动物胃提取物对实验性小鼠胃溃疡的保护作用

目的观察动物胃提取物对实验性胃溃疡小鼠模型的保护作用。方法用3种剂量(0.3,0.1,0.03 g/kg)的动物胃提取物及雷尼替丁0.02 g/kg给小鼠灌胃,观察各药对利血平、盐酸、无水乙醇型小鼠胃溃疡模型的影响。结果动物胃提取物能有效抑制利血平、盐酸、无水乙醇型小鼠胃溃疡所致黏膜损伤。结论动物胃提取物有抗实验性小鼠胃溃疡的作用。     

鳕鱼皮胶原蛋白肽的抗酒精性胃溃疡作用

目的探究鳕鱼皮胶原蛋白及其酶解梯级多肽的抗酒精性胃溃疡作用。方法从鳕鱼皮中提取胶原蛋白并酶解成不同分子量段的胶原肽,采用酒精诱导大鼠急性胃溃疡模型,试验组灌胃给予不同剂量的胶原肽,检测胃溃疡指数、胃溃疡抑制率并对胃溃疡病灶部位进行组织学观察。结果与模型组相比,各受试物均能够降低大鼠胃腺的出血损伤。低分子量胶原肽与高分子量胶原肽都能显著降低胃溃疡指数,胃溃疡抑制率分别为46.98%和46.46%(P<0.05);高剂量的胶原蛋白与中分子量胶原肽能极显著降低胃溃疡指数,胃溃疡抑制率分别为57.16%和65.16%(P<0.01)。结论鱼皮胶原蛋白及其酶解梯级多肽能够明显降低大鼠胃溃疡出血和溃疡指数,具有良好的抗酒精性胃溃疡作用。     

獐芽菜苦苷对乙醇致小鼠胃溃疡的保护作用

目的:探讨獐芽菜苦苷对无水乙醇致小鼠胃溃疡的保护作用.方法:采用无水乙醇灌胃造成小鼠急性胃溃疡,观察獐芽菜苦苷预防给药(96,48 mg·kg-1,qd,腹腔注射,给药5 d)对胃黏膜损伤的保护作用,计算溃疡指数和溃疡抑制率,测定胃液酸度和胃蛋白酶活性(meet毛细管法).结果:獐芽菜苦苷(96,48mg·kg-1)显著减轻无水乙醇引起的小鼠胃黏膜损伤,溃疡指数和胃蛋白酶活性均低于乙醇损伤组(P<0.01).大剂量獐芽菜苦苷与阳性对照药物雷尼替丁(50 mg·kg-1)的溃疡指数和溃疡抑制率无显著性差异,保护程度相似.结论:獐芽菜苦苷对无水乙醇诱导的小鼠胃溃疡有保护作用.     

博落回提取物对大鼠急性酒精性肝损伤的保护作用

目的探讨博落回提取物(Macleaya Cordataextract,MCE)对大鼠急性酒精性肝损伤的保护作用及其作用机制。方法采用白酒灌胃法建立大鼠急性酒精性肝损伤模型。将60只SD大鼠随机分为模型组,正常组,阳性药物组,MCE高、中、低剂量组,每组10只。检测各组大鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)和肝匀浆超氧化物岐化酶(SOD)活性及丙二醛(MDA)含量,观察肝脏病理形态学改变,并测定肝组织中肿瘤坏死因子(TNF-α)、白介素(IL-1β)的表达水平。结果与模型组相比较,经MCE预防性治疗后,大鼠血清中ALT、AST、LDH活性显著降低(P<0.01),肝组织中SOD活力明显增强、MDA含量显著下降、TNF-α与IL-1β表达水平显著降低(P<0.01),形态学观察显示MCE能明显改善肝组织病理形态。结论 MCE能改善肝功能,对大鼠急性酒精性肝损伤具有保护作用,其机制可能与其减轻肝脏炎症、抗脂质过氧化作用有关。     

