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1.
目的探讨溴氰菊酯中毒对大鼠胃黏膜的慢性病理损伤及其机制。方法染毒组大鼠分别给予不同剂量溴氰菊酯灌胃;对照组即橄榄油组仅给予相同剂量橄榄油。肉眼观察各组大鼠胃黏膜的大体损伤情况;取胃体部组织,制成切片,苏木精-伊红染色,镜下观察胃黏膜损伤情况,并对损伤程度进行累计积分;观察胃底腺的形态结构,计数壁细胞的数量。结果镜下对照组大鼠胃黏膜结构完整,胃底腺排列紧密规则,壁细胞形态结构较正常,无炎性细胞浸润。染毒组大鼠与对照组大鼠相比较,胃黏膜均呈现不同程度的损伤。高剂量组大鼠胃黏膜慢性病理损伤积分与其余各组比较差异有显著性(F=10.65,q=4.81~7.49,P<0.05);高剂量组大鼠胃黏膜壁细胞数量较对照组明显增多,差异有显著性(F=5.11,q=5.04,P<0.05)。结论溴氰菊酯对大鼠胃黏膜有较明显的慢性病理损伤的作用,尤其对胃底腺壁细胞的影响较为明显,损伤的机制可能与胃黏膜屏障功能的破坏和胃肠神经递质的变化有关。  相似文献   

2.
高青  刘兴  王丕龙 《重庆医学》2001,30(6):499-501
目的:观察阿斯匹林(ASA)对胃癌细胞株SGC-7901的细胞毒作用以及联用其它抗肿瘤药的增效作用。方法:应用流式细胞仪(FCM)测定细胞周期,噻唑蓝(MTT)法测定药物细胞的抑制率。结果:MTT显示体外ASA对SGC-7901有细胞毒作用,与ASA的浓度和作用时间有显著的相关性。同时可使SGC-7901细胞周期中S期及G2/M期比例升高,G1期比例下降,呈一定的剂量效应关系。低浓度ASA与5-氟脲噻啶(5-Fu)、阿霉素(DOX)和丝列霉素(MMC)合用,可增强它们对SGC-7901的杀伤作用,与各药物有相加或协同作用。结论:ASA体外对SGC-7901有细胞毒作用,可明显阻断SGC-7901细胞在S期和G2/M期;增强上述药物对SGC-7901的杀伤作用。鉴于所试药物对细胞周期的影响不同,提示ASA的体外增效作用可能与此相关。  相似文献   

3.
本研究应用透射电镜技术进行了十二指肠球部溃疡、胃溃疡及正常人胃壁细胞超微结构的对比分析。发现十二指肠球部溃疡组壁细胞组织形态学呈分泌活跃相,胃溃疡组和正常人对照组则无显著性差异。提示十二指肠球部溃疡的发生与高胃酸分泌状态的相关性,并对高胃酸分泌的机制进行了探讨  相似文献   

4.
目的:探讨一氧化氮(NO)在阿司匹林(ASA)致胃粘膜适应过程中可能发生的作用。方法:采用病理学、生化法检测连续ASA灌胃过程中,胃粘膜损伤指数以及血浆和胃粘膜中NO含量的量化。结果:经1天和3天ASA灌胃后损伤指数明显高于对照组(P<0.001),经7天和14天灌胃后,损伤指数显著下降(P<0.01),下降了90%。经1天和3天ASA灌胃后胃粘膜NO含量与对照组相比显著升高(P<0.001,P<0.01),且与损伤指数显著相关(r=0.8139,r=0.8686),而血浆NO含量变化相对较小(P<0.01,P<0.05,与对照组相比)。灌胃一周后,两者与对照组均无明显差异。结论:在阿司匹林致胃粘膜适应过程早期,NO可能起损伤作用,而适应性产生后,则发挥细胞保护效应。  相似文献   

