龙胆苦苷的保肝作用研究

目的：研究ig龙胆苦苷的肝保护作用及与龙胆草药理作用的一致性。方法：给动物ig给药，用CCl4、D－GlaN造急性肝损伤模型，测定小鼠血清ALT、AST及肝组织中谷胱甘肽过氧化物酶含量，采用麻醉大鼠，测定胆汁分泌量及胆汁成分。结果：ig龙胆苦苷后能明显降低CCl4急性肝损伤小鼠血清ALT、AST水平及增加肝组织中谷胱甘肽过氧化物酶活力，大鼠胆流量明显增加，胆汁中胆红素浓度提高。结论：龙胆苦苷具有明显肝保护作用。     

The protective effect and action mechanism of Vaccinium myrtillus L. on gastric ulcer in mice

Vaccinium myrtillus L. anthocyanoside (VMA) is used as a folk medicine to treat diseases related to gastric ulcers in northern Europe. However, the effects of VMA and its detailed mechanism on gastric ulcer have not been investigated sufficiently. Therefore, the aim of the present study was to investigate the protective effects of VMA on gastric mucosal damage in a murine gastric ulcer model. First the effects of VMA on ethanol‐induced gastric ulcers in mice were investigated. Then, the levels of lipid peroxide in murine stomach homogenates were measured to investigate the antioxidative effects of VMA. In addition, the free radical scavenging activity of VMA and its main anthocyanidins were evaluated by electron spin resonance measurement. Oral administration of VMA (10, 30 and 100 mg/kg) significantly protected gastric mucosa against HCl/ethanol‐induced gastric ulcers. Furthermore, VMA inhibited lipid peroxide levels in a concentration‐dependent manner and showed high scavenging activity against the superoxide anion radical (·O₂^‐) and the hydroxyl radical (·OH). Anthocyanidins also showed scavenging activity against the ·O₂^‐, while only delphinidin showed high scavenging activity against the ·OH. These findings indicate that the protective effects of VMA on HCl/ethanol‐induced gastric mucosal injury may be partially due to the antiperoxidative effects of anthocyanidins. Copyright © 2011 John Wiley & Sons, Ltd.     

Protective effects of astaxanthin from Paracoccus carotinifaciens on murine gastric ulcer models

The purpose of this study was to investigate the effect of astaxanthin extracted from Paracoccus carotinifaciens on gastric mucosal damage in murine gastric ulcer models. Mice were pretreated with astaxanthin for 1 h before ulcer induction. Gastric ulcers were induced in mice by oral administration of hydrochloride (HCl)/ethanol or acidified aspirin. The effect of astaxanthin on lipid peroxidation in murine stomach homogenates was also evaluated by measuring the level of thiobarbituric acid reactive substance (TBARS). The free radical scavenging activities of astaxanthin were also measured by electron spin resonance (ESR) measurements. Astaxanthin significantly decreased the extent of HCl/ethanol‐ and acidified aspirin‐induced gastric ulcers. Astaxanthin also decreased the level of TBARS. The ESR measurement showed that astaxanthin had radical scavenging activities against the 1,1‐diphenyl‐2‐picrylhydrazyl radical and the superoxide anion radical. These results suggest that astaxanthin has antioxidant properties and exerts a protective effect against ulcer formation in murine models. Copyright © 2011 John Wiley & Sons, Ltd.     

海洋岩盘深层水中药复方制剂对小鼠胃肠功能的影响

目的 :研究海洋岩盘深层水中药复方制剂(HYYPSCS)保护胃黏膜,调节肠胃功能的作用及机制。 方法 :采用乙醇ig给药法致正常小鼠胃溃疡,观察HYYPSCS(1 925,3 850,7 700 mg·kg^-1, qd, ig给药5 d)对胃黏膜的保护作用,计算溃疡指数和溃疡抑制率,测定胃SOD和MDA活性,并考察HYYPSCS对小肠推进率的影响。 结果 :HYYPSCS给药组溃疡指数和MDA活性均低于乙醇损伤组,中剂量组SOD活性显著高于乙醇损伤组( P <0.05),各给药组对小鼠肠运动的促进作用均显著高于空白组( P <0. 01)。 结论 :HYYPSCS显著促进胃肠蠕动且对乙醇致小鼠胃黏膜损伤具有保护作用,其作用机制可能与其抗氧化作用有关。     

