羧乙基锗倍半氧化物对实验诱发小鼠前胃癌变率的影响

用羧乙基锗倍半氧化物（Ｇｅ—１３２）处理ＮＳＥＥ诱发的小鼠前胃鳞状上皮增生、癌变，结果发现实验组的癌变率显著低于对照组（Ｐ＜０．０５），抑癌率为４２．９％，实验组核仁组成区相关嗜银蛋白（Ａｇ—ＮＯＲ）数目及不规则型颗粒的比例显著低子对照组（Ｐ＜０．０５），而实验组之癌周淋巴细胞浸润反应程度较对照组显著增强（Ｐ＜０，０５）。以上结果表明Ｇｅ—１３２可显著降低ＮＳＥＥ诱发小鼠前胃癌的癌变率，并可影响Ａｇ—ＮＯＲ在小鼠前胃鳞状上皮细胞中的表达，Ｇｅ—１３２的以上作用可能与其提高小鼠局部细胞免疫力有关。     

乌龙茶对小鼠前胃鳞状上皮癌变的影响

 本文阐述了小鼠前胃癌前，癌变实验治疗的结果。乌龙茶出产于食管癌高发区的汕头，它对由亚硝肌氨酸乙基乙酯(NSEE)诱发的小鼠前胃癌形成有抑制作用。给小鼠饮用乌龙茶后，其癌发生率从64.8%下降到25.0%。乌龙茶对小鼠无毒性副作用。     

热损伤对亚硝基肌氨酸乙酯诱发小鼠前胃癌变过程的影响

以６５℃热水灌喂ＮＩＨ小鼠１３周后，７８．５％的小鼠前胃粘膜鳞状上皮发生乳头状增生，固有膜血管充血和炎性细胞浸润等炎性粘膜改变。灌喂热水加亚硝基肌氨酸乙酯组，８５．７１％的小鼠前胃上皮发生癌变，明显高于对照组癌变率５３．５７％（Ｐ＜０．０１）。结果表明，热损伤可引起小鼠前胃粘膜炎症性改变，而炎症造成的粘膜损伤又增加了粘膜上皮对致癌物的敏感性。慢性热损伤可能是促癌因素之一。     

地塞米松不同剂量对小鼠前胃鳞状上皮癌变的研究

本文通过不同剂量地塞米松对小鼠前胃鳞状上皮癌变影响的实验研究,观察了大小剂量的作用效果。灌喂大剂量地塞米松(12mg/kg)经两次重复动物实验,70天和120天的抑制癌变率均在77.78％和46.15％左右,同时也促使癌组织向成熟方向分化。灌喂小剂量地塞米松(1mg/kg),70天和120天时诱发癌变率分别在43.75％和33.33％左右。并讨论了地塞米松抑制小鼠前胃鳞状上皮增生、癌变的机理。     

芦笋对小鼠前胃癌变和3T3细胞生长的影响

本实验分为体内体外两部分。体内实验证明芦笋对由肌氨酸乙酯亚硝胺诱发的小鼠前胃鳞状上皮癌变具有明显的抑制作用,对照组癌变率为63.0％,芦笋组为26.8％,两组癌变率与胃重比较在统计学上均有显著差异(P<0.01);形态学观察显示,芦笋不但可以降低癌变率而且可以阻止癌细胞的浸润。体外,芦笋对3T3细胞的生长曲线与分裂指数均有一定的抑制作用,细胞增殖缓慢,但无明显毒性。本文还讨论了芦笋抑制癌变的可能机理。     

6种中草药对小鼠前胃癌变的阻断作用与其硒含量关系的研究

目的研究抗癌中草药对癌变的阻断作用及与硒含量的关系。方法采用肌氨酸乙酯盐酸盐（ＮＳＥＥ）诱发的小鼠前胃鳞状上皮癌变模型，观察白花蛇舌草、冬菱草、斑蝥、山豆根、冬虫夏草、乌骨藤等６种中草药对小鼠前胃癌变的阻断作用，同时测定其硒的含量。结果和结论（１）６种中草药对小鼠前胃癌变均有不同程度的阻断作用；（２）６种中草药的癌变抑制率与其硒含量呈直线相关关系。     