娑罗子提取物对阿司匹林致胃溃疡作用的研究

目的研究娑罗子提取物（SAE）对阿司匹林所致胃溃疡的保护作用,为阿司匹林安全用药提供依据。方法用阿司匹林制备溃疡模型,小鼠连续5天灌胃给予SAE（3.5、7、14mg/kg）或在制备溃疡模型前、后不同时间点灌胃给予SAE（7mg/kg）,于显微镜下观察胃溃疡指数。结果与模型组比较,SAE（7、14mg/kg）显著降低溃疡指数（P〈0.05）。制备溃疡模型同时给予SAE（7mg/kg）可以明显降低溃疡指数。结论娑罗子提取物对阿司匹林所致胃溃疡有预防作用。     

艳山姜提取物对急性胃溃疡模型小鼠的保护作用研究

目的:探讨艳山姜提取物对急性胃溃疡模型小鼠的保护作用。方法:取小鼠48只,随机分为空白组、模型组、阳性组(三九胃泰颗粒,20 mg/kg)和艳山姜提取物高、中、低剂量组(2.34、1.17、0.59 g/kg,按生药量计),每组8只,每天灌胃生理盐水或相应药物1次,连续给药7 d后,除空白组外的其余组小鼠均一次性灌胃无水乙醇0.1 mL/10 g,以建立急性胃溃疡模型。另取小鼠48只,同法分组,连续给药15 d,并于给药第10天起对除空白组外的其余组小鼠连续6 d灌胃阿司匹林(20 mg/kg),以建立急性胃溃疡模型。在乙醇诱导模型实验中,观察各组小鼠胃溃疡形成情况并测定胃溃疡指数;采用苏木精-伊红染色法观察胃组织病理变化;采用酶联免疫吸附法(ELISA)检测血清中胃泌素(GAS)和胃组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)的水平。在阿司匹林诱导模型实验中,同法观察并测定各组小鼠胃溃疡形成情况、胃溃疡指数;采用ELISA法检测血清中GAS、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和胃组织中前列腺素E₂(PGE_2...     

瓦松提取物对实验性胃溃疡的治疗作用

目的：观察瓦松提取物对实验性胃溃疡的治疗作用。方法：以Wistar大鼠和昆明种小鼠为研究对象,复制5种实验性胃溃疡动物模型（小鼠束缚水浸应激致胃溃疡模型、吲哚美辛致小鼠胃溃疡模型、乙醇致大鼠胃溃疡模型、乙酸致大鼠胃溃疡模型和大鼠幽门结扎致胃溃疡模型）。将大鼠随机分为瓦松提取物400、200、100mg/kg剂量组、阳性对照组和模型对照组;小鼠随机分成瓦松提取物800、400、200mg/kg剂量组、阳性对照组和模型对照组。测定胃溃疡指数、胃液游离酸排出量及总酸排出量。结果：瓦松提取物400、800mg/kg剂量组能降低小鼠应激性溃疡溃疡指数（P〈0.05）;200～800mg/kg瓦松提取物对吲哚美辛致小鼠胃溃疡溃疡指数有明显的降低作用（P〈0.05或P〈0.01）;同时对乙醇引起的大鼠胃溃疡也具有明显的抑制作用（P〈0.05）,并可明显促进乙酸致大鼠胃溃疡溃疡的愈合,但对动物胃液分泌及胃蛋白酶活性无明显影响。结论：瓦松提取物对实验性胃溃疡有明显的预防和治疗作用。     