Attenuation of indomethacin- and HCl/ethanol-induced oxidative gastric mucosa damage in rats by kolaviron, a natural biflavonoid of Garcinia kola seed

Reactive oxygen species (ROS) have been implicated in the aetiology of HCl/ethanol- and indomethacin gastric mucosal damage. This study investigated the protective effects of kolaviron, a natural antioxidant from the seed of Garcinia kola, on oxidative gastric mucosal damage induced by HCl/ethanol, and indomethacin.A HCl/ethanol mixture (1.5 mL of 0.15 n HCl in 70% ethanol) and indomethacin (IND) caused severe gastric damage with an ulcer index of 2.90 +/- 0.8 and 2.5 +/- 0.4, respectively, and significant reductions in the gastric mucosal content of catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) (p < 0.001).Pre-treatment of animals with kolaviron (100 mg/kg) orally 1 h and once daily for 3 days prior to ulcer induction significantly reduced the formation of ulcers induced by HCl/ethanol with preventive ratios of 65 and 72, respectively, while rats treated with kolaviron 1 day and for 7 days prior to IND treatment attenuated ulcer formation by 59% and 77%. Pre-treatment with ranitidine 1 h prior to ulcer induction (50 mg/kg) elicited preventive ulcer ratio of 55.Kolaviron pre-treatment 1 h before ulcer induction attenuated the HCl/ethanol reduction in CAT, SOD and GSH by 43%, 42% and 30%, respectively, and 67%, 68% and 64% following 72 h treatment with kolaviron. Ranitidine elicited 24%, 41% and 29% protective effects, respectively.Similarly, kolaviron administered to rats 1 day and for 7 days before IND treatment attenuated the drug-induced inhibition of CAT by 44% and 70%; SOD by 23% and 43% and GSH by 32% and 55%, respectively.In a 1 h and 3-day treatment with kolaviron before HCl/ethanol administration, MDA was reduced by 35% and 55%, respectively, while kolaviron administration 1 day and for 7 days before IND elicited a 39% and 58% reduction in MDA. Ranitidine elicited 39% and 50% reduction in MDA following HCl/ethanol and IND treatment.The results indicate the gastroprotective activity of kolaviron, which may be linked to its intrinsic antioxidant properties.     

针刺足三阳经穴对胃黏膜损伤家兔生长抑素受体基因表达影响的比较

目的:比较针刺足三阳经对胃黏膜损伤的保护作用及对生长抑素受体基因表达的影响,探讨经脉脏腑相关的特异性.方法:乙醇灌胃造成家兔胃溃疡模型后,采用经络刺激仪进行针刺.治疗结束后用放射免疫及PC-PCR法测定胃黏膜表皮生长因子(EGF)、生长抑素(SS)及生长抑素受体(SSR1mRNA)表达.结果:模型组EGF含量较正常组明显降低;胃黏膜损伤指数、SS含量及SSR1mRNA表达则显著升高(P<0.01).与模型组比较,胃经组EGF明显升高,胃黏膜损伤指数、SS含量及SSR1mRNA表达显著降低(P<0.01).但胆经及膀胱经组与模型组比较上述指标未得到改善,与胃经组比较差异有非常显著性意义(P<0.01).结论:针刺足三阳经以胃经组对家兔胃黏膜损伤保护作用最强,其机制可能与调整有关脑肠肽及生长抑素受体基因表达有关.     