5.
Q H Qi  X Z Wu  J W Bai 《中西医结合杂志》1990,10(8):473-5, 453
Exocrine function of pancreas (BT-PABA test) in 13 patients with SYDS was examined and gastric membrane in 5 cases with SYDS other than gastric diseases was observed under light- and electro-microscopy. The results were as follows: urine rate of recovery of PABA in SYDS was 35. 42 +/- 14.33% and that in the control with same age was 64.70 +/- 10.55%. The rate in SYDS was decreased obviously (P less than 0.001). Under light microscopy gastric mucosa of patients with SYDS showed slight gland degenerative atrophy, smaller cytoplasm, eosinophilic decrease of parietal cells and infiltration of inflammatory cells in interstitial tissue. Under electro-microscopy, the main changes of the gastric mucosa with SYDS were severe mitochondria damage, inflating rough endoplasmic pools and large vacuole at which membrane major particles of ribosomes disappeared, degenerated secretory vessels and formation of myelin figure in parietal cells, decrease of secretory particles in main cells, degeneration in some degree and decrease of nervous secretory particles in G cells and damaged interstitial capillaries. The results in this study suggested that the exocrine function of pancreas in patients with SYDS after abdominal operation or with severe acute abdominal diseases was decreased and there were some damages in energy supply and protein manufacturing systems of the gastric mucosa and functional disturbances of main cells, parietal cells and G cells in patients with SYDS.  相似文献   

6.
目的检测目前常用化疗药物对体外培养的原代胃癌细胞的敏感性.方法用改良MTT法对88例胃癌患者的新鲜标本进行体外肿瘤细胞原代培养和化疗药物敏感性检测,并对其结果进行比较.结果试验成功率为94.3%,以细胞抑制率30%为判断标准的14种化疗药物中,5-FU、MMC、PYM、VP-16和DDP具有较高的敏感性(P<0.05).以上5种药物之间比较,其敏感性差异无显著意义(P>0.05);肿瘤分化程度的高低与肿瘤药敏无明显关系.结论体外胃癌细胞原代培养及化疗药物敏感试验对指导临床医生选择敏感化疗药物开展个体化化疗具有指导作用.  相似文献   

7.
Objective:To study the regulative action of mica monomer powder preparation on the chief and parietal cells as well as G and D cells in the gastric mucosa of the experimental atrophic gastritis(CAG)rats.Methods:Intervention therapy was given to the experimental CAG rats at three different doses of mica monomer powder preparation to evaluate the changes of chief and parietal cells as well as G and D cells in the gastric mucosa and the histopathological changes of gastric mucosa.Results:Mica monomer powder preparation at three different doses could increase the amount of chief and parietal cells as well as G and D cells in gastric mucosa of the experimental CAG rats and alleviate and control the inflammation of gastric mucosa and the atrophy of gastric mucosa glands.Especially,better effects were shown in the mid and high dose groups.Conclusion:Mica has the pharmacological action of protecting the gastric mucosa,promoting the regeneration of gastric glands,enhancing blood flow of the gastric mucosa,and consequently improving the inflammatory responses of the gastric mucosa.One of the mechanisms is associated with promoting the secretion of gastric acid and gastric pepsin and regulating the neuroendocrine mechanism including gut hormone secretion(gastrin and somatostatin)by increasing the number of chief and parietal cells as well as G and D cells.  相似文献   

8.
目的:探讨电针腧穴"胃病方"抗胃黏膜氧化损伤的作用机制。方法:将健康SD雄性大鼠24只随机分为正常组、模型组和治疗组,每组8只。采用阿司匹林灌胃制备胃黏膜损伤模型。正常组和模型组只抓取,不做其他处理;治疗组取"内关""、中脘"和"足三里",电针20 min,每天1次,连续3 d。治疗结束后,按GUTH法计算胃黏膜损伤指数(UI),取大鼠胃黏膜组织,HE染色,光学显微镜观察,免疫组织化学法检测胃黏膜组织中热休克蛋白70(HSP70)的表达。结果:与正常组比较,模型组UI升高(P<0.05);与模型组比较,治疗组UI降低、HSP70表达上调(P<0.01),炎细胞浸润减少(P<0.05)。结论:电针腧穴"胃病方"保护黏膜、减轻炎症反应,其机制可能与诱导HSP70表达上调有关。  相似文献   

9.
目的探讨泮托拉唑联合云南白药在心血管疾病高危患者急性非静脉曲张性上消化道出血止血后恢复服用阿司匹林预防再出血及改善内镜评分的疗效和效果。方法收治服用阿司匹林预防心血管疾病致急性非静脉曲张性上消化道出血患者126例,根据年龄、性别、内镜表现分层,按区组随机化方法分成十二指肠溃疡组(治疗组42例,对照组41例)和胃溃疡组(治疗组22例,对照组21例)。各组在应用泮托拉唑治疗止血后恢复服用阿司匹林,对照组用泮托拉唑40 mg静滴,1次/12 h,治疗组用同量泮托拉唑联合云南白药口服,0.5 g/次,4次/d,比较十二指肠溃疡组和胃溃疡组再出血情况及内镜表现。结果 泮托拉唑联合云南白药在降低再出血率方面比较,差异无统计学意义;但改善了十二指肠溃疡病例组的内镜评分,差异有统计学意义(P〈0.05)。结论 泮托拉唑联合云南白药对改善恢复服用阿司匹林后消化性溃疡的内镜表现优于单用泮托拉唑。  相似文献   

