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1.
通过研究饮茶对香烟中特异性亚硝胺-NNK诱发小鼠肺癌基因表达的影响,对饮茶可拮抗香烟致癌作用的结果做进一步验证,并对其作用机理进行探讨。所使用方法为国内外尚属新的技术,即非同位素标记探针测定基因表达。其结果表明阳性小鼠给NNK4周后,c-myc和c-raf基因表达水平明显增高,而小鼠若同时饮绿茶则可抑制这种增高,抑制率达50%和20%,到第8周时阳性对照组的c-myc和c-raf基因水平恢复正常。与此相对应,c-H-ras基因在第8周时表达增高,约为阴性组3倍,饮茶对此同样有抑制作用,抑制率为50%。在第2、4和8周均未见阳性对照组vsis基因表达水平的改变。 相似文献
2.
茶对促癌物(TPA)诱发小鼠皮肤癌基因表达的影响 总被引:7,自引:0,他引:7
通过研究在小鼠皮肤上涂抹儿茶素EGCG对促癌物(TPA)诱发小鼠皮肤组织某些癌症发生有重要关系的基因(c-myc,ODC、蛋白激酶C即PKC基因)表达水平的影响,对茶叶抗皮肤癌的机制做了较深入的探讨。其结果表明阳性小鼠皮肤涂10nmolTPA4h后,上皮组织中ODC基因表达水平比阴性组高出4.5倍,而EGCG对其有明显的抑制作用,1μmol和5μmolEGCG剂量组的抑制率分别为16%和56%,有一定的剂量-反应关系。C-myc与pKC基因表达水平在阳性组也有明显的升高,分别为5.0和1.9倍,EGCG同样具有抑制作用,5μmol的抑制率分别为24%和21%。 相似文献
3.
接触苯工人白细胞癌基因激活的研究 总被引:5,自引:1,他引:4
应用PCR-Blot和Dot-Blot技术检测了103名接触苯工人和70名对照组工人外周血白细胞c-Ki-ras2基因和c-myc基因。结果表明,103名接苯者中有4例其外周血白细胞检出c-Ki-ras2基因12位点G→T突变,其接苯工龄在6~10年,而70名对照者未检出该突变;c-Ki-ras2基因12位点(G→A突变在两组工人中均未检出阳性;c-myc基因亦未在两组工人中检出扩增现象。结果提示,c-Ki-ras2基因12位点G→T突变与慢性接触苯有关,有可能是苯白血病发生的分子机理。 相似文献
4.
本文对由致癌物苯并芘诱发的人肺癌建立的细胞系(BT)进行了染色体分析及myc,Rb和p53基因研究。发现许多异常染色体,以3号,5号,11号,13号,17号染色体改变较多,对定位于这些染色体上的Ha-ras,raf-1,p53,Rb和c-myc的表达、扩增及重排情况进行了分析,发现c-myc,p53,Rb三个基因发生了改变,说明染色体异常导致的基因改变与苯并芘诱发人肺癌的发生机制可能密切相关。 相似文献
5.
用免疫组化LSAB方法检测5例正常卵巢组织和35例卵巢肿瘤组织中的C-myc(原癌基因)和p53(抑癌基因)蛋白的表达水平。结果从良性卵巢腺瘤、交界性到恶性卵巢囊腺癌,C-myc和p53阳性表达呈增高趋势。其阳性表达率与卵巢肿瘤的细胞增殖状态、肿瘤分化及临床分期有关。检测卵巢肿瘤中C-myc及p53基因表达可了解卵巢囊腺癌的发生、发展,找出原癌基因及抑癌基因表达与卵巢瘤生物学行为间的关系。 相似文献
6.
本文观察了非选择性阳离子通道阻断剂链霉素(在脊椎动物心肌阻断牵张激活的钠离子跨膜内流)对缺氧大鼠右心室肥大和缺氧大鼠心肌中c─myc基因表达的影响。结果如下:(1)急性缺氧时,右心室收缩压明显增高,慢性间断性缺氧进一步增高右心室收缩压并明显增高右心室重量指数。(2)链霉素对急性缺氧性肺动脉增压反应无影响,但可明显降低慢性缺氧大鼠右心室收缩压和右心室重量指数。(3)缺氧引起右室心肌迅速一过性的c-myc基因表达增强,链霉素可降低c-myc表达水平。提示Na内流和C-myc表达可能参与了缺氧性右心室肥大的发生。 相似文献
7.