Effects of Nigella sativa oil on gastric secretion and ethanol induced ulcer in rats

The present work was done to investigate the possible effects of Nigella sativa oil (NSO) on gastric secretion and ethanol-induced ulcer in rats. Thirty two adult male rats were used in this study (four groups) and several parameters were determined to assess any degree of protection. It was found that the administration of NSO in rats produced a significant increase in mucin content and glutathione level and a significant decrease in mucosal histamine content. Ethanol administration produced a 100% ulcer induction with an ulcer score of 12.62+/-1.35 (mean+/-S.E., n=8). It caused a significant reduction in free acidity and glutathione level while it produced a significant increase in mucosal histamine content. When animals were pretreated with NSO before induction of ulcer, there was a significant increase in glutathione level, mucin content and free acidity and a significant decrease in gastric mucosal histamine content with a protection ratio of 53.56% as compared to the ethanol group. It can be concluded that NSO imparted a protective action against ethanol induced ulcer in rats.     

龙胆苦苷抗炎药理作用研究

目的 研究秦艽所含龙胆苦苷的抗炎作用。方法 分别用二甲苯致小鼠耳肿胀，冰醋酸致小鼠腹腔毛细血管通透性增加及小鼠扭体反应，酵母多糖A、角叉菜胶、制霉菌素致大鼠或小鼠足跖肿胀模型，ig给药，观察龙胆苦苷的抗炎作用。结果 龙胆苦苷能减轻二甲苯所致小鼠耳肿胀、冰醋酸所致小鼠腹腔毛细血管通透性增加、角叉菜胶、酵母多糖A所致大鼠足跖肿胀，但对制霉菌素所致的炎症模型无明显作用。结论 秦艽所含龙胆苦苷具有一定的抗炎作用，其机制涉及对多种炎症介质的抑制。抗炎作用能部分代表秦艽生药的传统功效。     

栀子总苷对小鼠实验性胃粘膜损伤的保护作用

目的:研究栀子总苷(TGZ)对小鼠实验性胃粘膜损伤的保护作用及其与氧自由基(OFR)和一氧化氮(NO)的关系。方法:制备小鼠无水乙醇型、阿司匹林型、消炎痛型胃粘膜损伤模型,测定胃粘膜损伤面积;测定胃组织内丙二醛(MDA)和NO含量。结果:TGZ(5 0 ,10 0 ,2 0 0 mg/ kg,ig)可剂量依赖性地抑制小鼠实验性胃粘膜损伤。TGZ可使阿司匹林致小鼠胃粘膜损伤过程中胃组织中升高的MDA含量降低,可使降低的NO水平回升。结论:TGZ对小鼠实验性胃粘膜损伤具有保护作用,其作用机理与TGZ抗氧化和促进NO水平恢复正常有关。     

两面针总碱抗胃溃疡作用研究

目的:研究两面针总碱对实验性胃溃疡的保护作用及其机制。方法:灌服两面针总碱7天后,用无水乙醇、束缚一冷冻法和幽门结扎法造胃溃疡模型,测量溃疡指数、胃液量、游离酸、总酸度、胃蛋白酶活性以及胃粘膜MDA含量、超氧化物歧化酶(SOD)活性、NO含量。结果:两面针组能使三种模型溃疡指数降低,对胃液量、游离酸、总酸度无明显影响,可降低胃液胃蛋白酶活性,使胃粘膜MDA含量降低,SOD活性和NO含量升高。结论:两面针总碱具有抗溃疡作用。     

铁皮石斛护肝及抗胃溃疡作用研究

目的:考察铁皮石斛对肝脏损伤及胃溃疡动物模型的保护作用。方法:建立四氯化碳急性肝损伤模型(CCl4造模剂量50μL.kg-1,腹腔注射)、亚急性酒精性肝损伤模型(酒精造模剂量7.5mL.kg-1.d-1×14 d,灌胃)、应激性胃溃疡模型(冷水浸泡法诱导)及化学性胃溃疡模型(消炎痛诱导,40 mg.kg-1,灌胃)。将成功造模的小鼠随机分为4组:模型组、阳性对照组、石斛榨汁高、低剂量组(含生药2,0.5 g.kg-1),并设立正常对照组,每组12只。各给药组连续灌胃给药若干天,每天1次;正常组和模型组同时给予等容量的蒸馏水。实验结束时,肝损伤动物麻醉后眼球取血,分离血清测定谷草转氨酶(AST)、谷丙转氨酶(ALT)的含量,同时剖取肝脏计算肝脏系数;胃损伤动物麻醉后,剖开腹腔取胃,观察腺胃部的胃黏膜损伤程度并采用Guth标准记分法计算溃疡指数。结果:铁皮石斛鲜榨汁液显著抑制CCl4肝损伤小鼠血清AST,ALT(P<0.05)及亚急性酒精性肝损伤小鼠血清AST的升高(P<0.05);显著降低应激性胃溃疡模型及消炎痛诱导的化学性胃溃疡模型的溃疡指数(P<0.01)。结论:铁皮石斛鲜汁具有保肝护胃的作用。     

