芪龙方防治大鼠胃癌癌前疾病的作用

目的;研究经验方芪龙方防治胃癌癌前疾病及其在胃癌发生发展中的作用。方法：用Ｎ－甲基－Ｎ‘－硝基－Ｎ－亚硝基胍（ＭＮＮＧ）诱恨新生大鼠胃癌前疾病及胃癌的动物模型,观察芪龙方对模型动物的病理组织学作用,结果：芪龙方能显著减少ＭＮＮＧ诱发的大鼠胃粘膜慢性萎缩性胃炎、胃粘膜异型增生和胃腺癌的发生率,与单纯病理模型组比较Ｐ〈０．０５,并呈现一定的剂量效应关系,结论：芪龙方有较强的防治胃癌癌前病变和胃癌发生发     

中药芪龙方抑制实验性胃肿瘤的作用

芪龙方是北京市中医研究所在临床应用治疗胃癌癌前疾病数十年的基础上,不断总结和发展起来的经验方剂．芪龙方具有健脾益气,清热活血解毒之功效．临床用于治疗胃癌癌前疾病不仅疗效确切,还未发现毒副作用．因此我们为了深入研究芪龙方的作用,以期初步阐明芪龙方治疗胃癌癌前疾病的作用机制,为临床更广泛的应用芪龙方,提供理论依据和实验研究的基础．本文以小鼠Ｌｅｗｉｓ肺癌、前胃癌（ＦＣ）为体内移植瘤,探讨芪龙方对实验性肿瘤的抑制作用,并以人胃腺癌ＢＧＣ＿８２３,ＢＧＣ＿８０３及ＭＮＫ＿２８等细胞株为材料,用ＭＴＴ法进…     

加味四君子汤对MNNG诱导大鼠胃癌的预防作用

[目的]观察加味四君子汤治疗对N-甲基-N-硝基-亚硝基胍(MNNG)诱发大鼠胃癌的预防作用.[方法]90只雄性Wister大鼠随机分成5组,正常对照组,模型组,加味四君子汤组,增液汤组,0.85%氯化钠组.每组18只,除正常对照组外,其余各组MNNG造模.喂养(28士2)周后观察各组大鼠的胃黏膜病变.[结果]83只(92.2%)大鼠完成实验.模型组大鼠胃癌发生率40.0%(6/15),显著高于加味四君子汤组5.9%(1/17),差异有统计学意义(P＜0.05),前者胃黏膜萎缩、肠上皮化生和异型增生发生率也显著高于后者(P＜0.05).增液汤组及0.85%氯化钠组与模型组大鼠胃癌及癌前病变发生率无明显差异(P＞0.05);正常对照组无胃癌发生.[结论]脾虚血瘀是胃癌及癌前病变发生发展过程中的重要促进因素之一,加味四君子汤健脾化瘀治疗能有效地抑制MNNG诱发大鼠胃癌及癌前病变的发生.     

复方参七汤治疗胃癌的基础研究

目的阐明复方参七汤治疗胃癌的作用机制.方法体外抑癌研究:体外培养人胃癌细胞株BGC-823,观察复方参七汤对人胃癌细胞株BGC-823的杀伤效应、细胞分裂及集落形成的抑制作用.在体实验研究:中药组(50只)大鼠每日喂MNNG 100 mg/L和含复方参七汤(18 mL/kg)的颗粒饲料,连续9mo.对照组(50只)大鼠每日喂MNNG 100mg/L和颗粒饲料,连续9mo.9mo后(除自然死亡外)杀死生存大鼠,切取鼠腺胃和十二指肠标本,应用10%福尔马林固定标本,石蜡包埋,组织切片HE染色.免疫组化研究:鼠腺胃标本的石蜡切片进行免疫组化染色,应用免疫组化S-P法检测Wistar大鼠腺胃粘膜的正常细胞、异型增生细胞和癌细胞PCNA和Cyclin D1表达.结果体外实验研究:复方参七汤抑制人胃癌细胞株BGC-823的细胞分裂和集落细胞形成,IC50为7g生药/L.高浓度时有直接杀死癌细胞作用,LC50为48 g生药/L.在体实验研究:中药组,50只Wistar大鼠中7只自然死亡,余下43只生存9 mo,将它们分批处死,32只大鼠腺胃粘膜细胞呈现正常(74.4%,32/43);8只大鼠腺胃粘膜细胞呈异型增生(18.6%,8/43)和3只大鼠腺胃癌(6.9%,3/43).对照组,50只Wistar大鼠中,11只自然死亡,余下39只生存9mo,将它们分批处死,16只大鼠腺胃粘膜细胞异型增生(41.1%,16/39),23只大鼠腺胃癌(58.9%,23/39),比较两组腺胃癌的发生率,中药组6.9%,明显低于对照组58.9%,P<0.01.免疫组化研究:中药组大鼠腺胃粘膜细胞的PCNA和Cyclin D1强阳性表达率分别为13.8%和22.8%,而对照组分别为75.7%和62.8%,两组相比较,中药组的大鼠腺胃PCNA和Cyclin D1的强阳性表达率明显低于对照组(P<0.05).结论复方参七汤治疗胃癌有良好的疗效,其作用机制可能抑制人胃癌细胞株BGC-823细胞分裂和集落形成;可能降低MNNG诱发Wistar大鼠腺胃癌发生率;可能抑制鼠腺胃增殖细胞和癌细胞的PCNA和Cyclin D1强阳性表达;可能阻止正常腺胃细胞向肿瘤细胞转化,抑制肿瘤细胞的过度增殖.     

