参香养胃胶囊的抗溃疡药效学研究

目的:研究参香养胃胶囊抗SD大鼠胃溃疡及抗胃黏膜损伤的作用。方法:采用水浸应激法、幽门结扎法、利血平法、醋酸等方法致大鼠胃溃疡,盐酸-乙醇、吲哚美辛致大鼠急性胃黏膜损伤,进行抗胃溃疡和胃黏膜保护实验。结果:参香养胃胶囊能明显抑制水浸应激、幽门结扎、利血平以及醋酸致大鼠胃溃疡;并对盐酸-乙醇、消炎痛所致大鼠急性胃黏膜损伤有明显的抑制作用;结论:参香养胃胶囊具有抗溃疡的作用。     

肚痛健胃整肠丸保护胃黏膜作用与调节肠道菌群功能研究

目的研究肚痛健胃整肠丸对胃黏膜的保护作用及其对肠道菌群的调节功能。方法采用无水乙醇致大鼠胃黏膜损伤模型、吲哚美辛致大鼠胃黏膜损伤模型和冰醋酸诱发大鼠胃溃疡模型等考察肚痛健胃整肠丸对胃黏膜的辅助保护作用;采用林可霉素制备小鼠肠道菌群失调模型,观察肚痛健胃整肠丸对肠道菌群（乳酸杆菌、双歧杆菌、肠球菌、产气荚膜梭菌和大肠埃希菌）的调节作用。结果肚痛健胃整肠丸可减轻乙醇和吲哚美辛所致大鼠急性胃黏膜损伤,对醋酸诱发大鼠胃溃疡亦有明显抑制作用,可增加肠道微生态失调小鼠体质量;增加肠道微生态失调小鼠模型乳酸杆菌、双歧杆菌数量,减少肠球菌、大肠埃希菌数量。结论肚痛健胃整肠丸具有保护胃黏膜作用和调节肠道菌群功效。     

黄连厚朴药对药理作用的研究

目的：比较黄连-厚朴药对、黄连-厚朴有效部位、盐酸小檗碱-厚朴酚不同比例的止泻、镇痛作用。方法：观察黄连-厚朴药对、黄连-厚朴有效部位、盐酸小檗碱-厚朴酚不同比例对冰乙酸致小鼠扭体反应的影响及对番泻叶致小鼠腹泻模型的影响。结果：黄连-厚朴药对1∶2、黄连-厚朴有效部位1∶2、和盐酸小檗碱-厚朴酚1：2的止泻、镇痛效果较好。结论：盐酸小檗碱-厚朴酚、黄连-厚朴有效部位和其药对具有同样的止泻、镇痛作用,且最佳组方配比为1∶2。     

干姜温中止痛作用研究

研究表明干姜石油醚提物能对抗水浸应激性、吲哚美辛加乙醇性、盐酸性和结扎幽门性胃溃疡形成；促进麻醉大鼠胆汁分泌，但对ＣＣｌ４引起的ＳＧＰＴ和ＳＧＯＴ升高无降低作用，能对抗蓖麻油引起的腹泻，但对番泻叶引起的腹泻无作用。水提物能对抗结扎幽门性溃疡形成，对抗番泻叶引起的腹泻。两种提取物都不影响小鼠胃肠推进运动。     

藿香正气不同剂型产品药效比较实验

摘 要：目的 比较藿香正气不同剂型产品以各自临床用量的相同倍数给药,其止泻、止吐及解痉作用。方法 采用番泻叶致小鼠腹泻实验模型,观察单次量 ig 给药后,小鼠的腹泻潜伏期、腹泻率、腹泻级数及腹泻指数;采用硫酸铜致家鸽呕吐实验模型,观察单次量 ig 给药后,家鸽的呕吐潜伏期、呕吐次数及呕吐持续时间;采用甲硫酸新斯的明致小鼠小肠痉挛实验模型,观察单次量 ig 给药后,炭末推进百分率。结果 藿香正气不同剂型产品均有不同程度的止泻作用;藿香正气胶囊、藿香正气软胶囊均有明显的止吐作用;藿香正气胶囊、藿香正气软胶囊、藿香正气滴丸均有明显的解痉作用。结论 藿香正气胶囊作用最强,藿香正气软胶囊次之,不同厂家的产品作用强度有差异。     

