唐古特大黄多糖对大鼠应激性胃溃疡的保护作用

目的：探讨唐古特大黄多糖(Rheum tanguticum polysaccharides，RTP)对大鼠应激性胃溃疡的保护作用。方法：用水浸束缚应激法(water immersion and restraint stress，WRS)复制大鼠应激性胃溃疡模型，提前灌胃给予大黄多糖，应激6h后处死动物，观察溃疡指数和胃粘膜损伤程度的变化，检测血清及胃粘膜组织中超氧物歧化酶(SOD)和丙二醛(MDA)的变化。结果：RTP能明显降低应激大鼠胃粘膜溃疡指数和胃粘膜MDA水平，升高血清和胃粘膜SOD活性。结论：RTP对水浸束缚应激引起的大鼠应激性胃溃疡有明显的保护作用，可能是大黄治疗应激性胃溃疡的有效成分之一。     

黄芪对应激性大鼠胃黏膜抗氧化作用研究

目的 测定黄芪注射液对应激状态下大鼠胃黏膜中超氧化物歧化酶(SOD)活性和丙二醛含量的影响,为临床应用黄芪治疗应激性溃疡提供理论依据.方法 采用水浸束缚应激方法复制大鼠应激性溃疡模型.健康雄性SD大鼠40只完全随机分为5组,每组8只,即对照组、模型组、黄芪低剂量组(低剂量组)、黄芪高剂量组(高剂量组)及硫糖铝组.对照组、模型组采用生理盐水,低剂量组采用10 g/kg黄芪注射液,高剂量组采用20 g/kg黄芪注射液,硫糖铝组采用硫糖铝500 mg/kg连续灌胃5 d,水浸束缚应激12 h后,采用黄嘌呤氧化酶法和硫代巴比妥酸法(TBA法)测定胃黏膜中SOD活性和丙二醛含量.结果 应激12 h后,对照组、模型组、硫糖铝组及低、高剂量组的丙二醛含量分别为(5.24±1.70)、(13.31±1.69)、(7.76±1.11)、(7.13±0.83)、(6.53±0.73)nmol/mg prot;上述5组的SOD活性水平分别为(191.87±24.38)、(112.00±16.74)、(203.00±16.24)、(174.00±19.74)、(197.75±18.43)U/mg prot.与对照组相比,其他4组大鼠胃黏膜丙二醛含量明显增高(P＜0.01).与模型组相比较,硫糖铝组和低、高剂量组大鼠胃黏膜丙二醛含量明显降低,差异具有统计学意义(P＜0.01).同时,与对照组相比较,模型组、低剂量组大鼠胃黏膜SOD活性明显降低,差异有统计学意义(P＜0.01或P＜0.05).与模型组相比较,硫糖铝组和低、高剂量组大鼠胃黏膜SOD活性明显增高,差异具有统计学意义(P＜0.01).高剂量组的胃黏膜SOD活性高于低剂量组,差异有统计学意义(P＜0.01).结论 黄芪对应激性溃疡大鼠具有显著的胃黏膜保护作用.其机制可能是增强大鼠血清和胃黏膜局部抗氧化能力.

Abstract：

Objective To investigate the antioxidation on gastric mucosa of radix injection in rats on stress ulcer, and to explore the possible mechanism. Methods Water immersion and restraint stress(WRS) induced acute gastric injury was used as the experimental model of stress ulcer of rats. All the animals were randomly divided into 5 groups, the control group, the model group, Radix injection 10, 20 g/kg and sucralfate 500 mg/kg group.Rats were orally administrated with Radix injection or sucralfate for 5 days before stressed. 12 h after WRS, The activity of total superoxide dismutase (SOD) and malondialdehyde (MDA) level in gastric mucosa were measured by xanthine oxidase method and thibabituric acid(TBA) method respectively. Results In radix 20 g/kg group, radix exhibited the strong ability to rise the activity of SOD in gastric mucosa( P ＜0.01 ) and lower the mucosal MDA concentration(P＜0. 01). Conclusions Radix exhibits remarkable protective effects on WRS induced stress ulcer in rats. The protective effects might be related to trigger the intrinsic protective mechanism by enhancing the antioxidatire effect. It provides theoretical principle for clinical application of radix on stress ulcer.     

