瞄准:学习 Helicobacter pylori (H pylori ) 由损坏人的胆囊上皮细胞(HGBEC ) 的机制。方法:从胆囊孤立的 H pylori 在液体媒介是有教养的。不同集中上层清液和 H pylori 房间的声音的 ated 摘录然后在一种主要文化被加到 HGBEC。在象在硷性磷酸酯酶(高山) 的层次的变化一样的 HGBEC 的词法变化, lactate 脱氢酶(LDH ) 和 glutamyltransferase (GGT ) 被测量。结果:根据 HGBEC 的文化曲线,由增加声音的 ated 提取的 H pylori 和 H pylori 文化上层清液在 HGBEC 学习变化是方便的。声音的 ated 提取的 H pylori 和 H pylori 文化上层清液在 HGBEC 形态学上有重要影响,即 HGBEC 更慢慢地成长了,他们的生存能力减少了,他们的分开增加了。而且, HGBEC 破裂了并且死。高山的层次( 33.84 +/- 6.00 对 27.01 +/- 4.67 , P 【 0.05 ), LDH ( 168.37 +/- 20.84 对 55.51 +/- 17.17 , P 【 0.01 )并且 GGT ( 42.01 +/- 6.18 对 25.34 +/- 4.33 , P 【 0.01 )显著地在一个时间依赖者和集中依赖者在 HGBEC 文化上层清液增加了。在 H pylori 文化液体的 HGBEC 的损坏比在 H pylori,声音的 ated 提取是更重要的。结论:H pylori 不导致明显的损坏到 HGBEC。
AIM: To study the mechanism by which Helicobacter pylori (H pylori) damages human gallbladder epithelial cells (HGBEC). METHODS: H pylori isolated from gallbladder were cultured in a liquid medium. Different concentration supernatants and sonicated extracts of H pylori cells were then added to HGBEC in a primary culture. The morphological changes in HGBEC as well as changes in the levels of alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and glutamyltransferase (GGT) were measured. RESULTS: According to the culture curve of HGBEC, it was convenient to study the changes in HGBEC by adding H pylori sonicated extracts and H pylori culture supernatants. Both H pylori sonicated extracts and Hpylori culture supernatants had a significant influence on HGBEC morphology, i.e. HGBEC grew more slowly, their viability decreased and their detachment increased. Furthermore, HGBEC ruptured and died. The levels of ALP (33.84 ± 6.00 vs 27.01 ± 4.67, P 〈 0.05), LDH (168.37 ± 20.84 vs 55.51 ± 17.17, P 〈 0.01) and GGT (42.01 ± 6.18 vs 25.34 ±4.33, P 〈 0.01) significantly increased in the HGBEC culture supernatant in a time- and concentrationdependent. The damage to HGBEC in H pylori culture liquid was more significant than that in Hpylori sonicated extracts. CONCLUSION: H pylori induces no obvious damage to HGBEC.