镉对小鼠肢芽细胞增殖细胞核抗原和c—myc基因表达的影响 总被引:2,自引:0,他引:2
目的探讨镉对胚胎肢芽细胞增殖抑制的机制。方法运用免疫组化SP法结合图像分析技术观察了CdCl2对增殖细胞核抗原(PCNA)和c-myc基因表达的影响。结果PCNA和c-myc基因在正常增殖的胚胎肢芽细胞中均呈强阳性免疫反应;0.1~0.8μg/mlCdCl2对细胞中PCNA和c-myc的表达均有明显的抑制作用,并呈现明显的剂量-效应关系。结论CdCl2可通过抑制PCNA和c-myc的表达而对胚胎细胞增殖产生抑制作用。 相似文献
8.
甲基叔丁基醚对原癌基因和功能基因表达的影响 总被引:3,自引:0,他引:3
甲基叔丁基醚(MTBE)是一种新型的汽油添加剂,被用来提高汽油燃烧效率,减少汽车尾气中有害物质的排放。MTBE具有一定的动物致癌性,但其机制目前并不清楚。本研究采用免疫组织化学方法,检测了MTBE对体外培养的NIH3T3细胞中c-myc和p21蛋白表达的影响;采用点杂交方法,从RNA水平检测了MTBE亚慢性染毒大鼠肝组织中原癌基因c-myc基因和功能基因GST-P基因的表达情况。免疫组化结果显示,MTBE可诱导c-myc基因的高表达,对p21蛋白的表达未见明显影响。点杂交结果显示,MTBE可明显诱导大鼠肝组织中c-myc基因的高表达,而对GST-P基因的表达未见明显影响。上述结果提示,MTBE可诱导细胞中c-myc基因表达活性增高,可能是其动物致癌性的机制之一。 相似文献
9.
茶对小鼠免疫功能的保护作用 总被引:9,自引:0,他引:9
目的探讨茶叶防癌的免疫调节机理。方法用致癌剂4甲基亚硝胺1(3吡啶)1丁酮(NNK)诱发小鼠肿瘤的实验模型,观察NNK所致小鼠免疫功能的改变及绿茶(GT)、复合茶(MT)和茶多酚(TP)的保护作用。结果小鼠注射NNK后,在观察的4周内,腹腔巨噬细胞吞噬功能、外周血白细胞化学发光、迟发型变态反应、脾细胞抗体生成细胞数、以及脾NK活性等免疫指标,与正常对照组比较均出现不同程度的增高或降低;而GT、MT和TP对所有这些免疫功能的不良改变有明显的保护作用。结论茶及其成分对NNK诱发小鼠肿瘤过程中早期所致免疫功能的改变具有保护作用 相似文献
10.
目的甲基叔丁基醚(MTBE)是一种新型的汽油添加剂,动物试验显示其具有一定的致癌性。为了解其动物致癌性的可能机制,我们检测了经MTBE亚慢性染毒的大鼠肝组织中原癌基因cmyc基因和功能基因谷胱甘肽S转移酶P(GSTP)基因的表达情况。方法40只雄性SD大鼠,体重180~200g,随机分为4组。将MTBE溶于适量豆油中,灌胃染毒,染毒剂量分别为200mg/kg,600mg/kg,1000mg/kg和对照组。每天1次,每周5天,共13周。动物肝组织于液氮速冻后,一步法提取总RNA。随机引物法地高辛标记cmyc和GSTP探针,与RNA进行点杂交,图像分析仪分析结果。结果大鼠肝组织中cmyc基因表达水平明显增高,GSTP基因表达未见增强。结论MTBE可明显诱导cmyc基因的高表达,提示其具有促进细胞增殖的作用,这是其动物致癌性的可能机制之一。 相似文献
11.
Green tea and its major components ameliorate immune dysfunction in mice bearing Lewis lung carcinoma and treated with the carcinogen NNK 总被引:2,自引:0,他引:2
The protective effects of tea and/or its components on dysfunction of immune functions during tumor growth and carcinogenesis in mice were studied using two experimental models: C57/BL6J mice transplanted with Lewis lung carcinoma (LLC) and Kunming mice treated with a single dose of 4-(methylnitrosamino-)-1-(3-pyridyl)-1-butanone (NNK). In C57/BL6J mice bearing LLC, the weight of the thymus decreased, the proportion of CD4(+)-positive T lymphocytes and the ratio of CD4+ to CD8+ decreased, luminol-enhanced chemiluminescence of white blood cells in peripheral blood stimulated by zymosan increased, and plaque-forming cells (PFC) decreased. However, in LLC-bearing mice given green tea as drinking water, all immune functions were improved, along with inhibition of tumor growth. In Kunming mice treated with NNK, during the four weeks of observation, their immunologic indicators, such as phagocytosis of macrophages in the abdominal cavity, luminol-enhanced chemiluminescence of white blood cells, plaque-forming cells, and delayed-type hypersensitivity, increased or decreased to various extents compared with normal controls. However, these changes were significantly prevented in the mice given green tea, mixed tea, or tea polyphenol as drinking water. In conclusion, tea and its components ameliorated immune dysfunction in mice bearing LLC or treated with the carcinogen NNK. 相似文献
12.