10.
提要自1991年10月以来,我们采用了保留交感神经的壁细胞迷走神经切断术(PCV-AP)治疗十二指肠溃疡,临床结果表明,PCV-AP针对性切断了支配壁细胞区域的迷走神经,同时保留了交感神经的支配,减少了对机体的损伤,其降酸作用与PCV手术相比更为显著,手术近期效果良好。术后2~3周胃镜复查溃疡基本愈合;胃酸分泌试验结果,平均BAO下降77.9%,PMPO下降56.3%,IMAOi及IMAO_2分别下降80.4%和71.4%。但是,PCV-AP手术操作比PCV更为精细。本文主要介绍了PCV-AP的手术方法和初步治疗结果。  相似文献   

11.
D H Loebl  R M Craig  D D Culic  A S Ridolfo  J Falk  F R Schmid 《JAMA》1977,237(10):976-981
The feasibility of determining the exact site and amount of drug-induced gastric bleeding was tested. Fourteen patients with rheumatoid arthritis received equivalent therapeutic doses of the antinflammatory drugs aspirin, 4 gm/day, and fenoprofen calcium, 2.4 gm/day, in randomized order for seven days. Acetaminophen was given for 14 days just prior to each of these periods. By fiberoptic gastroscopy, antral ulceration and acute mucosal lesions were found in seven patients following aspirin ingestion, in one taking fenoprofen, and in none taking acetaminophen. Fecal blood loss in four-day stool collections, quantitated by autologous chromium 51-labeled erythrocytes shed into the stool averaged 5.0 ml/day while taking aspirin, 2.2 ml/day while taking fenoprofen calcium, and 0.8 ml/day while taking acetaminophen. The mean blood loss was greater for those in whom gastric lesions developed while taking aspirin than for those in whom lesions did not develop. The short-term risk of erosive gastritis was greater for aspirin than fenoprofen.  相似文献   

12.
Effects of combined octreotide and aspirin on the growth of gastric cancer   总被引:10,自引:0,他引:10  
Gastricadenocarcinomaisstillthesecondmostcommoncancerandthesecondmostcommoncauseofcancerdeathintheworld Inspiteofconsiderableprogressinendoscopydiagnostics ,earlydiagnosisofgastriccancerisstilldifficultbecauseofthelackofsymptoms Advancedtumorsappeartobepoorprognosticfeatures Chemotherapyorradiationtherapyhasgenerallyshownsomeclinicalresponsebutlittlesurvivaladvantageandisintolerableinmanypatients 1Therefore,othertherapeuticregimensforgastricadenocarcinomaneedtobeexplored Ithasbeenreportedthat…  相似文献   

13.
采用HE染色显示壁细胞,结合生物体视学技术对链脲佐菌素诱导的糖尿病大鼠在胃底腺中的壁细胞进行了研究。结果显示:糖尿病状态的早期,胃底腺腺体上部壁细胞的体密度显著增加,而数密度却明显减少;腺体下部壁细胞的体密度和面密度均无显著变化,但数密度却显著地减少。提示糖尿病状态下,壁细胞数量显著减少,但体积却明显增大。根据正常情况下壁细胞的细胞动力学变化及上述实验结果,认为大鼠胃底腺峡部的干细胞向壁细胞分化成熟的功能在胰岛素缺乏的情况下受到一定程度的抑制,而这种功能的抑制可能是糖尿病状态下易出现目粘膜萎缩和胃酸分泌减少的重要原因之一。  相似文献   