蒲葛舒胃灵对实验性胃溃疡作用的研究

目的研究蒲葛舒胃灵抗实验性胃溃疡的作用。方法采用应激性胃溃疡模型、吲哚美辛致大鼠急性胃黏膜损伤模型、大鼠幽门结扎胃溃疡等模型观察蒲葛舒胃灵抗胃溃疡作用、对醋酸所致小鼠扭体反应的影响和体外抗幽门螺杆菌的作用。结果蒲葛舒胃灵能减少大鼠实验性胃溃疡面积,抑制醋酸所致小鼠扭体反应次数,对幽门螺杆菌具有明显抑制作用。结论蒲葛舒胃灵有显著的抗胃溃疡作用,实验结果与该药用于治疗胃溃疡的功效吻合。     

净厚朴与姜厚朴水煎液主要药理学比较

目的:观察净厚朴和姜厚朴的主要药理学变化。方法:小鼠灌胃数天后,利用经典的小肠推进、盐酸性溃疡、番泻叶致泻、二甲苯耳肿胀实验来比较炮制前后厚朴的双向调节胃肠活动和抗炎作用的变化。结果:以上4项作用,小肠推进作用净厚朴>姜厚朴,抗盐酸性溃疡作用净厚朴<姜厚朴,抗番泻叶腹泻和抗炎作用二者无明显差异。结论:中药厚朴的炮制是有必要的。本实验简单易行,易出结果。     

神农丸的药效学实验

目的观察神农丸对小白鼠胃粘膜损伤后有无止痛、保护作用以及对大白鼠胃液分泌有无调节作用。方法以醋酸致疼痛、乙醇致胃粘膜损伤两种小鼠模型和乙醇、去氧胆酸钠致慢性胃炎大鼠模型为实验对象,以小鼠扭体次数、溃疡指数、大鼠胃液游离酸度、胃蛋白酶活力、血活胃泌素量为指标,全面考察神农丸对胃粘膜损伤的保护作用和对胃液分泌的调节作用。结果神农丸能明显减少醋酸致疼痛模型小鼠的扭体次数,降低乙醇胃炎模型小鼠的溃疡指数,降低实验性慢性胃炎模型大鼠胃液中游离酸度,升高胃蛋白酶活力。结论神农丸对小白鼠胃粘膜损伤有止痛和保护作用,对大白鼠实验性慢性胃炎胃液分泌有调节作用。     

白藜芦醇对小鼠实验性胃黏膜损伤的保护作用

目的研究白藜芦醇对小鼠实验性胃黏膜损伤的保护作用。方法制备小鼠无水乙醇型、阿司匹林型、吲哚美辛型胃黏膜损伤模型,测定胃黏膜损伤面积;测定血清中丙二醛和超氧化物歧化酶含量。结果白藜芦醇（25,50,100mg·kg^-1, ig）可剂量依赖性地抑制小鼠实验性胃黏膜损伤。白藜芦醇可使阿司匹林致小鼠胃黏膜损伤过程中血清中升高的丙二醛含量降低,可使降低的超氧化物歧化酶水平回升。结论白藜芦醇对小鼠实验性胃黏膜损伤具有保护作用,其作用机制可能与抗氧化作用有关。     

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。     

胃脘合剂的药理研究

目的研究胃脘合剂治疗慢性萎缩性胃炎、消化道溃疡的药理作用。方法根据现代制药工艺理论制备胃脘合剂;通过醋酸扭体镇痛实验,对小鼠胃排空、对蓖麻油所致小鼠腹泻及无水乙醇诱发大鼠胃粘膜损伤的影响,研究胃脘合剂的药理作用。结果胃脘合剂可显著抑制小鼠醋酸引起的扭体反应,抑制小鼠的胃排空,具有较好的止泻作用,对大鼠胃粘膜损伤有显著的保护作用。结论胃脘合剂对慢性萎缩性胃炎、消化道溃疡有明显防治作用。     

Mast cells do not contribute to nonsteroidal anti-inflammatory drug-induced gastric mucosal injury in rodents