13.
Inhibition of lung carcinogenesis and effects on angiogenesis and apoptosis in A/J mice by oral administration of green tea 总被引:7,自引:0,他引:7
Oral administration of tea (Camellia sinensis) has been shown to inhibit the formation and growth of several tumor types in animal models. The present study investigated the effects of treatment with different concentrations of green tea on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in female A/J mice. Two days after a single dose of NNK (100 mg/kg body weight, i.p.), the mice were given 0.1, 0.2, 0.4, and 0.6% green tea solution (1, 2, 4, and 6 g of tea solids, respectively, dissolved in 1 l of water), 0.02% caffeine, or water as the sole source of drinking fluid until the termination of the experiment. Only the treatment with 0.6% tea preparation significantly reduced lung tumor multiplicity (mean +/- SE, 6.07 +/- 0.77 vs. 8.60 +/- 0.50 tumors per mouse, P = 0.018). Treatment with 0.6% tea also inhibited angiogenesis, as indicated by the lower microvessel density (number of blood vessels/mm2) based on immunostaining for the von Willebrand factor antigen (81.9 +/- 9.5 vs. 129.4 +/- 8.2, P = 0.0018) and anti-CD31 antibody staining (465.3 +/- 61.4 vs. 657.1 +/- 43.6, P = 0.0012). Significantly lower vascular endothelial growth factor immunostaining scores were also observed in the 0.6% tea-treated group (0.98 +/- 0.17 vs. 1.43 +/- 0.07, P = 0.006). The apoptosis index was significantly higher in lung adenomas from 0.6% tea-treated mice based on morphological analysis of cell apoptosis (2.51 +/- 0.18% vs. 1.57 +/- 0.11%, P = 0.00005), and the result was further confirmed using the TUNEL method. Inhibition of angiogenesis and the induction of apoptosis by green tea may be closely related to the inhibition of pulmonary carcinogenesis. 相似文献
14.
Treatment of SKH-1 mice with ultraviolet B light (UV-B, 30 mJ/cm2) twice a week for 22-23 weeks resulted in tumor-free animals with a high risk of developing malignant and nonmalignant tumors during the next several months in the absence of further UV-B treatment (high-risk mice). In three separate experiments, oral administration of green tea or black tea (4-6 mg tea solids/ml) as the sole source of drinking fluid for 18-23 weeks to these high-risk mice inhibited the formation and decreased the size of nonmalignant squamous cell papillomas and keratoacanthomas as well as the formation and size of malignant squamous cell carcinomas. In one experiment all these inhibitory effects of tea were statistically significant, whereas in the two other experiments many but not all of the inhibitory effects of tea were statistically significant. The decaffeinated teas were inactive or less effective inhibitors of tumor formation than the regular teas, and adding caffeine back to the decaffeinated teas restored biological activity. Oral administration of caffeine alone (0.44 mg/ml) as the sole source of drinking fluid for 18-23 weeks inhibited the formation of nonmalignant and malignant tumors, and this treatment also decreased tumor size in these high-risk mice. 相似文献
15.
目的 探讨ERK信号转导通路在CdCl2诱导HEK293细胞低剂量兴奋效应过程中的作用.方法 以0、0.0005、0.005、0.05、0.5、5、50和500μmol/L浓度的氯化镉(CdCl2)分别染毒HEK293细胞12h和24h;在染毒前分别用ERK1/2抑制剂PD98059(100μmol/L)、U0126(... 相似文献
16.
