参佛胃康对大鼠慢性萎缩性胃炎及胃癌前病变逆转作用的研究

目的：观察参佛胃康对大鼠慢性萎缩性胃炎及胃癌前病变的逆转作用,探讨其作用机制。方法：采用主动免疫、去氧胆酸钠、热水灌胃综合法连续造模90d,复制慢性萎缩性胃炎（CAG）大鼠模型,空白组自由饮水,模型组用等体积的蒸馏水灌胃,丽珠得乐组用丽珠得乐溶液0.018mg/kg灌胃,参佛胃康大剂量组、参佛胃康小剂量组分别用参佛胃康溶液2.44mg/kg和0.61mg/kg灌胃。肉眼观察胃黏膜的变化,光镜下观察胃黏膜的病理学改变,同时测定大鼠胃液pH值及胃蛋白酶活性的变化。结果：参佛胃康能保护大鼠慢性胃黏膜损伤,增加胃液酸度提高胃蛋白酶活性,且参佛胃康大剂量组效果显著。结论：参佛胃康对慢性胃萎缩性胃炎黏膜的各种病理变化具有明显的逆转作用。     

复胃汤对大鼠胃癌前病变的防治作用研究

 【摘要】　目的　探讨中药复胃汤预防和治疗胃癌前病变的机制和效果。方法　对140只胃癌前病变模型大鼠进行中药（复胃汤）和西药（维酶素）预防和治疗给药,观察胃黏膜病理改变和Caspase-3的变化。结果　中药及西药预防组不典型增生发生率分别为50.0 %（6／12）、42.86 %（6／14）,明显低于造模组的90.0 %（9／10）（H＝16.40,H＝16.86,均P＜0.05）。中药及西药治疗组不典型增生发生率为42.9 %（6／14）和41.7 %（5／12）,明显低于造模空白组的90.9 %（10／11）（H＝12.39,H＝12.18,均P＜0.05）,且多为轻、中度不典型增生[45.45 %（6／11）、36.36 %（4／11）]。造模组Caspase-3表达明显低于正常对照组（q＝3.05,P＜0.01）,中药及西药预防组Caspase-3表达均增加,均明显高于造模组和正常对照组（q＝5.45、q＝7.54、q＝8.51、q＝10.60,均P＜0.01）。中药及西药治疗组Caspase-3表达亦明显高于造模空白组和正常组,差异均有统计学意义（q＝15.66、q＝18.53、q＝15.66、q＝18.53,均P＜0.01）。结论　复胃汤通过促进Caspase-3的表达,抑制了胃黏膜上皮细胞不典型增生,达到对胃癌前病变的防治作用。。     

康赛迪胶囊治疗慢性萎缩性胃炎伴胃黏膜不典型增生的临床观察

2000年3月18日～2002年2月2日对伴有慢性萎缩性胃炎(chronic atrophic gastritis，CAG)和中度胃黏膜不典型增生(atypical delirium，ATP)的癌症患者．服用康赛迪胶囊进行治疗总结报道如下。     

慢性萎缩性胃炎的中医中药康复治疗

慢性胃炎包括浅表性胃炎和萎缩性胃炎。其中慢性萎缩性胃炎伴有胃黏膜肠上皮化生或中度、重度不典型细胞增生及幽门螺杆菌（HP）感染。由于胃酸分泌缺乏,胃排空时间延长,为致病菌或致癌物质的接触提供了有利的环境,致使病人常会集中表现胃部各种痛、胀等不适症状,     

康赛迪胶囊治疗慢性萎缩性胃炎伴胃黏膜不典型增生的临床观察

20 0 0年3月18日～2 0 0 2年2月2日对伴有慢性萎缩性胃炎(chronicatrophicgastritis ,CAG )和中度胃黏膜不典型增生(atypicaldelirium ,ATP)的癌症患者,服用康赛迪胶囊进行治疗总结报道如下。1　临床资料1.1　病例选择12例患者,男8例,女4例,病程3～2 0年。4例ATP为轻度,7例为中     