褪黑素对脑出血大鼠应激性胃黏膜损伤的保护作用

目的 探讨褪黑素对脑出血大鼠应激性胃黏膜损伤的保护作用。方法 将60只健康成年SD大鼠随机分为空白对照组、模型组、奥美拉唑组、褪黑素组。空白对照组、模型组大鼠给予生理盐水灌胃,奥美拉唑组以奥美拉唑悬液灌胃,褪黑素组给予褪黑素灌胃,预防性给药,连续灌胃7 d,末次给药后禁食水24 h,除了空白对照组外,其余3组均制作脑出血大鼠模型,通过酶联免疫吸附法检测大鼠血清中超氧化物歧化酶(superoxidedismutase,SOD)、丙二醛(malonaldehyde,MDA)含量,大体观察大鼠胃黏膜病变并计算溃疡指数(UI),HE染色光镜下观察胃黏膜组织形态学改变,并比较各组胃黏膜损伤的发病率。结果 褪黑素的治疗增加了SOD含量,降低MDA含量、降低大鼠胃黏膜UI及胃黏膜损伤的发病率(P<0.05)。结论 褪黑素可通过清除氧自由基而对应激性胃黏膜起到保护作用。     

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。     

Vanillyl nonanoate protects rat gastric mucosa from ethanol-induced injury through a mechanism involving calcitonin gene-related peptide

Previous studies have demonstrated that capsaicin-sensitive sensory nerves are involved in the protection of gastric mucosa against damage by various stimuli and calcitoin gene-related peptide (CGRP) is a potential mediator in this process. This study was performed to explore the effect of vanillyl nonanoate, a capsaicin analog, on ethanol-induced gastric mucosal injury and the possible underlying mechanisms. A rat model of gastric mucosal injury was induced by oral administration of acidified ethanol and gastric tissues were collected for analysis of gastric ulcer index, cellular apoptosis, the activities of caspase-3, catalase and superoxide dismutase (SOD), levels of CGRP, TNF-α and malondialdehyde (MDA). The results showed that acute administration of ethanol significantly increased gastric ulcer index concomitantly with increased cellular apoptosis, caspase-3 activity, TNF-α and MDA levels as well as decreased activities of catalase and SOD. Pretreatment with 1mg/kg vanillyl nonanoate significantly attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by increase of CGRP expression, and SOD activity and decrease of caspase-3 activity, TNF-α and MDA levels. The effects of vanillyl nonanoate were inhibited by capsazepine, an antagonist of capsaicin receptor. Our results suggested that vanillyl nonanoate was able to protect the gastric mucosa against ethanol-induced gastric mucosal injury. The underlying mechanism is related to stimulation of CGRP release and subsequent suppression of ethanol-induced inflammatory reaction, cellular apoptosis and oxidative stress.     

颈交感神经干离断减轻鼠急性胃黏膜损伤

目的 探讨颈交感神经干离断(TCST)对大鼠急性胃黏膜损伤的保护作用.方法 30只雄性SD大鼠,随机分为假手术(A)组、假手术后浸水(B)组和TCST后浸水(C)组,每组10只.B、c组大鼠垂卣浸水至剑突水平6h,测各组大鼠胃黏膜血流量(GMBF),评定黏膜溃疡指数(UI).采用放免法检测胃黏膜组织降钙素基因相关肽(CGRP)含量,硝酸还原酶法测定胃黏膜组织中一氧化氮合酶(NOS)含量.结果 B、C组胃黏膜见出血性溃疡,B组损伤较重.B组GMBF、CGRP降低及UI、NOS明显高于C组(P<0.05或P<0.01).结论 TCST对大鼠急性胃黏膜损伤有保护作用,其机制可能与调节胃黏膜组织CGRP及NOS含量有关.     