赶黄草提取物对大鼠酒精性脂肪肝的保护作用研究

目的:研究赶黄草提取物对酒精性脂肪肝的保护作用。方法:以1.5%的硫酸亚铁饲料进行饲养,应用灌胃乙醇法复制酒精性脂肪肝大鼠模型,复制模型6周后停止灌胃乙醇。实验分为7组,即正常对照,模型,槲皮素高、低剂量(50、25mg·kg-1),硫普罗宁(50mg·kg-1)和赶黄草提取物高、低剂量(4000、2000mg·kg-1)组。灌胃给药,每天1次,连续6周。计算肝脏系数;对大鼠肝脏行油红O染色,进行病理学检查;检测大鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆固醇(TC)、甘油三酯(TG)的含量。结果:灌胃酒精6周后大鼠形成酒精性脂肪肝。与模型组比较,赶黄草提取物高、低剂量组大鼠肝脏脂肪变明显改善,大鼠血清中ALT、AST、TC、TG均显著降低(P<0.01或P<0.05)。结论:赶黄草对大鼠酒精性脂肪肝具有保护作用。     

溃疡灵对实验性胃溃疡的影响

本实验观察了溃疡灵对实验性胃溃疡模型的作用,结果表明,溃疡灵对束缚应激法,消炎痛加乙醇所致小鼠胃溃疡和盐酸损伤法及幽门结扎法所致的大鼠胃溃疡模型均有明显的抑制作用。     

黄皮果提取物对急性乙醇中毒致小鼠肝损伤的保护作用

目的探讨黄皮果提取物(EFCL)对小鼠急性乙醇中毒致肝损伤的保护作用及其可能的作用机制。方法 ICR小鼠40只,随机分为正常对照、模型及EFCL 1.5和3.0 g·kg-1组。EFCL 1.5和3.0 g·kg-1组小鼠分别ig给予相应剂量的EFCL;30 min后ig给予52℃二锅头白酒12 ml.kg-1;24 h后处死小鼠,制备血清,取肝组织制备10%肝组织匀浆,采用试剂盒方法检测血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)活性,以及肝组织匀浆中超氧化物歧化酶(SOD)活性、丙二醛(MDA)和谷胱甘肽(GSH)含量,常规HE染色和淀粉酶-过碘酸希夫法染色观察肝组织病理形态改变,并用免疫组织化学法测定肝组织中NF-κB和α-平滑肌肌动蛋白(α-SMA)的表达。结果与正常对照组比较,模型对照组小鼠血清ALT和AST活性分别升高28.0%和28.9%(P<0.01),肝组织匀浆中SOD活性和GSH含量分别由(706±46)kU·g-1蛋白和(251±61)mg.g-1蛋白降低至(515±68)kU·g-1蛋白和(126±18)mg.g-1蛋白,而MDA含量由(204±21)μmol·g-1蛋白升高至(258±50)μmol·g-1蛋白(P<0.05);肝组织中NF-κB和α-SMA表达增加(P<0.01)。与模型对照组比较,EFCL 1.5和3.0 g·kg-1组小鼠血清ALT活性分别降低了18.3%和19.8%,血清中AST活性分别降低了6.4%和9.7%(P<0.05,P<0.01);EFCL 3.0 g·kg-1组肝组织匀浆中GSH水平和SOD活性分别升高了61.4%和14.8%(P<0.05,P<0.01)。肝组织中NF-κB和α-SMA的表达水平明显低于模型对照组(P<0.01)。肝组织病理形态检测可见,EFCL 1.5和3.0 g·kg-1组小鼠对乙醇引起的肝细胞脂肪样变、水样变和炎症细胞浸润等均有明显改善。结论 EFCL对小鼠急性乙醇中毒所致肝损伤具有保护作用,其机制可能与升高抗氧化酶活性、促进自由基清除、降低NF-κB的表达及抑制肝星状细胞活化有关。     

Protective effect of tetrahydrocoptisine against ethanol-induced gastric ulcer in mice