番茄酱对大鼠食管癌前病变抑制作用的研究

目的 研究番茄酱通过抑制脂质过氧化反应而影响甲基戊基亚硝胺（MANA）致癌的效果。方法 Wistar大鼠随机分为三组,对照组、干预组（MANA 番茄酱）,单亚组和干预组大鼠每周肌注MANA1次,剂量5mg/kg,持续20周,干预组番茄酱添加至实验结束,实验期26周,共分5次处死动物,测定血清活性氧单位（ROS单位）、超氧化物歧化酶活性（SOD）、丙二醛（MDA）含量以及全血谷胱甘肽过氧化物酶（GSH-Px)活力的变化,并重点观察大鼠食管组织病理改变。结果 单亚组和干预组大鼠食管上皮均发生癌前病变,干预组癌前病变的发生率低于单亚组,干预组大鼠ROS单位,SOD和GSH-Px活性有明显提高,MDA含量有明显降低。结论 番茄酱对大鼠食管癌前病变的发生有预防作用;番茄酱通过提高大鼠的抗氧化能力。抑制脂质过氧化反应,是影响亚硝胺诱发大鼠食管癌的可能机制之一。     

BRM释介素抗肿瘤作用及作用机理研究

目的：研究中药复方胶囊BRM释介素的抗癌活性及诱导人神经胶质瘤细胞SHG-44、人乳腺癌细胞MCF-7的凋亡作用。方法：运用MTT法检测BRM对体外人癌细胞株的抑制作用；运用小鼠移植瘤模型观察BRM体内瘤活性，应用电镜、AnnexinV-FITC／PT双染流式细胞胞仪分析、琼脂糖凝胶电泳观察BRM诱导SHG-44，MCF-7细胞发生凋亡的作用。结果：BRM释介素体外对SHG-44，MCF-7细胞具有明显的抑制作用。体内对小鼠移植性肿瘤：胰腺癌(MPC-83)、艾氏腹水癌(EAC)、肉瘤(S-180)、神经胶质瘤(G422)表现出较显著的抗癌活性，SHG-44和MCF-7在BRM水提液作用下发生细胞凋亡，表现为细胞固缩、核染色质靠边，出现马蹄形，半月形。Annexin V-FITC／PT流式细胞仪分析，BRM作用24—38h，早期和中晚期凋亡细胞明显增多。BRM水提液(2．5mg生药)作用24～48h，细胞DNA裂解片断呈典型的梯带。结论：BRM释介素的抗肿瘤活性与诱导细胞凋亡有关。     

丁酸钠治疗胃粘膜癌前病变的实验研究

给大鼠自由饮用５０μｇ／ｍｌＭＮＮＧ溶液共２０周，诱发脾胃粘膜病变。实验从第３６周起，按１５０ｍｇ／ｋｇ体重，每日１次给大鼠喂服丁酸钠共８周，以后处死动物进行观察。丁酸钠治疗组大鼠腺胃粘膜肠化生、硫酸粘液阳性肠化生、中重度异型增生及胃癌的发生率（各为６０．０％、４０．０％、２０．０％、０％）显著低于未加治疗的对照组（各为８８．０％、７６．０％、４８．０％、１６．０％）（Ｐ＜０．０５）；治疗组大鼠幽门腺与胃底腺平均肠化腺体数（各为７０．３±４６．８、３９．８±２９．６）亦显著地低于治疗前对照组（各为２１６．３±９８．４、１３０．７±５９．２）和未加治疗的对照组（各为２４１．４±１１３．９、１４６．４±６６．３）（Ｐ＜０．０１）；经丁酸钠治疗后，大鼠病变胃粘膜血流量改善，泌酸功能好转，跨膜电位差及血和组织中ＬＰＯ含量恢复接近正常水平。说明丁酸钠对大鼠实验性腺胃粘膜癌前病变有部分逆转和阻断治疗作用。这为探讨人类胃癌前病变的防治提供了新的途径。     