Background: By releasing pro-ulcerogenic mediators, mast cells may contribute to the mucosal injury associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs).
Methods: To study this, rat and mouse models of NSAID-induced gastric damage were used in which administration of indomethacin causes haemorrhagic injury in the corpus region of the stomach, and the "re-feeding" model in which penetrating antral ulcers are induced in the rat by naproxen. Mast cell degranulation was determined histologically and by measurement of tissue and serum levels of rat mast cell protease-II, a mediator specific to mucosal mast cells. The effects of either increasing or decreasing the number of gastric mucosal mast cells on the susceptibility of the stomach to injury induced by indomethacin were also studied.
Results: Gastric injury induced by indomethacin was not accompanied by significant mast cell degranulation. Moreover, neither increasing nor decreasing the number of gastric mucosal mast cells had a significant effect on the susceptibility of the gastric mucosa to damage induced by indomethacin. In the re-feeding model, prior depletion of gastric mucosal mast cells did not significantly affect the severity of antral ulceration induced by naproxen, nor the ability of prostaglandin E₂ to prevent this damage. Finally, indomethacin-induced damage was similar in severity in mice with a genetic defect resulting in the complete absence of mast cells as it was in normal, congenic littermates.
Conclusion: Mast cells do not play a significant role in the development of gastric injury induced by acute NSAID administration in the rat or mouse.     

中药芡实预防急性胃粘膜损伤药理作用的研究

目的探讨中药芡实对小鼠急性胃粘膜损伤的保护作用,并初步探讨其作用机制。方法采用乙醇制备小鼠急性胃粘膜损伤模型,测定胃粘膜损伤指数包括小鼠胃组织SOD活性、MAD及PEG2含量。结果预防给药可以明显降低小鼠胃溃疡指数;模型组小鼠胃粘膜SOD活性明显降低,胃粘膜中MAD含量明显升高;预防性给药可以升高小鼠急性胃粘膜损伤后SOD活性,并抑制胃粘膜中MAD含量的增多;模型组小鼠胃组织中PGE2含量较空白对照组降低,预防性给药组小鼠胃粘膜中PGE2含量明显回升。结论中药芡实对急性胃粘膜损伤具有预防作用。     

五种不同基源石斛对小鼠胃粘膜损伤的保护作用及机制研究

目的:研究叠鞘、金钗、铁皮、马鞭和鼓槌石斛对小鼠乙醇性胃粘膜损伤的保护作用及其与氧自由基(OFR)、一氧化氮(NO)和前列腺素(PG)的关系.方法:制备小鼠乙醇性胃粘膜损伤模型,测定胃粘膜损伤指数;测定胃组织内SOD、MDA、NO和PGE2含量.结果:石斛可剂量依赖性地抑制无水乙醇诱发的小鼠胃粘膜损伤,使小鼠胃粘膜损伤过程中胃组织中升高的MDA含量降低,使降低的SOD活性和NO水平回升,对胃组织中PGE2含量无明显影响.结论:石斛对小鼠乙醇性胃粘膜损伤具有保护作用,其作用机制与石斛抗氧化作用有关,叠鞘石斛可能与促进NO水平恢复正常也有关系.     

温胃化湿汤对小鼠急性腹泻及胃排空作用的研究

目的观察温胃化湿汤对番泻叶所致的腹泻模型作用及胃排空作用的影响,探讨其作用机制。方法采用番泻叶煎剂致小鼠腹泻模型,连续4 d观察温胃化湿汤给药后3 h内的腹泻指数,并观察小鼠小肠墨汁推进率;采用甲基橙为标志物,观察温胃化湿汤对新斯的明致小鼠胃排空亢进的影响。结果温胃化湿汤各组均能明显降低小鼠腹泻指数,减慢小鼠小肠推进速度,与模型组比较有显著性差异(P<0.05),与香连丸组比较,高、中剂量组有显著性差异(P<0.05);温胃化湿汤各组能增加新斯的明致胃排空亢进小鼠的胃残留率,与模型组比较有显著性差异(P<0.05),与香连丸组比较,高、中剂量组有显著性差异(P<0.05)。结论温胃化湿汤对小鼠腹泻和胃排空亢进有较好的防治作用,其作用优于香连丸。     

Inhibition by leukotriene inhibitors, and calcium and platelet-activating factor antagonists, of acute gastric and intestinal damage in arthritic rats and in cholinomimetic-treated mice.