Tea catechins prevent the development of atherosclerosis in apoprotein E-deficient mice 总被引:14,自引:0,他引:14
Miura Y Chiba T Tomita I Koizumi H Miura S Umegaki K Hara Y Ikeda M Tomita T 《The Journal of nutrition》2001,131(1):27-32
Green tea contains various antioxidative flavan-3ols (tea catechins), such as (-)-epigallocatechin gallate (EGCg, the major catechin), which exert potent inhibitory effects on LDL oxidation in vitro and ex vivo in humans. In this study, the antiatherogenic effects of tea catechins were examined in atherosclerosis-susceptible C57BL/6J, apoprotein (apo)E-deficient mice. Male apoE-deficient mice (10 wk old) were fed an atherogenic diet for 14 wk; during that time, one group (tea) was supplied drinking water supplemented with green tea extract (0.8 g/L), and another group (control) was offered the vehicle only. The tea extract consisted of the following (g/100 g): EGCg, 58.4; (-)-epigallocatechin (EGC), 11.7; (-)-epicatechin (EC), 6.6; (-)-gallocatechingallate (GCg), 1.6; (-)-epicatechin gallate (ECg), 0.5; and caffeine, 0.4. The estimated actual intake of tea catechin was 1.7 mg/(d. mouse). Tea ingestion did not influence plasma cholesterol or triglyceride concentrations. Plasma lipid peroxides were reduced in the tea group at wk 8, suggesting that the in vivo oxidative state is improved by tea ingestion. Atheromatous areas in the aorta from the arch to the femoral bifurcation and aortic weights were both significantly attenuated by 23% in the tea group compared with the control group. Aortic cholesterol and triglyceride contents were 27 and 50% lower, respectively, in the tea group than in the control group. These results suggest that chronic ingestion of tea extract prevents the development of atherosclerosis without changing the plasma lipid level in apoE-deficient mice, probably through the potent antioxidative activity of the tea. 相似文献
17.
茶对二甲基苯并蒽诱发金黄色地鼠口腔癌预防作用的研究 总被引:1,自引:0,他引:1
选用二甲基苯并蒽( D M B A)诱发的金黄色地鼠口腔癌模型,研究绿茶、茶色素和混合茶对口腔癌的预防作用,并探讨其防癌机制。试验设阳性对照组(局部涂05% D M B A,每周3次,共15周)、3个饮茶试验组(在涂 D M B A2周前开始分别饮15% 绿茶、01% 茶色素和05% 混合茶至15周实验结束)和阴性对照组(仅涂丙酮)。结果表明,与阳性对照组相比,绿茶、茶色素和混合茶组对平均瘤数目的抑制率分别为426% 、508% 和672% ,平均瘤负荷抑制率分别为794% 、885% 和955% ;在3组中以混合茶对口腔癌的抑制效果最强。在涂 D M B A 后的第6、10和15周,3个茶试验组中均见到口腔上皮细胞微核形成,每核银染核仁组织区( Ag N O R)颗粒数目和表皮生长因子受体( E G F R)的表达低于阳性对照组。表明饮茶对 D M B A 诱发的动物口腔癌有明显的预防作用,而茶预防 D M B A 引起的粘膜细胞 D N A 损伤和抑制粘膜细胞增殖可能是其预防口腔癌的重要作用机制。 相似文献
18.
Lack of effects of selenium on N-nitrosomethylbenzylamine-induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice. 总被引:1,自引:0,他引:1
The effects of dietary selenium deficiency and excess on N-nitrosomethylbenzylamine-(NMBA) induced esophageal neoplasia in rats and forestomach tumors in mice and the effects of dietary selenium on DNA adduct formation and on the activities of DNA adduct-repairing enzyme and oncogene expression in rat esophagus were investigated. The esophageal and forestomach tumors were induced by administration of NMBA by gavage with a total dose of 39 mg/kg body wt in rats and 12 mg/kg body wt in mice. Neither selenium dietary deficiency (Se < 0.02 ppm) nor selenium excess (2.0 ppm) showed any significant effect on the incidence of tumors or number of tumors per tumor-bearing animal. For the DNA adduct formation studies, rats were given a dose of NMBA intraperitoneally after six weeks on the different selenium-containing diets. No significant difference in the amount of the DNA adduct O6-methyldeoxyguanosine was found among the different selenium-treated groups. In a parallel group of rats that did not receive NMBA, the levels of esophageal O6-methyldeoxyguanosine DNA methyltransferase were not significantly altered by dietary selenium levels. The c-myc oncogene expression in rat esophagus was induced by the administration of NMBA (3 mg/kg body wt) by gavage once a week for eight weeks. Dietary selenium did not show any effects on its expression. On the basis of the results of these studies, dietary selenium has no effects in the NMBA-induced tumor model. 相似文献