尼美舒利对吲哚美辛诱导的大鼠胃黏膜损伤的保护作用

目的探讨尼美舒利对胃黏膜的保护作用及其可能的作用机制。方法大鼠禁食12h后,ig给予吲哚美辛30mg·kg-1制备急性胃黏膜损伤模型,5min后分为模型对照、尼美舒利100mg·kg-1、塞来昔布100mg·kg-1、美洛昔康4mg·kg-1、双氯芬酸钠50mg·kg-1和布洛芬600mg·kg-1组,分别ig给予相应药物;另设正常对照组。6h后处死所有大鼠,测定胃溃疡面积。生化比色法检测大鼠胃组织和血清中谷胱甘肽(GSH)和丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果正常对照组大鼠胃黏膜表面光滑,黏膜皱襞纹理清晰;模型组大鼠均见急性胃溃疡,溃疡面积为(10.6±7.4)mm2;与模型组比较,尼美舒利和塞来昔布组胃溃疡面积显著减小,分别为4.1±1.7和(4.9±3.2)mm2(P<0.01);美洛昔康组未见明显变化,为(8.1±3.5)mm2;双氯芬酸钠和布洛芬组胃溃疡面积明显增加,分别为15.4±4.8和(16.0±7.3)mm2(P<0.01)。与正常对照组比较,模型组大鼠胃组织中GSH含量和SOD活性明显降低(P<0.05),MDA含量显著升高(P<0.01);血清中MDA含量显著升高(P<0.01),而GSH含量和SOD活性变化不明显。与模型组相比,尼美舒利组胃组织中GSH含量和SOD活性明显升高(P<0.05,P<0.01),MDA含量明显降低(P<0.01);血清中GSH含量明显增加(P<0.01),MDA含量明显降低(P<0.01);塞来昔布组大鼠胃组织中SOD活性明显升高(P<0.01),血清中MDA含量明显降低(P<0.01),其他指标无明显变化;美洛昔康、双氯芬酸钠和布洛芬对模型大鼠胃组织和血清中GSH,MDA含量及SOD活性均无明显影响。结论尼美舒利对吲哚美辛诱导的大鼠急性胃黏膜损伤具有明显的保护作用,作用机制可能与其抗氧化活性有关。     

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。     

维生素E对胃黏膜损伤模型小鼠的保护作用研究

目的:观察维生素E(VE)对胃黏膜损伤模型小鼠的保护作用。方法:取小鼠50只随机均分为正常对照组、模型组、西咪替丁(25mg·kg-1)组和VE低、高剂量(25、50mg·kg-1)组,灌胃给予相应药物30min后,后4组灌胃给予吲哚美辛25mg·kg-1,4h后处死小鼠,检测各组小鼠胃黏膜损伤程度及血清中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量。结果:与正常对照组比较,模型组小鼠胃黏膜损伤指数和SOD活性、MDA含量均明显升高(P<0.01);与模型组比较,西咪替丁组和VE低、高剂量组小鼠胃黏膜损伤指数和SOD活性、MDA含量均明显降低(P<0.01);与西咪替丁组比较,VE高剂量组小鼠胃黏膜损伤指数和SOD活性均明显降低(P<0.01)。结论:VE可能通过抗氧化、清除氧自由基和抑制脂质过氧化过程发挥预防胃黏膜损伤的作用,且VE高剂量(50mg·kg-1)组对胃黏膜损伤的保护作用强于西咪替丁(25mg·kg-1)组。     

银杏叶提取物的胃粘膜保护作用(英文)

目的:研究银杏叶提取物的胃粘膜保护作用.方法:采用大鼠束缚-冷冻应激(RCS)模型和小鼠无水乙醇损伤模型观察GbE对胃粘膜损伤指数的影响;采用幽门结扎法收集胃液,观察GbE对胃液分泌量,胃液酸度和胃蛋白酶活性的影响;采用硫代巴比妥酸(TBA)法测定胃粘膜及血清中丙二醛(MDA)含量.结果:GbE(25,50,100 mg/kg,bid×5 d,ig)剂量依赖性地抑制RCS和无水乙醇引起的胃粘膜损伤.用药组应激后的胃粘膜损伤指数分别为对照组的58％,43％和31％;用药组乙醇诱发的胃粘膜损伤指数降至对照组的62％,36％和26％;GbE尚能增强西米替丁对胃粘膜的保护作用,但对大鼠胃液分泌量、胃液酸度及胃蛋白酶活性GbE并无明显影响.小鼠经无水乙醇ig后1 h,胃粘膜和血清中的MDA含量显著升高(P<0.01),而GbE(25,50,100 mg/kg,ig)预处理则可以明显抑制MDA的升高.结论:GbE具有胃粘膜保护作用,并且与西米替丁在治疗急性胃粘膜损伤方面具有协同作用.     