两种不同剂量Ge—132对二甲肼诱发大鼠大肠癌的作用

在以二甲肼(DMH)诱发大鼠大肠癌的同时,给大鼠灌胃Ge-132 100mg/kg体重或300mg/kg体重共27周。Ge-132 100mg/kg体重组大鼠的平均癌灶数和平均癌灶体积,均显著少于对组照和Ge-132 300mg/kg体重组(P均<0.01)。Ge-132 300mg/kg体重组与对照组差异无显著意义(P>0.05)。肠镜检查显示,Ge-132 100mg/kg体重组致癌物所致结肠粘膜的炎症、萎缩和不典型增生明显轻于对照组(P<0.05),癌肿发生的潜伏期比对照组长3周。Ge-132 300mg/kg体重组与对组照差异无显著意义(P>0.05)。结果表明,Ge-132对化学诱癌的预防作用具有剂量依赖性。     

复合核黄素抗亚硝胺致癌作用的动物实验研究

本文应用ＮＳＥＥ诱发ＮＩＨ小鼠前胃鳞癌的动物模型，观察了复合核黄素和纯核黄素对小鼠前胃鳞状上皮癌变的影响。结果表明，复合核黄素对ＮＳＥＥ诱发小鼠前胃鳞癌有明显抑制作用，其抑制率为５４．８４％（Ｐ＜０．０５）。而纯核黄素未发现明显的阻断癌变的作用。提示，其有效成分可能不是核黄素，而是核黄素以外的其它成分或是核黄素与其它成分的协同作用。本研究为食管癌的预防研究提供了实验依据。     

六种中草药阻断食管上皮癌变的实验研究

为研究中草药对食管上皮癌变的阻断作用，我们选用了冬凌草、冬虫夏草、山豆根、乌骨膝、白花蛇舌草、斑蠢等6种文献报道具有抗癌作用的中草药，对380只小鼠前胃鳞状上皮癌变进行了阻断实验研究。现报告如下材料与方法8周龄雌性昆明小鼠380只，体重18－22g。共分对照组80只，其余300只按中草药名称分组，每组50只。参照蔡海英方法（中华医学杂志，1980，60（2）：87）进行诱癌。即用亚硝酸钠0．3g／kg体重和肌氨酸乙酯盐酸盐（NSEE）2g/kg体重，两者分别用0．lIIx）lxL的HCI配成3％和20％的水溶液，灌喂前等量混合，每周灌OW给药2次，…     

复合核黄素抗亚硝胺致癌作用的动物实验研究

本文应用ＮＳＥＥ诱发ＮＩＨ小鼠前胃鳞癌的动物模型，观察了复合核黄素和纯核黄素对小鼠前胃鳞状上皮癌变的影响。结果表明，复合核黄素对ＮＳＥＥ诱发小鼠前胃鳞癌有明显抑制作用，其抑制率为５４．８４％（Ｐ〈０．０５）。而纯核黄素未发现明显的阻断癌变的作用。提示，其有效成分可能不是核黄素，而是核黄素以外的其它成分或是核黄素与其他成分的协同作用。本研究为食管癌的预防研究提供了实验依据。     

羧乙基锗倍半氧化物对实验诱发小鼠前胃癌变过程中的免疫作用

Ｎ—亚硝基肌氨酸乙酯（ＮＳＥＥ）诱发昆明小鼠前胃癌变，再以羧乙基锗倍半氧化物（Ｇｅ－１３２）治疗结果发现实验组中癌细胞的浸润深度显著浅于对照组（Ｐ＜０．０５）；实验组核仁组成区相关嗜银蛋白（ＡｇＮＯＲ）计数及细小、不规则颗粒所占比例均低于对照组（Ｐ＜０．０５）；实验组癌周淋巴细胞浸润反应则较对照组显著（Ｐ＜０．０５）。提示Ｇｅ－１３２对ＮＳＥＥ诱发的小鼠前胃癌有一定的治疗作用；并从免疫形态学证实介导宿主免疫反应可能是Ｇｅ－１３２发挥抗癌作用的机制之一。本研究为Ｇｅ－１３２用于临床提供理论依据。     

