Brzozowski Tomasz, Konturek Peter C, Mierzwa Marzena, Drozdowicz Danuta, Bielanski Wladyslaw, Kwiecien Slawomir, Konturek Stanislaw J, Stachura Jerzy, Pawlik Wieslaw W, Hahn Eckhart G
Department of Physiology Jagiellonian University School of Medicine, Cracow, Poland.
Helicobacter. 2006 Feb;11(1):10-20. doi: 10.1111/j.0083-8703.2006.00373.x.
Helicobacter pylori infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis that mimics H. pylori-positive patients developing gastric ulcer and gastric cancer, but the effect of probiotic therapy on functional aspects of this infection remains unknown.
We compared the effects of intragastric inoculation of gerbils with H. pylori strain (cagA+ vacA+, 5 x 10(6) colony forming units/ml) with or without triple therapy including omeprazole, amoxicillin, and tinidazol or probiotic bacteria Lacidofil. Histology of glandular mucosa, the viable H. pylori, and density of H. pylori colonization were evaluated. The gastric blood flow was measured by H2-gas clearance method; the plasma gastrin and gastric luminal somatostatin were determined by RIA and expression of cyclooxygenase (COX)-2 and apoptotic Bax and Bcl-2 proteins were evaluated by Western blot.
The gastric H. pylori infection was detected in all animals by histology and H. pylori culture. Basal gastric acid was significantly reduced in H. pylori-infected animals but not in those with triple therapy or Lacidofil. Early lesions were seen already 4 weeks upon H. pylori inoculation and consisted of chronic gastritis and glandular atypia associated with typical regenerative hyperplasia and increased mitotic activity and formation of apoptotic bodies. The H. pylori infection was accompanied by the fall in gastric blood flow, the marked increase in plasma gastrin, the significant fall in gastric somatostatin levels and Bcl-2 protein expression, and the rise in expression of COX-2 and Bax proteins. These mucosal changes were counteracted by the triple therapy and Lacidofil.
H. pylori infection in gerbils, associated with regenerative hyperplasia of glandular structure, results in the suppression of gastric secretion, overexpression of COX-2, and enhancement in apoptosis and impairment of both, gastric blood flow and gastrin-somatostatin link that were reversed by anti-H. pylori triple therapy and attenuated by probiotics.
蒙古沙鼠幽门螺杆菌感染是一种已确立的胃癌发生实验模型，可模拟幽门螺杆菌阳性患者发生胃溃疡和胃癌的情况，但益生菌疗法对这种感染功能方面的影响尚不清楚。
我们比较了用幽门螺杆菌菌株（cagA+ vacA+，5×10⁶ 菌落形成单位/毫升）对沙鼠进行胃内接种，同时或不同时给予包括奥美拉唑、阿莫西林和替硝唑的三联疗法或益生菌Lacidofil的效果。评估了腺黏膜的组织学、存活的幽门螺杆菌以及幽门螺杆菌定植密度。通过氢气清除法测量胃血流量；通过放射免疫分析法测定血浆胃泌素和胃腔内生长抑素，并通过蛋白质印迹法评估环氧合酶（COX）-2以及凋亡相关蛋白Bax和Bcl-2的表达。
通过组织学和幽门螺杆菌培养在所有动物中均检测到胃幽门螺杆菌感染。幽门螺杆菌感染的动物基础胃酸显著降低，但接受三联疗法或Lacidofil治疗的动物则未出现这种情况。在接种幽门螺杆菌后4周就已出现早期病变，包括慢性胃炎和腺异型增生，伴有典型的再生性增生、有丝分裂活性增加以及凋亡小体形成。幽门螺杆菌感染伴随着胃血流量下降、血浆胃泌素显著升高、胃生长抑素水平和Bcl-2蛋白表达显著下降，以及COX-2和Bax蛋白表达升高。这些黏膜变化被三联疗法和Lacidofil抵消。
沙鼠的幽门螺杆菌感染与腺结构的再生性增生相关，导致胃分泌受抑制、COX-2过表达、凋亡增强以及胃血流量和胃泌素 - 生长抑素联系受损，而抗幽门螺杆菌三联疗法可逆转这些情况，益生菌则可使其减轻。