一氧化氮参与艾灸对大鼠急性胃粘膜损伤的保护作用

本实验用70％酒精胃内注射建立大鼠急性胃粘膜损伤模型，研究了艾灸足三里对胃粘膜保护作用的可能机理。结果发现：与对照组相比，艾炙组大鼠胃粘膜血流量、跨膜电位差、血清及胃窦、胃体中一氧化氛含量均升高（P＜0．05），粘膜损伤指数下降（P＜0．05）；NW-硝基-L-精氨酸（L-NNA）能阻断上述效应（P＜0．05）；用左旋精氨酸（L－Arginine）或硝普钠（Snap）预处理，均能明显减轻大鼠胃粘膜损伤（P＜0．05）。提示NO参与艾灸对冒粘膜的保护作用。     

复方蜥蜴散不同微粒组合剂对大鼠急性胃黏膜损伤修复作用的实验研究

目的：观察复方蜥蜴散不同微粒组合剂对急性酒精性胃黏膜损伤模型大鼠血清PGE2及胃黏膜组织NOS水平的影响,探讨其保护胃黏膜损伤的作用机制。方法：用无水乙醇诱导的急性胃黏膜损伤大鼠模型,在造模前分别灌胃给予生理盐水、复方蜥蜴散不同微粒组合剂及铝碳酸镁等不同药物干预,用ELISA和硝酸还原酶法分别测定血清PGE2及胃黏膜组织NOS的水平。结果：预防治疗组大鼠血清PGE2及胃黏膜组织NOS的水平明显高于模型组（P〈0．01）,且胃黏膜病理组织学损伤有明显改善。结论：复方蜥蜴散不同微粒组合剂对急性胃黏膜损伤有预防保护作用。     

基于均匀设计法评价白及制川乌配伍对胃溃疡模型小鼠的影响

目的 研究白及与制川乌不同配比和剂量变化对无水乙醇致胃溃疡模型小鼠胃黏膜损伤的影响.方法 采用均匀设计法,按2因素7水平,以小鼠胃溃疡指数和胃黏膜病理损伤积分为指标,观察白及制川乌合煎液灌胃给药后对胃溃疡小鼠的影响,并选取有显著意义的配比和剂量进行验证.结果 白及制川乌总剂量在3.64~29.32 g/kg范围内,小鼠溃疡指数和病理损伤积分随合煎液中白及剂量的增加而降低、随制川乌剂量的增加而升高,但二药未见交互作用;当总剂量固定不变,小鼠溃疡指数和病理损伤积分即随合煎液白及配比增加而降低、随制川乌配比增加而升高.结论 白及和制川乌合煎液对小鼠胃溃疡的影响与二药的剂量和配比密切相关,为十八反中白及与制川乌反药组合作用的深入研究提供实验依据.     

娑罗子提取物对实验小鼠胃肠道的保护作用研究

目的观察娑罗子提取物对实验小鼠胃肠道的影响。方法采用易蒙停建立小鼠便秘模型和肠蠕动抑制模型,通过鼠肠道炭末推进法测定小鼠排便和小肠推进,观察不同剂量组(3.5,7,14 mg/kg)娑罗子提取物对便秘小鼠的首次排便时间、粪便粒数、粪便重量和小肠内容物推进率的影响;采用无水乙醇造成小鼠急性胃粘膜损伤,观察娑罗子提取物各组溃疡指数、溃疡抑制率的变化。结果与模型组比较,娑罗子提取物各剂量组均能明显提高小肠推进率(P<0.05),显著减少溃疡指数(P<0.01),低,中,高各剂量组溃疡抑制率分别达到75.2%,77.0%,72.9%;低剂量组能显著增加小鼠粪便粒数(P<0.01)和粪便重量(P<0.05)。结论娑罗子提取物对实验小鼠胃肠道具有明显的保护作用。     