芪龙方对荷瘤小鼠T细胞亚群和自然杀伤细胞的作用

目的：观察芪龙方对荷瘤小鼠Ｔ细胞亚群和自然杀伤细胞的作用。方法；用６１５小鼠移植前胃癌，观察芪龙方，阿霉素及其联合用药对荷瘤小鼠的Ｔ细胞亚群ＣＤ＾４＋，ＣＤ８＾＋数量和ＮＫ细胞的活性，抑瘤作用及体重的作用。结果；给药第７，１３天，芪龙方组ＣＤ４＾＋数量明显上升，ＣＤ＾＋８数量有所升高，但无显著性差异；联合用 组ＣＤ＾＋４升高，优于对照组及单纯化疗组。     

实验性胃癌模型

用化学致癌剂诱发胃癌模型的研究始于30年代,但因缺乏特异的致癌剂而较难在大鼠等啮齿类动物中诱发成与人体胃癌相似的胃腺癌.50年代中期,有些学者曾试用芳香多环烃类化合物如3-甲基胆蒽、3,4-苯并芘、7,12-二甲基苯蒽等进行胃壁内直接注射或包埋,但均因胃腺癌诱发率较低而未获推广.1967年,日本Sugimura等应用N-甲基-N'-硝基-N-亚硝基胍(N-Methyl-N'-Nitro-N-Nitrosoguanidine简称MNNG)溶于饮水中给药,成功地诱发了Wistar大鼠的胃腺癌,使实验性胃癌模型的研究有了突破性进展.以后许多学者相继在小鼠、仓鼠、犬等动物中用MNNG诱发胃腺癌成功.用MNNG饮水法诱发胃癌方法简便,特异性较高,重复性好,诱     

MNNG诱发动物实验性腺胃癌机理的研究进展

本文综述了N-甲基-N’-硝基亚硝基胍(MNNG)诱发大鼠及狗实验性胃癌方面的研究进展。     

芪龙方对荷瘤小鼠T细胞亚群和自然杀伤细胞的作用

目的：观察芪龙方对荷瘤小鼠Ｔ细胞亚群和自然杀伤（ＮＫ）细胞的作用。方法：用６１５ 小鼠移植前胃癌（ＦＣ）,观察芪龙方（１ ０００ ｍ ｇ／ｋｇ）、阿霉素（１．５ ｍ ｇ／ｋｇ）及其联合用药对荷瘤小鼠的Ｔ细胞亚群ＣＤ＋４ 、ＣＤ＋８ 数量和ＮＫ 细胞的活性、抑瘤作用及体重变化的作用。结果：给药第７、１３ 天,芪龙方组ＣＤ＋４ 数量明显上升（Ｐ ＜ ０．０５）,ＣＤ＋８ 数量有所升高,但无显著性差异（ Ｐ＞ ０．０５）;联合用药组ＣＤ＋４ 升高,优于对照组及单纯化疗组（Ｐ＜ ０．０５）。给药第７、１３天,芪龙方组ＮＫ细胞活性明显升高（ Ｐ＜ ０．０５）,联合用药组升高趋势优于单纯化疗组,但无显著性差异（ Ｐ＞ ０．０５）。给药第７、１３ 天,芪龙方组抑瘤作用分别为２５．０％ 、４０．５％ ,联合用药组分别为４１．７％ 、５４．２％ 。结论：芪龙方具有直接抑制肿瘤生长、改善与提高机体的免疫功能状态和一般状况的综合作用     

