的治疗作用。方法建立乙醇致大鼠胃黏膜损伤模型,通过观察胃组织病理学改变、计算胃黏膜损伤指数、检测胃黏膜组织一氧化氮(NO)、丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性评价PREA对乙醇型胃黏膜损伤的保护作用。采用幽门结扎模型,观察PREA对大鼠胃液分泌和胃黏液分泌的影响。结果与模型组比较,PREA可剂量依赖性地降低乙醇所致胃黏膜损伤指数,明显改善胃黏膜损伤的病理变化,抑制乙醇引起的胃黏膜MDA含量升高及NO水平和SOD活性降低,并显著减少胃酸分泌、抑制游离胃酸酸度和总酸度,对胃蛋白酶活性没有明显影响。另外,可显著抑制幽门结扎模型大鼠胃腔游离黏液以及胃壁结合黏液的分泌。结论PREA对乙醇型胃黏膜损伤具有明显的保护作用,提示PREA可能成为预防或治疗乙醇所致胃损伤的药物。     

和胃冲剂对大鼠急性胃黏膜损伤的保护作用

目的：观察中药复方和胃冲剂对大鼠急性胃黏膜损伤的保护作用。方法：将40只健康♂性Spaque-Dawley大鼠随机分为5组：正常对照纽、模型对照组、和胃冲剂低、中、高剂量组，采用无水乙醇诱导大鼠急性胃黏膜损伤，分别测定各组大鼠的胃黏膜损伤指数、血浆超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量，并在光镜下观察胃黏膜病理学改变。结果：和胃冲剂各剂量组的损伤指数较模型对照组显著降低（P〈0．01），且呈剂量依赖性；血浆中SOD活性显著升高，MDA含量下降，黏膜损伤程度明显减轻。结论：和胃冲剂对无水乙醇诱导的急性胃黏膜损伤有明显的保护作用，其机制可能与抗氧化作用有关。     

竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用

目的观察竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用。方法取40只小鼠随机均分为对照组、模型组、维生素E(50 mg/kg)组以及竹叶黄酮25、50 mg/kg组。各组连续ig给药7 d,1次/d。末次给药1 h后,各组按10 mg/kg ig给予无水乙醇,制作胃黏膜损伤模型。建模4 h后,观察胃黏膜损伤面积,计算胃黏膜损伤指数和损伤抑制率。测定小鼠胃黏膜组织中一氧化氮(NO)、前列腺素(PEG2)含量以及血清中超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果与模型组比较,竹叶黄酮25 mg/kg组小鼠胃黏膜损伤面积减少,50 mg/kg组小鼠损伤程度最小。与模型组比较,竹叶黄酮25、50 mg/kg组小鼠胃黏膜损伤指数均明显降低(P0.01);胃黏膜组织NO、PEG_2含量明显升高(P0.01);血清SOD、MDA水平明显降低(P0.01),SOD/MDA比值明显升高(P0.01)。结论竹叶黄酮能拮抗乙醇诱导的胃黏膜损伤,其机制可能与其抗氧化、抑制氧自由基产生并升高胃黏膜NO、PEG_2含量有关。     

微米大黄炭对乙醇诱导大鼠急性胃黏膜损伤的保护作用及炎症因子的影响

目的：探讨微米大黄炭对乙醇所致急性胃黏膜损伤的保护作用及机制。方法：采用无水乙醇灌胃诱导大鼠急性胃黏膜损伤模型,测定各组大鼠胃黏膜一般状况、损伤指数,以及血清TNF-α、IL-6、IL-4水平。结果：模型组大鼠的胃黏膜损伤指数、IL-6、TNF-α水平均显著高于正常组（P<0.01）,IL-4水平显著低于正常组（P<0.05）。微米大黄炭组及奥美拉唑镁肠溶片组胃黏膜损伤指数低于模型组（P<0.05）,且微米大黄炭降低更明显（P<0.01）。微米大黄炭组较模型组的TNF-α、IL-6水平显著降低,IL-4水平显著升高,但较奥美拉唑镁肠溶片组比较无统计学差异（P>0.05）。结论：微米大黄炭对乙醇诱导的急性胃黏膜损伤具有一定的保护作用,其作用机制可能与抑制TNF-α、IL-6的释放,增加IL-4水平有关。     

牛磺酸对乙醇性胃粘膜损伤的保护机制初探

目的为了探讨牛磺酸抗乙醇性胃粘膜损伤的作用机制。方法采用大鼠实验性乙醇胃粘膜损伤模型，测定胃粘膜局部一氧化氮合成酶（ＮＯＳ）、内皮素（ＥＴ）和部分胃肠激素含量。结果牛磺酸可明显减轻胃粘膜损伤，抑制ＥＴ释放，增加ＮＯＳ活性及生长抑素（ＳＳ）和血管活性肠肽（ＶＩＰ）的含量。结论牛磺酸可明显减轻实验性乙醇胃粘膜损伤，其可能机制为调节胃粘膜局部ＥＴ、ＮＯＳ、ＳＳ、ＶＩＰ的活性和含量。     

Drugs acting at the GABAA receptor attenuate ethanol-induced gastric mucosal damage in vitro