羧乙基锗倍半氧化物抗移植瘤实验

将移植了ＨｅｐＡ鼠肝癌的ＮＩＨ鼠随机分为四组，一组作对照组，另三组分别给予Ｇｅ－１３２、ＣＹ、Ｇｅ－１３２＋ＣＹ治疗。２周后处死，测定血清中ＳＯＤ活性，对瘤体进行病理切片检查。结果表明：治疗组肿瘤重量较轻，ＳＯＤ活性较高（Ｐ＜０．０５）。Ｇｅ－１３２组的癌组织中白细胞浸润程度较高，细胞免疫力较强。对鼠肝癌的抑制率，Ｇｅ－１３２与ＣＹ合用有相加作用。     

双β-羧乙基锗倍半氧化物对小鼠和裸鼠移植性肿瘤生长的影响

我们研究了双β-羧乙基锗倍半氧化物(Ge—132)的抗瘤作用,结果表明对小鼠Harding—Passey黑色素瘤(M—HP)、艾氏腹水癌实体瘤(ESC)和裸鼠移植人肺鳞癌的生长有明显的抑制作用,并发现Ge—132与DDP合并应用对抗裸鼠移植人肺鳞癌有协同作用。     

Experimental Studies of the Therapeutic Effect of Gypsophila Oldhamiana Gypsogenin on Lewis Lung Cancer in Mice

OBJECTIVE To observe the inhibitory effect of Gypsophila oldhamiana gypsogenin (GOG) on Lewis lung cancer growth,and to investigate the mechanism of its anti-tumor effect. METHODS A mouse model bearing Lewis lung cancer was used.The 5 experimental groups were divided into a positive control (cis-diaminedichloroplatinum),a negative control,and high,medium and low-GOG dosage groups.The inhibitory action of GOG administration on the lung cancer was observed.After GOG treatment,the lungs were taken out and a lung coefficient computed.The expressions of VEGF,Bcl-2,Bax and P53 in the cancers were determined using immunohistochemical staining. RESULTS The tumor weight of the mice given various doses of GOG was significantly lower compared to the negative-control group (P<0.01),and the lung coefficient of the groups given high and low GOG doses was significantly lower compared to the negative-control group (P<0.01).Immunohistochemical results were shown as follows:i) The VEGF and Bcl-2 expressions in the GOG groups were significantly lower than that of the negative-control group (P<0.05);ii) Bax expression in the groups treated with high and medium GOG doses was significantly higher compared to the negative-control group (P<0.05);iii) The mutant P53 expression in the GOG-treated groups was significantly lower compared to the negative-control group (P<0.05).CONCLUSION GOG can inhibit the growth and metastasis of Lewis lung cancer,and may exert its mechanism of tumor control by inhibition of tumor angiogenesis and induction of apoptosis.     

三种有机锗（G－132，Ge－162，Ge－164）对小鼠骨髓嗜多染红细胞微核率的影响

本文以三种有机锗（Ｇｅ－１３２，Ｇｅ－１６２．Ｇｅ－１６４）对小鼠进行灌胃处理，以测定对环磷酰胺（ＣＰ）诱发的骨髓嗜多染红细胞微核率的抑制作用，结果表明，三种有机锗均能降低微核率，与阳性对照组比较有显著性差异（Ｐ＜０．０５）．而三种有机锗之间抑制微核率的效能无差异（Ｐ＜０．０５）。提示，三种有机锗均可拮抗ＣＰ的致突变作用。     

Systemic two-stage carcinogenesis in the epithelium of the forestomach of mice using 7,12-dimethylbenz(a)anthracene as initiator and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate as promoter.

In a modified two-stage carcinogenesis experiment, the effectiveness of the initiator 7,12-dimethylbenz(a)anthracene (DMBA) and the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) in the epithelium of the forestomach of the mouse has been investigated. Fifty mice were treated intragastrically with a single dose of DMBA (50 mg/kg body weight), followed by repeated intragastric administration of TPA (10 mg/kg body weight) over a period of 35 weeks. In comparison with the corresponding control groups (no treatment, DMBA initiation only, and TPA treatment only), the initiated and promoted group clearly showed the highest tumor incidence in the target organ (45 tumor-bearing animals of 50 animals). No tumors of the forestomach were found in the untreated control group and the TPA-treated group, whereas in the DMBA-initiated group, ten animals had developed tumors of the forestomach. In addition to the mouse skin model for two-stage carcinogenesis, the mouse forestomach appears to respond to DMBA initiation-TPA promotion. This organ provides an additional tissue with which to investigate tumor promotion and further to ascertain specific parameters of the promotion step.     