胃癌前状态注墨标记及随访研究

为观察胃粘膜癌前状态的转归，对２０８例癌前状态病人前瞻性随访５年。常规胃粘膜取材随访２年后，采用胃粘膜内注墨标记癌前病变，定期原位取材，追踪癌前状态的发展。在随访期间，以胃粘膜活检病理积分法观察癌前变化，大部分癌前病变减轻或无进展，胃粘膜癌前变化病理积分显著下降，但在随访初期检出早期胃癌７例，提示癌前状态可能预示有隐藏癌，强调应加强近期随访初诊为胃癌状态者。此外，观察叶酸治疗癌前状态其效果与一般胃病治疗药无显著差异     

β-胡萝卜素治疗慢性萎缩性胃炎

慢性萎缩性胃炎 ( CAG)是胃癌的癌前疾病 ,近年来认为它是在慢性浅表性胃炎的基础上发生的 ,与胃癌的发生关系密切。 Correa提出肠型胃癌的发生模式为 :正常胃粘膜→浅表性胃炎→CAG→肠上皮化生→不典型增生→胃癌[1] 。如何使其逆转 ,减少胃癌的发生 ,是目前研究的热点。β-胡萝卜素和肿瘤的关系报道很多 ,本文就其治疗 CAG及基因表达方面进行初步探讨。1　资料与方法1 .1　临床资料 :2 0 0 2年 8月～ 2 0 0 2年 3月在我院行胃镜检查的患者 ,根据 2 0 0 0年 5月井冈山制定的慢性胃炎标准 ,经病理学检查证实为 CAG者 1 86例 ,男 1 1 …     

胃癌及癌前病变中p53蛋白的检测及意义

探讨p53蛋白表达与胃癌及癌病变的相互关系,方法：用免疫组化染色示检测33例肠化,26例异型增生和26例胃癌组织中p53蛋白的表达。结果：p53蛋白在胃癌组织中表达率最高（61．5％）,在异型增生和肠化组织中的表达率分别为34．6％和12．1％,组间有显著差异,各期胃癌组织中p53蛋白的表达无显著差异,结论：p53蛋白在胃癌前病变中已有阳性表达,在肠化、异型增生及胃癌组织中,其表达率依次增高,p53蛋白积累主要发生在癌前病变晚期及胃癌早期,其表达与胃癌发生密切相关。     

Effect of jianpiyiwei capsule on gastric precancerous lesions in rats

AIM：To evaluate the therapeutic effect of compound Chinese drugs,Jianpiyiwei capsule(JPYW)on gastric precancerous lesions in rats and to explore its mechanism of action.METHODS:Model of gastric precancerous lesions was constructed in male Wistar rats:a metal spring was inserted and fixed through pyloric sphincter.One week after recovery,each rat was given50-60℃hot paste containing150g/LNaCl2mLorally,twice a week for 15weeks.Then10normal and11model rats were anaesthetized,after the measurement of gastric mucosa blood flow(GMBF),the rats were killed and the mucosal hexosamines and malonic dialdehyde(MDA)were measured.The morphological changes of gastric mucosa were observed macroscopically and microscopically,and by an automatic imaging analysis system.Other rats were treated with JPYW1.5g/kg-d^&#183;1 0r4.5g/kg&#183;d^-1.ordistilled water as negative control respectively(n=10in each group).After 12weeks,all the rats were examined as above.RESULTS:The gastric mucosa of model rats showed chronic atrophic gastritis with dysplasia and intestinal metaplasia(IM).GMBFand hexosamine content were reduced significantly and MDAwas increased as compared to the normal group(P&lt;0.01).After12weeks treatment,the pathological changes of the negative control group became worsened.while in JPYWtreated groups the changes were modified with significant increase of GMBF and reduction of MDA,although the hexosamine concentration increased only mildly.CONCLUSION:JPYW increases GMBFand reducesMDAcontent in gastric mucosa and has therapeutic effects on gastric precancerous lesions.     