Beneficial effects of capsiate on ethanol-induced mucosal injury in rats are related to stimulation of calcitonin gene-related Peptide release

Capsiate is a non-pungent analogue of capsaicin from CH-19 Sweet peppers. Capsaicin is reported to trigger calcitonin gene-related peptide (CGRP) release through activation of transient receptor potential vanilloid subfamily member 1 (TRPV1) and produces beneficial effects on gastric mucosa. This study aimed to investigate whether capsiate is able to produce beneficial effects on gastric mucosa and whether the protective effects of capsipate occur through a mechanism involving the activation of TRPV1 and CGRP release. A rat model of gastric mucosal injury was established by the oral administration of acidified ethanol. Gastric tissues were collected for analysis of the gastric ulcer index, cellular apoptosis, activities of caspase-3, catalase and superoxide dismutase (SOD), and levels of CGRP, TNF-α, and malondialdehyde (MDA). Our results show that the acute administration of ethanol significantly increased the gastric ulcer index concomitantly with an increase in cellular apoptosis, caspase-3 activity, and TNF-α and MDA levels, as well as a decrease in the activities of catalase and SOD. Pretreatment with 1 mg/kg capsiate attenuated ethanol-induced gastric mucosal injury and cellular apoptosis accompanied by an increase in CGRP level, catalase, and SOD activities, and a decrease in caspase-3 activity, and TNF-α and MDA levels. The effects of capsiate were inhibited by capsazepine, an antagonist of TRPV1. These results suggest that capsiate is able to produce beneficial effects on ethanol-induced gastric mucosal injury. These effects are related to the stimulation of CGRP release through the activation of TRPV1.     

猴头菇胃肠保健口服液对胃黏膜损伤的保护功能研究

目的评价猴头菇胃肠保健口服液对胃黏膜损伤的保护功能。方法建立灌胃酒精致大鼠急性胃黏膜损伤和胃壁注射冰醋酸致大鼠慢性胃溃疡两种模型,连续灌胃30 d,实验结束时测量各实验组胃黏膜损伤面积或体积,检查猴头菇胃肠保健口服液对胃黏膜损伤的保护功能[1]。结果猴头菇胃肠保健口服液对大鼠慢性胃溃疡有明显的保护作用,低剂量组差异非常显著(P<0.01),中、高剂量组差异显著(P<0.05);对大鼠急性胃黏膜损伤无明显的保护作用(P>0.05)。结论猴头菇胃肠保健口服液对大鼠慢性胃溃疡具有保护功能。     

慢性萎缩性胃炎病人胃粘膜MDA和SOD测定及其意义

目的 探讨自由基在慢性萎缩性胃炎(CAG)病人胃粘膜中的变化及其意义。方法 采用比色法及放射免疫法分别检测了36例CAG病人和17例正常人胃粘膜丙二醛(MDA)含量,胃粘膜超氧化物歧化酶(SOD)含量。结果 CAG病人胃粘膜MDA含量明显升高,胃粘膜SOD含量则明显减少,与正常对照组相比差异有高度显著意义(P<0.01);同时CAG病人胃粘膜MDA含量与胃粘膜SOD含量之间呈负相关,差异并有高度显著意义(P<0.01)。结论 检测自由基对阐明CAG的发病机制可能有重要意义。     

牛乳铁蛋白对实验性胃黏膜损伤及胃溃疡大鼠模型的影响

目的 观察牛乳铁蛋白对实验性大鼠胃黏膜损伤及胃溃疡的保护作用。方法 建立无水乙醇、幽门结扎致大鼠胃黏膜损伤模型,水浸应激、乙酸灼烧致大鼠胃溃疡模型,测定模型大鼠胃黏膜损伤程度、溃疡面积、溃疡指数,以及胃黏膜中氨基己糖、PEG₂含量和血流动力学的变化,观察牛乳铁蛋白对实验性胃黏膜损伤和胃溃疡的保护作用。此外,通过连续喂养正常大鼠牛乳铁蛋白,观察其对大鼠胃液量、胃液酸度和胃蛋白酶活性的影响。结果 牛乳铁蛋白能降低乙醇及幽门结扎致胃黏膜损伤大鼠的溃疡指数,增加乙醇致胃黏膜损伤大鼠受损胃黏膜的氨基己糖和PEG₂含量以及血流量。同时,牛乳铁蛋白还能降低水浸应激以及乙酸灼烧致胃溃疡大鼠胃部的溃疡面积。此外,连续灌胃高剂量牛乳铁蛋白能抑制正常大鼠胃液分泌,减少胃液酸度。结论 牛乳铁蛋白对实验性胃黏膜损伤及胃溃疡大鼠模型胃黏膜损伤具有保护作用。     