有机锗(Ge-132)对大鼠肝细胞色素P_(450)、EROD活性抑制作用的研究

利用雄性ＳＤ大鼠每日经口给予有机锗（Ｇｅ－１３２）１００、２５０、５００ｍｇ／ｋｇ连续二十五ｄ，发现高剂量组的肝细胞色素Ｐ４５０受到明显抑制（Ｐ＜０．０５）。对Ｐ４４８的标志酶乙氧基异吩口恶唑脱乙氧基酶（ＥＲＯＤ）的抑制也近５０％；动物以Ｇｅ－１３２５００ｍｇ／ｋｇ／ｄ预先处理２０ｄ，再分别给予苯巴比妥钠盐（ＰＢ）、３－甲基胆蒽（３－ＭＣ），发现Ｇｅ－１３２对ＰＢ诱导Ｐ４５０的抑制不明显，而对３－ＭＣ诱导ＥＲＯＤ的抑制仍达３３％。     

Suppression of tumor growth by peritoneal macrophages isolated from mice treated with carboxyethylgermanium sesquioxide (Ge-132)

In a murine model it has been shown that the antitumor activity of carboxyethylgermanium sesquioxide (Ge-132) can be depleted by administration of macrophage (M phi) blockers. In the present study, the role that M phi play in the antitumor activity of the compound was investigated. Oral administration of Ge-132 in mice was demonstrated to be effective in activating M phi (Ge-132-cytotoxic M phi), and the cytotoxic activity of these M phi appeared in the peritoneal cavity of mice 48 hours after the oral administration of the compound. Co-cultivation of RL male-1 leukemia or Ehrlich carcinoma cells with Ge-132-cytotoxic M phi in vitro resulted in marked suppression of the growth of tumor cells. The transfer of peritoneal exudate cells (PEC), or purified M phi fractions of PEC from Ge-132-treated mice to mice bearing Ehrlich or RL male-1 ascites tumors resulted in significant protection. However, when the cytotoxic M phi were depleted by carbonyl-iron treatment in vitro, no antitumor effect was demonstrated in mice bearing Ehrlich or RL male-1 ascites tumors. Macrophage fractions obtained from PEC of Ge-132-treated mice exhibited an inhibitory effect against certain tumors both in vivo and in vitro suggesting that the antitumor effect of Ge-132 observed in vivo resulted from the activation of M phi.     

黄腐酚类似物通过cAMP/Wnt/β-catenin信号通路抑制卵巢癌细胞增殖降低对顺铂的耐药性

目的:探究黄腐酚（xanthohumol,XN）类似物通过cAMP/Wnt/β-catenin信号通路调控卵巢癌细胞增殖的作用及对顺铂耐药性的影响。方法:以人卵巢癌细胞株HO-8910为研究材料,分为不同浓度(0、5、7.5、15、20 μmol/L)黄腐酚类似物组、对照组、顺铂组、黄腐酚类似物+顺铂组。采用四甲基偶氮唑蓝（methyl thiazolyl tetrazolium,MTT）法、实时荧光定量酶链式反应（quantitative real-time polymerase chain reaction,qRT-PCR）、蛋白免疫印迹法（Western blot,WB）检测黄腐酚类似物对HO-8910细胞增殖及对顺铂耐药性的影响。结果:与对照组比,黄腐酚类似物能够明显抑制HO-8910细胞增殖,差异具有统计学意义（P<0.05）;黄腐酚类似物a13+顺铂组HO-8910细胞对顺铂的半数抑制浓度（half maximal inhibitory concentration,IC50）显著低于顺铂组,细胞活性抑制率（inhibition rate,IR）显著高于顺铂组,差异具有统计学意义（P<0.05）;PKIβ（cAMP抑制剂）、IWP-2（Wnt/β-catenin抑制剂）可降低黄腐酚类似物a13对HO-8910细胞增殖的抑制作用,逆转黄腐酚类似物a13抑制HO-8910细胞对顺铂的耐药作用,差异具有统计学意义（P<0.05）。结论:黄腐酚类似物可提高顺铂对卵巢癌细胞增殖的抑制作用,降低细胞对顺铂的耐药性,作用机制与激活cAMP/Wnt/β-catenin信号通路有关。