参芪消痞汤对慢性萎缩性胃炎癌前期病变胃黏膜修复作用和血管生成机制及血清p53、MDA、GSH-Px的相关影响

目的:观察参芪消痞汤对慢性萎缩性胃炎(CAG)癌前期病变大鼠胃黏膜表皮生长因子(EGF)、表皮生长因子受体(EGFR)表达水平与缺氧诱导因子(HIF-1α)、血管内皮生长因子(VEGF)及血清p53、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)的相关影响.方法:选择60只健康SD雄性大鼠喂养1周后,根据体重随机...     

A model of gastric precancerous lesions for rats

AIM To establish an ideal model of gastric precancerous lesions for rats.METHODS Fifty rats were fed with carcinogen MNNG for 35 wk and heat-plaste at 60C for 20 wk, thepathological changes were observed. Data in the groups were analyzed by Ridit test.RESULTS The occurrence rate of dysplasia in rats due to MNNG and heat-damage was 65%, which wasobviously higher than that due to MNNG only. The differences between the two groups were significant.CONCLUSION The animal model made by MNNG and heat-damage was an ideal one which could be usedto investigate the pathologic mechanism of gastric precancerous lesions.     

莪蚕健胃方治疗大鼠胃癌前病变作用机制的探讨

[目的]通过观察莪蚕健胃方对胃癌前病变大鼠胃黏膜组织细胞增殖、凋亡及Bcl-2蛋白表达的影响,探讨莪蚕健胃方治疗胃癌前病变的作用机制.[方法]采用N-甲基-N-硝基-N-亚硝基胍(MNNG)配合饥饱失常法诱导造模.设空白对照组,模型对照组,莪蚕健胃方大、中、小剂量组,进行常规病理检测,采用免疫组化SP法、TUNEL法检测胃黏膜组织细胞增殖核抗原(PCNA)、Bcl-2蛋白及凋亡指数(AI)的表达情况.[结果]莪蚕健胃方各剂量组胃黏膜组织病理学变化,中、重度异型增生率与模型对照组相比明显降低(均P＜0.05);莪蚕健胃方能明显下调胃癌前病变组织细胞的PCNA、Bcl-2的表达,上调AI.[结论]莪蚕健胃方对大鼠实验性胃黏膜癌前病变有逆转作用,抑制细胞增殖、诱导细胞凋亡可能是该方的作用机制之一.     

Effect of Helicobacter pylori infection on Bax protein expression in patients with gastric precancerous lesions

AIM: To investigate the effect of Helicobacter pylori (H pylori) infection on Bax protein expression, and explore the role of H pylori in gastric carcinogenesis. METHODS: H pylori was assessed by rapid urease test and Warthin-Starry method, and expression of Bax protein was examined immunohistochemically in 72 patients with pre-malignant lesions. RESULTS: Bax protein was differently expressed in intestinal metaplasia and gastric dysplasia, and showed 63.99% positivity. The positivity of Bax protein expression in Hpylori-positive gastric precancerous lesions (72.3%) was significantly higher than that in H pylori-negative gastric precancerous lesions (48.0%, X~2=4.191, P<0.05). H pylori infection was well correlated with the expression of Bax protein in gastric precancerous lesions (r=0.978, P<0.01). After eradication of H pylori, the positivity of Bax protein expression significantly decreased in H pylort-positive gastric precancerous lesions (X~2=5.506, P<0.05). In the persisting H pylori-infected patients, the positivity of Bax protein expression was not changed. CONCLUSION: H pylori infection may be involved in the upregulation of Bax gene, which might be one of the mechanisms of H pylori infection-induced gastric epithelial cell apoptosis. H pylori might act as a tumor promoter in the genesis of gastric carcinoma and eradication of H pylori could inhibit gastric carcinogenesis.     