14.
阿司匹林抑制胃癌细胞生长及其机制探讨   总被引:9,自引:2,他引:7  
目的 研究阿司匹林对 SGC- 790 1胃癌细胞生长的影响 ,并初步探讨其作用的分子机制。方法 采用 3H- Td R法及流式细胞术检测不同浓度阿司匹林对胃癌细胞 DNA合成及细胞周期的影响 ;用免疫细胞化学法检测阿司匹林对胃癌细胞 COX- 2表达的影响 ;Western blotting法及 EMSA法检测阿司匹林对胃癌细胞 c- fos表达及 AP- 1活化的影响。结果 胃癌细胞经不同浓度的阿司匹林作用后 ,其 3H- Td R掺入值明显降低 ,且与阿司匹林浓度呈高度负相关 ( r=- 0 .9,P<0 .0 5 )。细胞周期分析显示 ,阿司匹林主要作用于胃癌细胞 S期。免疫细胞化学染色显示 ,阿司匹林能下调胃癌细胞 COX- 2表达 ,且具有良好的量效关系。Western blotting检测表明 ,阿司匹林能降低胃癌细胞 c- fos蛋白的表达。EMSA分析显示 ,阿司匹林能有效抑制血清刺激的 AP- 1的 DNA结合活性。结论 阿司匹林能有效抑制胃癌细胞的生长 ,这种作用可能是其通过抑制胃癌细胞 c- fos表达以及 AP- 1活化 ,进而抑制COX- 2表达所致  相似文献   

15.
ObjectiveTo investigate the protective effect of the combination of turmeric (Curcuma domestica), cardamom pods (Amomum compactum) and sembung leaf (Blumea balsamifera) on gastric mucosa in aspirin-induced gastric ulcer model rats.MethodsThirty male Wistar rats weighing 150–200 g were divided into 6 groups. Four groups were administered with the hot water extracts combination consisted of cardamom pods 36.6 mg/200 g body weight and sembung leaf 91.5 mg/200 g body weight (fixed doses). The herbal extracts combination were also consisted of turmeric in various doses i.e. 10 mg/200 g body weight in the second group, 30 mg/200 g body weight in the first and third groups, and 50 mg/200 g body weight in the fourth group. The fifth group rats received sucralfate 72 mg/200 g body weight. Ten minutes after receiving herbal extracts combinations or sucralfate, the rats were induced with aspirin 90 mg/200 g body weight except the first group. Another group (sixth group) only received aspirin without any protective agent. All treatments were adsministered orally for seven days. The number and area of the gastric ulcers were counted and measured macroscopically. Score of mucosal damage and the number of eosinophils as well as the number of mast cells were observed in paraffin sections stained with hematoxylin eosin and toluidine blue, respectively.ResultsThe groups receiving herbal infuse combination exhibited less number and smaller area of gastric ulcers as well as smaller score of mucosal damage in comparison to those of aspirin group (P<0.05). The number of mast cells and eosinophil of herbal groups were also smaller than that of aspirin group.ConclusionsThe herbal extracts combination of turmeric (Curcuma domestica), cardamom pods (Amomum compactum) and sembung leaf (Blumea balsamifera) has potential gastroprotective effects.  相似文献   

16.
During the year 1991, 43 patients with upper gastrointestinal bleeding and one with severe epigastric pain associated with intake of non-steroidal anti-inflammatory drugs were admitted for emergency endoscopy to our unit. Fourteen patients (33%) had been treated with 100-325 mg aspirin daily, 11 of them for at least one year. The mean age of this group was 71. Only two patients had a previous history of peptic ulcer. Five patients used anticoagulants or antiplatelet drugs concomitantly with aspirin. The endoscopic diagnosis of the sources of bleeding was erosive gastritis in eight patients, gastric ulcer in four, duodenal ulcer in five and oesophageal ulcer in one. Our results support findings by other groups, showing that doses of aspirin as low as 75 mg daily should be used in the management of elderly patients with thrombo-embolic disease.  相似文献   

17.
目的 评价楹树提取物对大鼠急性胃溃疡的影响并研究其与H+,K+-ATP酶(质子泵)相关的作用机制.方法 采用水浸拘束和腹腔注射吲哚美辛建立大鼠急性胃溃疡模型,造模前30 min灌胃给予楹树提取物,以溃疡数和溃疡抑制率评价楹树提取物对急性胃溃疡的药效;HE染色观察楹树提取物对胃溃疡组织病理学变化的影响;生化法检测楹树提取物对大鼠离体胃壁细胞H+,K+-ATP酶活性的影响;细胞免疫荧光实验法观察楹树提取物对离体胃壁细胞H+,K+-ATP酶转位的影响.结果 楹树提取物300 mg/kg灌胃对水浸拘束和吲哚美辛致大鼠急性胃溃疡的抑制率分别为70.0%和75.4%.楹树提取物(15、30、60、120、240和480 mg/L)对胃壁细胞H+,K+-ATP酶活性的抑制率分别为21.5%、29.4%、44.1%、51.9%、57.7%和62.9%,较空白对照组均具显著差异(均P<0.01),ID50为130 mg/L.但楹树提取物对H+,K+-ATP酶的转位无明显影响.结论 楹树提取物300 mg/kg对急性胃溃疡有保护作用,抑制H+,K+-ATP酶的活性是其作用机制之一.  相似文献   