健脾理气等中药对大鼠肝脏癌前病变阻断作用的实验研究

在肿瘤形成过程中用化学药物进行干预,阻断其发展,在肿瘤防治中具有重要意义。我们用二乙基亚硝胺作诱癌剂,巴比妥钠作促癌剂建立大鼠肝癌模型,甩健脾理气、活血化瘀、清热解毒中药处理实验动物,以大鼠肝脏癌前病变γ-GT酶变灶的定量分析为实验指标,观察不同治则的中药对大鼠肝脏癌变过程的影响。现将结果报告如下。     

慢性萎缩性胃炎患者及胃癌患者的免疫状态研究

 本文用OKT单克隆抗体间接SPA菌花环法和非特异性酯酶柒色法对慢性萎缩性胃炎（CAG）患者进行了外周血T淋巴细胞亚群的检测，同时还测定了CAG患者的血清IgG、IgA和IgM。实验结果：两种方法均显示CAG患者的辅助T亚群明显降低，辅助T/抑制T亚群的比值显著下降，表明CAG患者的T亚群处于失调状态。OKT单抗花环法测定CAG重度患者的T亚群失调甚于CAG轻中度患者的失调。本文还将CAG患者与术前胃癌患者的T亚群检测作了对比，发现后者的T亚群失调状态比前者的更甚。CAG患者的血清IgG、IgA和IgM测定无明显改变，属正常值范围。     

慢性萎缩性胃炎治疗初探

目的 探讨塞来昔布对胃癌前疾病——慢性萎缩性胃炎的干预作用。方法 胃镜活检经病理证实为慢性萎缩性胃炎的病人97例（男51例，女46例，男女比例1．11：1）。随机分为两组：塞来昔布组（接受塞来昔布0．2，1次／d，po）和空白对照组（不接受特异性治疗），疗程均为6mo。治疗前，治疗3mo及疗程结束各行胃镜检查1次。活检组织行常规病理检查及免疫组化染色检测COX-2的表达。结果 治疗3mo时，塞来昔布组cox-2蛋白表达明显下降（P〈0．05），但两组胃粘膜萎缩程度无明显差异；疗程结束后，塞来昔布组cox-2蛋白表达明显下降（P〈0．05），且胃粘膜萎缩程度有所减轻，但两组间无统计学差异。结论 塞来昔布可以明显抑制胃粘膜cox-2蛋白的表达，提示对慢性萎缩性胃炎有一定的逆转作用。     

塞来昔布治疗慢性萎缩性胃炎的疗效及安全性

目的初步评价塞来昔布治疗胃癌前疾病-慢性萎缩性胃炎过程中的疗效及副作用。方法胃镜活检经病理证实为慢性萎缩性胃炎的病人78例（男41例,女37例,男女比例1．11：1）。随机分为两组：塞来昔布组（接受塞来昔布0．2,1次/d,po）和空白对照组（不接受特异性治疗）,疗程均为6mo。治疗前,治疗3mo及疗程结束各行胃镜检查1次。活检组织行常规病理检查及免疫组化染色检测cox-2的表达。治疗过程中记录胃黏膜损害、肾功能损害、血清脂蛋白水平变化及心脑血管事件。结果治疗3mo时,塞来昔布组cox-2蛋白表达明显下降（P〈0．05）,但两组胃黏膜萎缩程度无明显差异;疗程结束后,塞来昔布组cox-2蛋白表达明显下降（P〈0．05）,且胃黏膜萎缩程度有所减轻,但两组间无统计学差异。塞来昔布组治疗前、治疗中及治疗后未发现急性胃黏膜损害及心脑血管事件;治疗前后血清脂蛋白水平及肾功能无明显变化。结论塞来昔布可以明显抑制胃黏膜cox-2蛋白的表达,提示对慢性萎缩性胃炎有一定的逆转作用。应用塞来昔布治疗慢性萎缩性胃炎安全性良好。     