Excessive alcohol consumption can lead to gastric ulcer and the present work was aimed to examine the protective effect of tetrahydrocoptisine (THC) in the model of ethanol-induced gastric ulcer in mice. Fasted mice treated with ethanol 75% (0.5 ml/100 g) were pre-treated with THC (10 or 20 mg/kg, ip), cimetidine (100 mg/kg, ip) or saline in different experimental sets for a period of 3 days, and animals were euthanized 4 h after ethanol ingestion. Gross and microscopic lesions, immunological and biochemical parameters were taken into consideration. The results showed that ethanol induced gastric damage, improving nitric oxide (NO) level, increased pro-inflammatory cytokine (TNF-α and IL-6) levels and myeloperoxidase (MPO) activity, as well as the expression of nuclear factor-κB (NF-κB) in the ethanol group. Pretreatment of THC at doses of 10 and 20 mg/kg bodyweight significantly attenuated the gastric lesions as compared to the ethanol group. These results suggest that the gastroprotective activity of THC is attributed to reducing NO production and adjusting the pro-inflammatory cytokine, inhibited neutrophil accumulation and NF-κB expression.     

Protective effect of l-citrulline against ethanol-induced gastric ulcer in rats

We examined the protective effect of l-citrulline on ethanol-induced gastric ulcer in rats. Administration of l-citrulline at doses of 300, 600 and 900mg/kg body weight prior to ethanol ingestion protected the stomach from ulceration. The gastric lesions were significantly attenuated by all doses of l-citrulline as compared to the ethanol group. Pre-treatment with l-citrulline prevented the oxidative damage and the decrease of nitric oxide content as well as the increase of the myeloperoxidase activity. Consequently, significant changes observed included the attenuation in the elevation in total nitric oxide synthase activity and inducible nitric oxide synthase activity as well as the decrease in constitutive nitric oxide synthase activity in the gastric mucosa induced by ethanol. Analysis of serum cytokines of ethanol-induced rats showed a moderate decrease in interleukin-10 with considerable increase of interleukin-6 while l-citrulline inhibited the acute alteration of cytokines. These results suggested the gastroprotective effect of l-citrulline.     

獾子油对小鼠乙醇性胃溃疡的保护作用

目的研究獾子油对小鼠胃溃疡的保护作用。方法以乙醇致小鼠胃溃疡为模型,以奥美拉唑作为阳性药对照,通过计算溃疡指数,测定小鼠胃液PH值,胃组织匀浆中一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量,研究獾子油高、中、低剂量(0.2、0.1和0.05 mL·10 g~(-1))对小鼠胃溃疡的保护作用及其与剂量的关系。结果与模型组比较,各剂量组的獾子油对乙醇致小鼠胃溃疡均有一定的改善作用,能抑制胃酸的分泌,减小溃疡面积,降低胃组织中NO的含量,使SOD、MDA含量升高,而且随着浓度的增加作用效果逐渐增强,其中高剂量组有显著性差异(P<0.05)。结论獾子油对乙醇致小鼠胃溃疡具有一定的保护作用,且高剂量效果最好。     

Protective effects of escin against indomethacin-induced gastric ulcer in mice

Escin, a natural mixture of triterpenoid saponin isolated from the seed of the horse chestnut, is reported to have a potent antiulcer activity against ethanol-induced gastric mucosal lesions. This study investigated the possible mechanisms underlying the gastroprotective effect of escin against indomethacin-induced gastric ulcer in mice. Gastric ulceration was induced by a single intragastric administration of indomethacin (18?mg/kg). The mice underwent intragastric treatment with escin at doses of 0.45, 0.9 or 1.8?mg/kg. Gastric lesion was estimated morphometrically and histopathologically 6?h after the indomethacin administration. The antioxidative parameters in gastric mucosa were measured. Moreover, the activity of myeloperoxidase and the contents of TNF-α, P-selectin and VCAM-1 in gastric tissues were determined. The results showed that escin protected gastric tissues against indomethacin-induced gastropathy as demonstrated from a reduction in the ulcer index and an attenuation of histopathologic changes. Escin caused significant reductions of the contents of malondialdehyde, TNF-α, P-selectin, VCAM-1 and myeloperoxidase activity. The altered activities of superoxide dismutase, catalase and glutathione peroxidase in the stomach tissues were also ameliorated by escin treatment. The present study demonstrated that escin had a protective effect against indomethacin-induced gastric ulcer in mice, not only by virtue of its antioxidant potential, but also due to its anti-inflammatory effect.     