加味左金丸对胃癌前病变大鼠胃黏膜组织细胞增殖与凋亡的影响

[目的]探讨加味左金丸对胃癌前病变大鼠胃黏膜组织细胞增殖与凋亡的影响。[方法]将以饮用甲硝基亚硝基胍为主24周制成的胃癌前病变模型大鼠随机分为模型组，维甲酸组，加味左金丸高、中、低剂量组，治疗16周，采用免疫组化SP法，TUNEL法检测胃黏膜组织细胞增殖细胞核抗原（PCNA）、Bcl-2蛋白及凋亡指数（AD）的表达情况。[结果]加味左金丸能明显下调胃癌前病变组织细胞的PCNA、Bcl-2的表达，上调AI。[结论]抑制细胞增殖，诱导细胞凋亡可能是该方的作用机制之一。     

血清胃蛋白酶原检测在胃癌及其癌前病变筛查中的价值

目的:探讨血清胃蛋白酶原(PG)检测在胃癌及其癌前病变筛查中的价值.方法:在胃癌高发区对35岁以上无症状、有胃病史及胃癌家族史者进行内镜筛查.同时采用免疫比浊法测定受检者血清PG水平,结合内镜活检和病理检查结果,对比分析接受受检者血清PGⅠ、PGⅡ水平和PGⅠ/Ⅱ值与胃癌及其癌前病变的关系.结果:内镜筛查共计918例,其中PG阴性718例(78.21%);阳性200例(21.79%),阳性人群中以40-60岁最多139例(69.50%);总体胃癌检出率7/918(0.76%),早期胃癌检出率为5/7(71.43%),进展期为2/7(28.57%);PG阳性癌检出率3/200(1.50%),高级别上皮内瘤变检出率2/200(1.00%),低级别上皮内瘤变检出率23/200(11.50%);PG阴性癌检出率4/718(0.56%),高级别上皮内瘤变检出率0/718(00.00%),低级别上皮内瘤变检出率54/718(7.52%);PG阳性与PG阴性之间胃癌及其癌前病变检出率有显著性差异(P<0.01).PG阳性中早期胃癌检出率为2/3(66.67%),胃癌诊断的敏感性42.86%,特异性78.38%.结论:以血清...     

Blood levels of natural antioxidants in gastric and colorectal precancerous lesions and cancers in Slovakia

A long-term sufficient intake of fruits and vegetables reduces significantly the risk of gastric and colorectal carcinoma. It is anticipated that natural antioxidants are involved in this effect in addition to other substances. The aim of this study was to determine levels of vitamins A, C and E, as well as beta-carotene, selenium, zinc and copper in blood of 249 patients with precancerous lesions (atrophic gastritis, gastric hyperplastic polyp, gastric, colonic and rectal adenoma, chronic ulcerative colitis) and in 96 individuals with gastric, colonic or rectal carcinoma and to compare these levels with the values of a control group of 130 healthy individuals. We have found that the frequency of average values of analyzed micronutrients in precancerous groups was decreasing in the order vit C > vit E/vit A > Se > beta-car. The average levels of vitamins and beta-carotene were significantly reduced in all carcinoma groups, while selenium level showed a decrease only in the gastric carcinoma group. Copper level was elevated in the ulcerative colitis group and in all groups with carcinoma. The results indicate a frequent insufficient saturation of organism by natural antioxidants in groups with precancerous lesions and carcinomas of stomach and colorectum. Therefore, it is necessary to increase the general consumption of fruits and vegetables in Slovakia as a part of primary prevention of malignant diseases in these organs. Chemoprevention may be recommended in individuals with precancerous lesions.     

盐酸小檗碱抗大鼠胃癌前病变及其作用机制

[目的]探讨盐酸小檗碱对实验性大鼠胃癌前病变的影响及与细胞凋亡和P53、Bcl-2蛋白、mRNA表达水平的关系.[方法]采用N-甲基-N-亚硝基胍饮水法建立大鼠胃癌前病变模型,用盐酸小檗碱预防和大、中、小3种剂量干预治疗,观察大鼠的一般情况,以光镜观察胃癌前病变的发生率,并运用末端DNA标记法检测凋亡率(AI),免疫组化法检测细胞中P53和Bcl-2蛋白表达,逆转录多聚酶链式反应检测P53和Bcl-2的mRNA水平.[结果]经盐酸小檗碱干预大鼠,其癌前病变的发生率明显降低,与模型组比较P＜0.05,AI显著提高,3种剂量组与模型组比较均P＜0.05,并伴有Bcl-2、突变型P53基因蛋白表达水平降低,野生型P53基因mRNA水平升高,Bcl-2基因mRNA水平下调,其中以大剂量组尤为显著,与模型组比较P＜0.01.[结论]盐酸小檗碱能预防和治疗实验性大鼠胃癌前病变,其机制与提高细胞凋亡率和调控基因表达有关.