Epidemiologic findings on serologically defined chronic atrophic gastritis strongly depend on the choice of the cutoff-value

Chronic atrophic gastritis (CAG), a precursor of intestinal gastric cancer, is mostly ascertained noninvasively by serum pepsinogens in epidemiologic studies. However, serological definitions vary widely. We aimed to investigate the impact of this variation on estimated prevalence of CAG and its association with its main risk factors, age and Helicobacter pylori infection. Serum pepsinogen I and II and antibodies against H. pylori were measured by ELISA among 9,444 women and men aged 50-74 years in a population-based cohort study in Saarland/Germany. Application of the various definitions resulted in a wide range of prevalence estimates of CAG prevalence (2.1%-8.2%, with an outlier of 18.8% for one particular definition) and its associations with age and H. pylori infection (age adjusted odds ratios, OR, for CagA positive H. pylori infection: 0.98-4.48). Definitions of CAG based on both pepsinogen I and the pepsinogen I/II ratio or on the pepsinogen I/II ratio only revealed much clearer associations with both age and H. pylori infection than definitions of CAG based on pepsinogen I only (ORs for H. pylori infection: 1.45-4.48 and 0.86-1.30, respectively). Epidemiologic findings on CAG lack comparability due to the heterogeneity in serologic definitions of CAG. The association of age and H. pylori infection with CAG may be strongly underestimated in studies in which CAG is defined by pepsinogen I only.     

Association of Helicobacter pylori infection with chronic atrophic gastritis: Meta-analyses according to type of disease definition

Helicobacter pylori is a major risk factor for chronic atrophic gastritis (CAG). A large variety of definitions of CAG have been used in epidemiologic studies in the past. The aim of this work was to systematically review and summarize estimates of the association between H. pylori infection and CAG according to the various definitions of CAG. Articles on the association between H. pylori infection and CAG published until July 2007 were identified. Separate meta-analyses were carried out for studies defining CAG based on gastroscopy with biopsy, serum pepsinogen I (PG I) only, the pepsinogen I/pepsinogen II ratio (PG I/PG II ratio) only, or a combination of PG I and the PG I/PG II ratio. Numbers of identified studies and summary odds ratios (OR) (95% confidence intervals) were as follows: gastroscopy with biopsy: n = 34, OR = 6.4 (4.0-10.1); PG I only: n = 13, OR = 0.9 (0.7-1.2); PG I/PG II ratio: n = 8, OR = 7.2 (3.1-16.8); combination of PG I and the PG I/PG II ratio: n = 20, OR = 5.7 (4.4-7.5). Studies with CAG definitions based on gastroscopy with biopsy or the PG I/PG II ratio (alone or in combination with PG I) yield similarly strong associations of H. pylori with CAG. The association is missed entirely in studies where CAG is defined by PG I only.     

Alcohol consumption and chronic atrophic gastritis: Population‐based study among 9,444 older adults from Germany

Moderate alcohol consumption has been suggested to facilitate elimination of Helicobacter pylori infection which is a key risk factor for chronic atrophic gastritis (CAG) and gastric cancer. The aim of our study was to assess the association of alcohol consumption with CAG among older adults from Germany. In the baseline examination of ESTHER, a population‐based study conducted in Saarland, serological measurements of pepsinogen I and II (for CAG definition) and H. pylori antibodies were taken in 9,444 subjects aged 50–74 years. Moderate current (<60 g/week) and lifetime (≤51,376 g, lowest quartile) alcohol consumption were found to be associated with significantly reduced CAG risk compared to alcohol abstinence with adjusted odds ratios of 0.71 (0.55–0.90) and 0.73 (0.55–0.96), respectively. Inverse associations with CAG were observed for moderate alcohol consumption from both beer and wine, and were slightly attenuated after additional adjustment for H. pylori infection. Our results are consistent with the hypothesis that moderate alcohol consumption may be inversely related to CAG, partly through facilitating the elimination of H. pylori. However, the observed patterns suggest that other mechanisms are likely to contribute to the association as well. © 2009 UICC     

Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer

We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori- and CAG-status was performed. No cancer developed in the H. pylori(-)/CAG(-) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori-free healthy stomach. With the progression of H. pylori-induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG-free gastritis [H. pylori(+)/CAG(-) group] (HR=7.13, 95%CI=0.95-53.33) to CAG [H. pylori(+)/CAG(+) group] (HR=14.85, 95%CI=1.96-107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(-)/CAG(+) group] (HR=61.85, 95%CI=5.6-682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori-induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis-metaplasia-carcinoma sequence.     

胃癌与慢性萎缩性胃炎基因表达谱的差异和关联

背景与目的:胃黏膜自慢性炎症演变为胃癌的过程中,隐伏着一系列的基因变化.本研究采用高通量基因芯片,检测慢性萎缩性胃炎和胃癌组织的基因表达,结合病理资料,分析和比较两者基因表达的异常及其生物学意义.方法:收集23例胃癌以及15例慢性萎缩性胃炎的病变及配对非病变部位胃粘膜组织,以载有13824个基因/EST序列的基因芯片检测基因表达谱,结合病理等临床资料,应用系统聚类法、t检验、Fisher确切概率法等统计学方法进行分析.结果:胃癌组和慢性萎缩性胃炎组分别筛选出符合条件的基因53个和21个.胃癌组的特征性表达基因中,STS、HAP1等基因与Borrmann分型等病理改变相关联;慢性萎缩性胃炎组的特征性表达基因中,BRD3、BF508879等基因与肠化等病理改变相关联;慢性萎缩性胃炎和胃癌组中共同存在的SLC26A3等基因与癌前病变相关联.结论:慢性萎缩性胃炎和胃癌组织基因的表达既有相似性,又有异质性.肿瘤基因表达与癌前状态和癌前病变相关.基因表达的相似性提示慢性萎缩性胃炎与胃癌这两者病理发展的相关性和延续性.     

慢性萎缩性胃炎的胃镜与病理诊断的对比分析

目的:对胃镜下慢性萎缩性胃炎的肉眼诊断结果与黏膜活检的病理诊断结果进行对比分析,探讨二者的一致性及临床意义。方法:收集我院内镜诊治中心2013年7月至2016年7月行内镜检查的67 727例患者中,胃镜下诊断慢性萎缩性胃炎的患者2 484例,对比胃镜下肉眼诊断和黏膜活检的病理诊断的一致性。结果:拒绝送病理38例,慢性浅表性胃炎1 196例,慢性萎缩性胃炎1 250例,其中伴有肠上皮化生322例,伴有非典型增生108例,伴有上皮内瘤变218例。胃镜诊断萎缩性胃炎的准确率为50.32%,内镜下表现为黏膜粗糙不平,呈颗粒状或者结节状改变的病理符合率为32.59%。内镜下表现为黏膜粗糙不平,呈颗粒状或者结节状改变,黏膜红白相间,以白为主的病理符合率为23.40%,其符合率之间比较差异无统计学意义（P＞0.05）。内镜下表现为黏膜粗糙不平,呈颗粒状或者结节状改变,黏膜红白相间,以白为主,黏膜的血管暴露并透明可见,皱襞变薄,变平或消失的病理符合率为83.77%。其符合率之间比较差异有统计学意义（P＜0.05）。结论:胃镜下诊断慢性萎缩性胃炎与黏膜活检的病理诊断结果有差异,为提高准确性,应在胃镜检查时根据内镜下慢性萎缩性胃炎表现的特征性,并结合病理取材避免漏诊,达到积极预防,早期发现慢性萎缩性胃炎的目的。