Protective effect of propranolol on ethanol-induced gastric lesions in mice

The non-selective beta-adrenoceptor antagonist, propranolol, has a protective effect on ethanol-induced gastric haemorrhagic lesions in mice when given in doses of 2.5, 5.0 and 10 mg/kg either parenterally (i.p.) or orally. The effect was more marked after oral administration. Another non-selective beta-adrenoceptor antagonist, timolol, failed to protect against ethanol-induced gastric lesions. Thus, beta-adrenoceptor blockade does not seem to play a role in the gastroprotective effect of propranolol. Pretreatment with the cyclo-oxygenase inhibitor, indomethacin, abolished the protective effect of 2.5 and 5.0 mg/kg i.p. propranolol but only attenuated the effect of the higher i.p. dose (10 mg/kg) and the three oral doses. These results indicate that the gastroprotective effect of propranolol is mediated partly by the prostaglandin pathway and partly by another mechanism which, we suggest, may involve its membrane-stabilising action.     

胡椒碱抗实验性胃溃疡的作用

目的：研究胡椒碱抗大鼠或小鼠实验性胃溃疡的作用。方法：实验性胃溃疡是由应激、吲哚美辛、盐酸和幽门结扎引起,实验前5h ig胡椒碱。结果：胡椒碱25、50、100mg/kg能抑制大鼠或小鼠胃粘膜损伤,对应激性型胃粘膜损伤,抑制率分别为16．9％,36．0％,48．3％;吲哚美辛型胃粘膜损伤为4．4％,51．1％,64．4％;盐酸型胃粘膜损伤为19．2％,41．5％,59．6％;对幽门结扎型胃粘膜损伤为4．8％,11．9％,26．2％;胃液分泌减少;胃酸、胃蛋白酶活性降低。结论：胡椒碱具有抗实验性胃溃疡作用。     

Gastroprotective effect of cirsilineol against hydrochloric acid/ethanol-induced gastric ulcer in rats

This study was designed to evaluate the gastroprotective activity of cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon cirsilineol administration. These results ultimately suggest that cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.     

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     

Protective effect of butyrate against ethanol-induced gastric ulcers in mice by promoting the anti-inflammatory,anti-oxidant and mucosal defense mechanisms

Gastric ulcers (GUs) are a common type of peptic ulcer. Alcohol overdose is one of the main causes of GU, which is difficult to prevent. Although the protective effect of butyrate on inflammation-related diseases is well understood, its effect on GUs has not been reported. We investigated the protective effects of butyrate against ethanol-induced lesions to the gastric mucosa in mice and the underlying mechanisms. BALB/c mice were orally pretreated with butyrate for 30 min prior to the establishment of the GU model by challenge with absolute ethanol. Ethanol administration produced apparent mucosal injuries with morphological and histological damage, whereas butyrate pretreatment reduced the gastric mucosal injuries in a dose-dependent manner. Butyrate pretreatment also significantly ameliorated contents of malondialdehyde (MDA) and carbonyl proteins, and decreased levels of IL-1β, TNF-α and IL-6. The Western blot results consistently demonstrated that butyrate pretreatment attenuated the phosphorylation of NF-κB p65, p38 MAPK and ERKs in the gastric tissues. Additionally, gastric wall mucus (GWM), a parameter reflecting mucosal defense, was clearly increased by butyrate pretreatment. Butyrate pretreatment protects the gastric mucosa against ethanol-induced lesions by strengthening the mucosal defense and anti-oxidant and anti-inflammatory activities. As a necessary substance for the body, butyrate may be applied to the prevention and treatment of GUs.