1. Benzodiazepines (BZ) have been reported to protect against ethanol-induced gastric damage in rats in both in vivo and in vitro models. However, the effects of some drugs in the new in vitro model do not agree with results reported previously in in vivo studies. 2. Therefore, the aim of the present study was to modify the new in vitro model to a model that more closely resembles the in vivo model and, using the new in vitro model, to reassess the gastroprotective effects of some BZ and to assess the effects of some new compounds. 3. The rat stomach was isolated from the whole animal and kept in aerated Krebs' solution at 37 degrees C in an organ bath. Gastric mucosal damage was induced by instillation of 1 mL of 100% ethanol into the stomach. Drugs or their vehicle were administered inside the bath 15 min before ethanol instillation into the stomach. One hour after the instillation of ethanol, the stomach was removed from the organ bath, opened along the greater curvature and then examined for gastric mucosal damage. 4. The results indicate that, compared with vehicle pretreatment, ethanol-induced gastric mucosal damage was significantly reduced in a dose-dependent manner by pretreatment with clonazepam, a drug that acts as an agonist at central BZ sites of the GABAA receptor, and Ro 15-4513, a partial inverse agonist at BZ sites of the GABAA receptor. Flumazenil (an antagonist of central BZ sites of the GABAA receptor) did not affect gastric mucosal lesions provoked by ethanol. However, flumazenil significantly reversed the mucosal protective effects of clonazepam and Ro 15-4513. 5. CGS 9896 (a partial agonist at BZ sites of the GABAA receptor, with anxiolytic and anticonvulsant but no sedative effects) did not offer any protection against ethanol-induced gastric mucosal damage. Ro 5-3663, an atypical BZ that binds to the picrotoxin site of the GABAA receptor and reported to be a potent convulsant and only a weak antagonist of GABA, did not show any protection against the development of lesions. 6. The results suggest local gastric mediation of the effects of ethanol, as well as the gastric protective effects of BZ, through an action at local central-type BZ sites of the GABAA receptor located in the rat stomach.     

Surgical vagotomy enhances the Indomethacin–Induced gastrointestinal mucosal damage in rats

Karádi O, Bódis B, Király á, Abdel-Salam OME, Sütō G, Vincze á, Mózsik Gy. Surgical vagotomy enhances the indomethacin-induced gastrointestinal mucosal damage in rats. Inflammopharmacology. 1994;2:389-399. Indomethacin (IND)-induced gastrointestinal mucosal lesions and changes of vascular permeability were studied in rats with and without acute bilateral surgical vagotomy. The aims of study were (a) to compare IND-induced mucosal lesions in the stomach, small intestine and large bowel of rats with intact vagus and acute surgical vagotomy and (b) to evaluate the changes of vascular permeability following these treatments. The gastrointestinal (GI) mucosal damage was produced by IND (20 mg/kg s.c.) at 24 and 48 h after IND administration. Sham operation (laparotomy alone) or surgical vagotomy alone was carried out in control animals. The number and severity of GI mucosal damage was determined. The changes of mucosal vascular permeability were determined by Evans Blue assays in the GI mucosa and in the contents of stomach, small intestine and colon. Evans Blue was given into the tail vein at 15 min before the killing of animals. It was found that (a) no ulceration and change in mucosal vascular permeability was found in any parts of GI tract after sham operation or surgical vagotomy (without IND); (b) IND caused mucosal injury coincidental with vascular permeability in the stomach and small intestine, but not in the large bowel; (c) surgical vagotomy aggravated the IND-induced mucosal damage and increased vascular permeability in the stomach and small intestine, but not in the colon. In conclusion, the intact vagal nerve is required for the prevention of gastric and small intestinal mucosa to protect against IND injury.     

HPLC法检查阿司匹林及阿司匹林片中的游离水杨酸

目的:建立HPLC法检查阿司匹林及阿司匹林片中的游离水杨酸.方法:以十八烷基硅烧键合硅胶为填充剂,甲醇-水-冰醋酸(8:4 : 1)为流动相,检测波长302nm.结果:水杨酸在0.13～5.01μg·ml-1(r=0.99996)的浓度范围内线性关系良好;阿司匹林中水杨酸的方法平均回收率为101.0%,RSD为1.64%(n=6);阿司匹林片中水杨酸的方法平均回收率为99.83%,RSD为1.75%(n=6).结论:本方法快速、准确,可用于检查阿司匹林及阿司匹林片中的游离水杨酸.     

Inhibition of gastric mucosal damage by santonin pretreatment in rats

The effect of santonin pretreatment on gastric mucosal injuries caused by 80% ethanol, 25% NaCl, 0.2 M NaOH, indomethacin, and combined treatment of ethanol and indomethacin was investigated in rats. The effects caused by ethanol on gastric mucus secretion, gastric levels of non-protein sulfhydryl groups, and malondialdehyde and histopathological effects were also investigated. Santonin pretreatment at oral doses of 30, 60, and 120 mg/kg (121.8, 243.6, and 487.2 μmol/kg) provided a dose-dependent protection against the ulcerogenic effects of different necrotising agents used. Further pretreatment with santonin afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, proteins, nucleic acids, non-protein sulfhydryl groups, and an increase in malondialdehyde levels in gastric tissue. The histopathological lesions induced by ethanol in the gastric mucosa were also protected by santonin pretreatment. The protective effect of santonin against alcohol damage to the gastric-wall mucosa may be mediated through its effects on mucus production, nucleic acids, and non-protein sulfhydryl generation and its free-radical scavenging. © Wiley-Liss, Inc.