尼莫地平与西咪替丁治疗大鼠脑震荡后急性胃溃疡的比较

目的：比较尼莫地平与西咪替丁对大鼠重型脑损伤后急性胃溃疡的疗效。方法：将４０只ＳＤ大鼠随机分为对照组、创伤组、西咪替丁及尼莫地平组,共４组,用Ｄｉｘｏｎ等方法致伤后西咪替丁组即予西咪替丁０．１ｍｇ／ｋｇ,尼莫地平组予尼莫地平５ｍｇ／ｋｇ,均ｉｐ,ｔｉｄ,７２ｈ后观察各组大鼠胃粘膜血流量（ＧＭＢＦ）,胃液ｐＨ及胃粘膜损伤指数。结果：与创伤组相比,尼莫地平组ＧＭＢＦ升高（Ｐ＜０．０５）,胃液ｐＨ值增加（Ｐ＜０．０１）,胃粘膜损伤指数减少（Ｐ＜０．０１）。西咪替丁组除ＧＭＢＦ略有下降（Ｐ＞０．０５）外,其余２项与尼莫地平组相似。结论：尼莫地平对大鼠脑损伤后急性胃溃疡疗效与西咪替丁近似。     

沙棘原花青素对应激性胃溃疡大鼠上皮细胞凋亡与增殖的影响

目的探讨沙棘原花青素对应激性胃溃疡大鼠上皮细胞凋亡与增殖的影响及其可能的机制。方法60只♂W ist-ar大鼠随机分为6组:正常组,对照组,低、中、高剂量组及雷尼替丁阳性对照组。采用束缚-浸水应激的方式造应激性胃溃疡模型,造模前灌胃不同剂量的SBPC或阳性药物。测定溃疡指数、大鼠血浆EGF及NO的水平;大鼠血浆NOS及iNOS的活性;免疫组化的方法测定胃粘膜组织中iNOS、EG-FR及PCNA的表达;采用原位末端标记法检测胃粘膜上皮细胞的凋亡。结果与对照组相比,高剂量组SBPC(150 mg.kg-1)的溃疡指数明显降低(P<0.01);血浆EGF的水平升高(P<0.05),血浆NO的浓度(P<0.01)降低;NOS及iNOS的活力降低(P<0.05);粘膜中的iNOS的表达降低(P<0.01),EGFR的表达增强((P<0.01),PCNA的表达增强(P<0.05),凋亡指数降低(P<0.05)。结论SBPC可能通过调节EGF和NO促进大鼠的细胞增殖抑制细胞凋亡,从而对应激性胃溃疡的发生起保护作用。     

蒲元和胃胶囊对内毒素血症大鼠急性胃粘膜病变的保护作用

目的观察蒲元和胃胶囊对大鼠内毒素血症模型胃黏膜的保护作用.方法 30只大鼠随机分为对照组及干预组.每组大鼠15只,干预组以1.0g?kg-1蒲元和胃灌胃,每日1次,对照组予等量生理盐水灌胃.7d后两组均经静脉注射内毒素建立内毒素血症模型.48h后处死动物,检测胃组织丙二醛含量,并进行胃粘膜溃疡指数评定.结果干预组胃MDA含量及指数评定明显小于对照组(P<0.05).结论在大鼠内毒素血症中蒲元和胃胶囊对胃胶囊黏膜有明显保护作用.     

