Study on stomach cancer and liver cancer by Helicobacter pylori in feetion and sterigmatocystin or nitrite treatment in mongorian gerbils

本研究研究了幽门螺杆菌、幽门螺杆菌上清液和ST对蒙古沙鼠胃和肝脏的影响。将214只9周龄蒙古沙鼠分为5组(1)对照组，(2)幽门螺杆菌组，(3)幽门螺杆菌上清液组，(4)幽门螺杆菌带ST组（100 ppb）和(5)幽门螺杆菌带ST组（1000 ppb）。幽门螺杆菌浓度为5.6 × 10^<12> CFU/ml。幽门螺杆菌培养上清液（含毒素VacA，下文简称毒素）和ST（浓度分别为100 ppb和1000 ppb）分别给药2年和4个月，分别加入饲料和混合。ELISA法检测血清IgG抗体，RIA法检测血清胃泌素。胃行HE、PAS、阿利新蓝（PH 2.5）染色等组织病理学检查。(1)幽门螺杆菌感染率（表1）各组血清IgG检测幽门螺杆菌感染率如下：幽门螺杆菌伴ST （100 ppb）组，83.3%；与ST （1000 ppb）组比较，占72.2%；幽门螺杆菌组63.3%；毒素组，0%；对照组，0%。幽门螺杆菌和幽门螺杆菌与ST组间差异无统计学意义。(2)血清胃泌素（表2）各组血清胃泌素平均值为：对照组，131.9 pg/ml；毒素组，126.0 pg/ml；幽门螺杆菌组，138.2 pg/ml；幽门螺杆菌与ST (1000 ppb), 179.4 pg/ml；幽门螺杆菌ST (100 ppb) 156.8 pg/ml。ST组幽门螺杆菌的胃泌素值高于其他组。幽门螺杆菌组与幽门螺杆菌伴ST （1000 ppb）组有显著性差异。提示ST对胃泌素排泄有一定影响。(3)病理（肉眼观察）（表1）对照组和毒素组沙鼠胃粘膜未见明显变化。大多数感染幽门螺旋杆菌的沙鼠胃黏膜出现不同程度的扩张和增厚，粘液丰富，糜烂性病变伴出血、溃疡或明显的癌变。各组胃癌发生率分别为：(1)幽门螺杆菌伴ST （100 ppb）组，72.2%；(2)幽门螺杆菌伴ST （1000 ppb）组，63.9%；(3)幽门螺杆菌组，40.9%；(4)毒素组，0%；(5)对照组，0%。幽门螺杆菌给药组胃癌发生率明显高于未给药组。幽门螺杆菌ST组胃癌发病率明显高于幽门螺杆菌组。提示幽门螺杆菌可诱发胃癌，而ST可增强幽门螺杆菌的作用。少

In this study, the effects of H.pylori, H.pylori supernatants and ST on the stomach and liver were investigated in Mongolian gerbils. 9-week-aged 214 Mongolian gerbils were divided into five groups (1)control, (2) H.pylori, (3) H.pylori supernatants (4) H.pylori with ST(100 ppb) and (5) H.pylori with ST(1000 ppb) groups. H.pylori were administered at 5.6x10^<12> CFU/ml. H.pylori culture supernatants (containing toxin VacA, we call it toxin below) and ST (in the concentration of 100 ppb and 1000 ppb each) which were administered for a period of two years and four months to animals, were added to feed and mixed respectively. Serum IgG antibody was determined by ELISA, and serum gastrin was determined by RIA. Stomach was examined by histopathological method including HE, PAS and Alcian blue (PH 2.5) staining.(1) Infection rate of H. pylori (table 1) Infection rate of H.pylori of every group which was determined by serum IgG is as follows : H. pylori with ST (100 ppb) group, 83.3 % ; H.pyl … More ori with ST (1000 ppb) group, 72.2 % ; H.pylori group, 63.3 % ; Toxin group, 0 % ; control group, 0 %. There is no significant difference between H.pylori and H.pylori with ST groups. (2) Serum gastrin (table 2) Average value of serum gastrin in every group is : control group, 131.9 pg/ml ; toxin group, 126.0 pg/ml ; H.pylori group, 138.2 pg/ml ; H.pylori with ST (1000 ppb), 179.4 pg/ml ; H.pylori with ST (100 ppb) 156.8 pg/ml. The gastrin values of H.pylori with ST groups were higher than the other groups. There is a significant difference between H. pylori group and H.pylori with ST (1000 ppb) group. It is suggested that ST has some effects on gastrin excretion. (3) Pathology (Macroscopic findings) (table 1) The gastric mucosa of all gerbils in the control and toxin groups showed no visible changes. The gastric mucosa of most H.pylori infected gerbils appeared expanded and thickened in varying degrees, covered with abundant mucus, erosive lesions with bleeding, ulcer, or showed marked cancers. The gastric cancer incidence of every group was : (1) H.pylori with ST (100 ppb) group, 72.2 % ; (2) H.pylori with ST (1000 ppb) group, 63.9 % ; (3) H.pylori group, 40.9 % ; (4) toxin group, 0 % ; (5) control group, 0 %. The gastric cancer incidence of H.pylori administered groups is significantly higher than that of none administered groups. The gastric cancer incidence of H.pylori with ST groups is significantly higher than that of H.pylori group. These results suggest that H.pylori can induce gastric cancer, and that ST can enhance the effect of H. pylori. Less