18.
目的 O6-甲基鸟嘌呤-DNA-甲基转移酶(O6-methylguanine-DNA-methylt ransferase,MGMT)是修复烷化剂对DNA损伤的关键酶,同时也是烷化剂类抗肿瘤药物耐药的主要因素之一。p53蛋白是p53抑癌基因的蛋白产物,其基因突变与肿瘤的发生、发展密切相关。文中探讨了MGMT蛋白在进展期胃癌患者肿瘤组织中的表达与临床病理参数及预后的关系,以及MGMT蛋白与p53蛋白在进展期胃癌组织中表达的相关性及对预后的影响。方法采用免疫组织化学法检测158例进展期胃癌切除标本中MGMT的表达水平,并分析其与胃癌临床病理特征及联合分析MGMT蛋白表达和临床检测指标p53蛋白表达与患者预后的关系。结果进展期胃癌组织中MGMT蛋白的阳性率为76.58%(121/158)。MGMT蛋白表达情况与患者的肿瘤部位及大小、肿瘤分期、分化程度、神经是否侵犯、脉管是否存在癌栓均无相关性(P>0.05)。Spearman相关系数分析显示MGMT与p53的表达呈负相关:r=-0.2534,P=0.0023。COX回归多因素分析显示MGMT(相对危险度:1.339,P=0.1363)和p53(相对危险度:1.174,P=0.4082)不能作为生存时间的独立预测指标。MGMT(+)、p53(-)组的总生存期显著长于MGMT(+)、p53(-)组,差异有统计学意义(P<0.05)。p53(+)、MGMT低表达组的总生存期要显著高于p53(+)、MGMT高表达组(P<0.05)。结论 MGMT蛋白的表达缺失及p53蛋白的表达增强可能共同参与了胃癌的发展过程,联合分析MGMT和p53蛋白的表达情况对于进展期胃癌患者的预后评估可能具有一定的参考价值;而MGMT蛋白低表达相较高表达时的总生存期略长可能存在其他影响因素。  相似文献   

19.
目的:探讨阿司匹林对胃溃疡愈合的影响和机制。方法:用乙酸诱导大鼠胃溃疡,然后随机分为模型对照组、生理盐水对照组、阿司匹林组。用组织学方法检测溃疡形态、溃疡面积和肉芽组织中的炎细胞数:用免疫组织化学方法检测核因子-κB、肿瘤坏死因子-α和白细胞介素-8在胃黏膜中的表达。结果:阿司匹林组的溃疡面积高于模型和生理盐水对照组(P〈0.05);炎细胞数、核因子-κB、肿瘤坏死因子-α和白细胞介素-8的积分光密度都高于模型和生理盐水对照组(P〈0.01)。结论:阿司匹林通过增加核因子-κB的表达上调肿瘤坏死因子-α和白细胞介素-8的表达,加重炎症反应,进而抑制溃疡愈合。  相似文献   

20.
阿司匹林抗氧化作用机制的探讨   总被引:5,自引:0,他引:5  
目的 探讨阿司匹林(AS)抗氧化作用的机制。方法 观察不同浓度的AS在抗H2O2损伤内皮细胞过程中诱导铁蛋白(Fn)表达的情况,以及添加外源性FeCI3和细胞内铁螯合剂去铁胺时对AS诱导Fn表达的影响。结果 极低剂量(0.1mmol/L)的AS即可诱导内皮细胞Fn表达超过对照25%(P<0.05),使乳酸脱氢酶(LDH)释放率减少50%,保护74.4%的细胞避免H2O2的损伤,同时使氧自由基指标丙二醛明显下降。AS与Fn表达之间表现出剂量与时间依赖关系,且对细胞的保护作用逐渐增强。但使用去铁胺去除细胞内游离铁能明显降低AS诱导Fn表达的作用,而加入FeCI3后诱导Fn表达的作用增强。结论 初步证实AS的抗氧化作用是通过影响细胞内铁代谢变化,增加Fn表达实现的。  相似文献   

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