The leukotrienes, platelet activating factor and intracellular calcium have been implicated in the development of gastro-intestinal lesions induced by non-steroidal anti-inflammatory drugs (NSAIDs) but the relative significance of these inflammatory mediators in lesion formation has not been established in sensitive and specific models of gastro-intestinal ulceration. In the present study the effects of drugs affecting 5-lipoxygenase activity, the actions of platelet activating factor and intracellular calcium on the development of gastric and intestinal ulceration induced by NSAIDs were investigated in highly sensitive models of ulcerogenicity induced by treatment with either the cholinomimetic, acetyl-beta-methyl choline chloride, in mice (gastric mucosal lesions) or adjuvant-induced polyarthritis in rats (gastric and intestinal mucosal lesions) as well as in normal mice (intestinal mucosal lesions). The 5-lipoxygenase inhibitors, such as MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-+ ++dimethylpropanoic acid), given at doses shown to reduce the indomethacin-induced increase in mucosal leukotriene B4 concentrations were found to partially prevent the development of gastric and intestinal lesion induced by indomethacin and gastric lesions from aspirin, but the same doses of MK-886 did not affect gastric lesions from diclofenac. Pretreatment with these inhibitors at both 3-5 h and 0-0.25 h was required to achieve protection against gastric mucosal damage from indomethacin. Immediate prior administration of platelet activating factor antagonists (e.g. WEB-2086) with the 5-lipoxygenase inhibitors did not affect gastric or intestinal lesions induced by indomethacin. The calcium antagonist, verapamil, was slightly protective against gastric and intestinal lesions induced by indomethacin. Gastric lesions were further prevented by combinations of a single dose of verapamil with a platelet activating factor antagonist but not combined with a 5-lipoxygenase inhibitor; other combinations of verapamil with lipoxygenase inhibitors or platelet-activating factor antagonists being without inhibitory effects on gastric or intestinal lesions compared with the drugs alone. These results show that 5-lipoxygenase products and intracellular calcium play a major role in acute gastric and intestinal damage by the NSAIDs, but platelet-activating factor has little or no appreciable involvement.     

越鞠胶囊内容物的药理作用

目的考察越鞠胶囊内容物 (theInclusionofYuejuCapsule ,IYC)与临床药效有关的药理作用。方法口服给药 ,采用乙醇致小鼠胃粘膜损伤模型、冰醋酸致大鼠胃溃疡模型、醋酸致小鼠疼痛模型、二甲苯致小鼠耳肿胀模型等考察受试物的药理学作用。结果在所选剂量范围内 ,IYC对乙醇致小鼠胃粘膜损伤和冰醋酸致大鼠胃溃疡模型均有显著的保护作用 ,且有一定的量效关系 ;对醋酸致小鼠扭体反应和对二甲苯致小鼠耳肿胀均有明显抑制作用 ;同时有显著的利胆作用。结论IYC对大、小鼠实验性溃疡的发生有明显的拮抗作用 ,并有一定的消炎、镇痛、利胆作用     

养胃颗粒对实验性胃溃疡的治疗作用研究

目的 研究养胃颗粒对实验性鼠胃溃疡的治疗作用。方法 分别采用水浸应激性大鼠胃溃疡、乙酸烧灼性大鼠胃溃疡、吲哚美辛致小鼠胃溃疡、利血平致小鼠胃溃疡等4种胃溃疡动物模型,考察养胃颗粒对胃溃疡的治疗作用;采用乙酸引起小鼠扭体反应动物模型,考察养胃颗粒的镇痛作用。结果 养胃颗粒灌胃给药对4种模型动物的胃溃疡均具有较好的保护效果,可以减轻胃黏膜损伤程度,降低溃疡指数,抑制溃疡形成,减少溃疡发生率;对乙酸引起小鼠扭体反应模型动物具有较好的镇痛效果,可以减少乙酸引起小鼠扭体反应的扭体次数。结论 养胃颗粒具有明显的治疗实验性胃溃疡的作用,可以用于胃及十二指肠等消化性溃疡的治疗。     

三油酸甘油酯抗胃粘膜损伤及作用机制

考察了三油酸甘油酯对无水乙醇所致大鼠胃粘膜损伤的保护作用及其对抗aspirin、reser pine所致小鼠胃溃疡的作用 .并进一步探讨了三油酸甘油酯抗溃疡作用的机制 .实验结果表明 ,三油酸甘油酯可降低上述各模型中大鼠及小鼠的溃疡指数 ,其作用是以增强胃的防御因子为主 .主要机制研究表明 ,三油酸甘油酯是通过促进胃内前列腺素E2 (PGE2 )和粘液的合成及分泌而起到保护胃粘膜的作用