黄花倒水莲提取物对实验性胃黏膜损伤的保护作用

目的研究黄花倒水莲提取物对小鼠胃黏膜损伤的保护作用。方法无水乙醇法、阿司匹林法、水浸应激法和利血平法制备小鼠胃黏膜损伤模型,测定给药后胃黏膜损伤面积。结果黄花倒水莲提取物对4种胃黏膜损伤均有显著的抑制作用。结论黄花倒水莲提取物对实验性胃黏膜损伤具有明显保护作用。     

虎杖苷对实验性急性胃黏膜损伤的保护作用

目的研究虎杖苷(polydatin,PD)对实验性急性胃黏膜损伤的保护作用及其与抗氧化的关系。方法制备小鼠无水乙醇型、吲哚美辛(消炎痛)型、大鼠束缚-冷冻(restraint-cold stress,RCS)应激型胃黏膜损伤模型,测定胃黏膜损伤指数;测定大鼠血清SOD活性和MDA含量。结果PD可剂量依赖性地抑制实验性急性胃黏膜损伤。PD可使大鼠束缚-冷冻应激型胃黏膜损伤过程中血清中升高的MDA含量降低,可使降低的SOD水平回升。结论PD对实验性急性胃黏膜损伤具有保护作用,其作用机制与PD抗氧化有关。     

龙胆中龙胆苦苷的分离纯化

目的建立龙胆中高纯度龙胆苦苷的快速分离纯化方法。方法坚龙胆药材的乙醇提取液经AB-8大孔吸附树脂柱进行粗分,乙醇-水系统进行梯度洗脱,30%乙醇溶液洗脱下来的流份粗龙胆苦苷部分冷冻干燥后经MCI树脂柱进一步纯化,洗脱剂为乙醇-水,所得的龙胆苦苷的纯度经高效液相色谱进行检测。结果在此条件下,可以分离得到纯度大于97%的龙胆苦苷。结论该法简便、快速、低毒、所得产物纯度高,适用于分离较高纯度的龙胆苦苷及龙胆苦苷标准品的制备。     

金葵胃药对实验性胃粘膜损伤的保护作用

目的:观察金葵胃药(JK)对小鼠胃粘膜损伤的作用.方法:无水乙醇法、阿司匹林法、水浸应激法和利血平法制备小鼠胃粘膜损伤模型,测定药后胃粘膜损伤面积.结果:JK 100、200、400mg/kg ig对四种胃粘膜损伤均有不同程度的抑制作用.结论:JK对实验性胃粘膜损伤具有保护作用.     

黄连总碱对乙醇致大鼠胃粘膜损伤的保护作用及其机制研究

目的:研究黄连总碱(TA)对乙醇致大鼠胃粘膜损伤的保护作用机制。方法:建立乙醇致胃粘膜损伤动物模型,通过胃粘膜损伤指数和病理学改变来观察TA的保护作用。检测胃粘膜一氧化氮(NO)、丙二醛(MDA)和活性氧(·OH)的含量以及超氧化物歧化酶(SOD)的活力。免疫组织化学方法分析神经型一氧化氮合成酶(nNOS)、内皮型NOS(eNOS)和诱导型NOS(iNOS)在胃粘膜的表达。结果:TA剂量依赖性地抑制乙醇致大鼠胃粘膜损伤,且作用强于等量的小檗碱(Ber)。TA明显阻遏乙醇引起的胃粘膜MDA、·OH升高以及NO、SOD降低。TA抑制乙醇所致的nNOS、eNOS在胃粘膜表达降低以及iNOS过表达。结论:黄连能抗人类酒精性胃粘膜损伤,该作用是各生物碱相互增效的结果。作用机制涉及:抑制氧自由基产生;促进自由基清除;减轻脂质过氧化;阻遏nNOS、eNOS表达降低以及iNOS过表达,维持胃粘膜的NO含量在正常水平。