Antiulcer activity of levcromakalim and nicorandil in albino rats: a comparative study

The objective of the present study was to investigate and compare the antiulcer effect of potassium channel openers, nicorandil and levcromakalim in the models of ulcer induced by pylorus ligation, aspirin and water immersion plus restraint stress in albino rats. Levcromakalim (250 microg/kg) and nicorandil (10 mg/kg) were administered intraduodenally immediately after pylorus ligation. Ulcer index was determined and gastric juice was subjected to analysis of total acid output (TAO) and pH. In aspirin-induced gastric ulcer model, the drugs were administered orally 30 min prior to noxious challenge, and in water immersion restraint stress model, the drugs were administered orally and ulcer index was determined. A significant reduction in ulcer index was observed after treatment with both potassium channel openers in all the gastric ulcer models. In pylorus-ligated rats, a significant decrease in TAO was noted. The conclusion is that potassium channel openers possess antiulcer activity. Antiulcer activity of levcromakalim is better than nicorandil but comparable to that of cimetidine. The antiulcer action of potassium channel openers is mediated partially by a decrease in gastric acid secretion, increase in gastric mucosal resistance and improvement in gastric mucosal blood flow.     

美洲大蠊提取物Ento-A对大鼠急性胃炎胃黏膜的保护作用

目的研究美洲大蠊提取物Ento-A对急性胃炎胃黏膜的保护作用及其初步作用机制。方法将大鼠分为正常对照组,模型对照组,康复新液组,西咪替丁组,美洲大蠊提取物Ento-A高、低剂量组,连续给药8 d后,采用80%乙醇与20 mg·mL-1水杨酸钠溶液等体积混合后灌胃建立胃黏膜损伤模型,以胃炎发生计分及病理组织学评分评价Ento-A对胃黏膜的保护作用;酶联免疫法检测大鼠血清中丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)、白介素-1β(IL-1β)及胃组织匀浆中表皮细胞生长因子(epidermal growth factor,EGF)的表达水平,探究Ento-A对胃黏膜的保护作用机制。结果与模型对照组比较,康复新液、西咪替丁及Ento-A能显著降低急性胃炎大鼠血清中TNF-α、MDA、IL-1β和升高SOD的表达水平(P<0.05,P<0.01),并能提高大鼠急性胃炎胃组织匀浆中EGF的表达(P<0.05,P<0.01)。结论美洲大蠊提取物Ento-A具有明显的胃黏膜损伤保护作用,其机制可能与减少炎性因子分泌,抗自由基损伤及促进组织修复有关。     

大柴胡汤及其组方中单味药对胃黏膜损伤防护作用的研究

目的 探讨大柴胡汤对大鼠无水乙醇性胃黏膜损伤的防护作用,研究其组方中单味有效药物.方法 66只雄性SD大鼠按随机数字表法分为正常对照组、模型组和9个治疗组(大柴胡汤组、柴胡组、黄芩组、枳实组、半夏组、大黄组、白芍组、生姜组、大枣组),每组各6只.正常对照组和模型组以生理盐水2ml灌胃,各治疗组以相应的药液2ml灌胃,2h后,正常对照组予生理盐水1ml灌胃,其余各组均予无水乙醇1ml灌胃.灌胃2h后,11组大鼠均乙醚麻醉下剖腹取胃,观察胃黏膜改变,计算溃疡指数和溃疡抑制率;光镜下观察病理组织学改变.制备胃组织匀浆,检测超氧化物歧化酶(SOD)和丙二醛(MDA)含量.结果 大体观察及病理组织切片显示,大柴胡汤组、黄芩组、枳实组、生姜组、大枣组胃黏膜与正常对照组接近,未见明显损伤;柴胡组、半夏组、大黄组及白芍组大鼠胃黏膜与模型组相似,胃黏膜有明显损伤.大柴胡汤组、黄芩组、枳实组、生姜组、大枣组与正常对照组SOD、MDA含量比较,差异无统计学意义(P＞0.05);而模型组、柴胡组、半夏组、大黄组和白芍组与正常对照组比较,SOD含量降低[(121±13)、(244 ±23)、(252±16)、(242±18)、(249±12) U/g比(357±21) U/g]、MDA含量升高[(15.0±1.6)、(14.4±1.3)、(13.9±1.0)、(14.5±1.1)、(14.1 ±0.7) μmol/g比(9.8±0.6) μmol/g],差异均有统计学意义(均P＜0.05).结论 大柴胡汤及其单味药黄芩、枳实、生姜和大枣可有效对抗无水乙醇致大鼠胃黏膜损伤,其防护胃黏膜的机制很可能是通过抗氧化起作用.