作者: N. Kalia , C. Jones , K.D. Bardhan , M.W.R. Reed , J.C. Atherton
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摘要: Helicobacter pylori induces a number of disturbances in rodent gastric microcirculation vivo. These events may result from direct necrotic or apoptotic damage to endothelial cells. This study therefore aimed investigate the effects genotypically different H. strains on microvascular cell (MVEC) viability vitro. Four extracts were prepared with cagA vacA status. MVECs plated into 96-well plates and coincubated 50 μl extract vehicle for 24, 48, 72, 96 hr. An MTT assay quantified overall MVEC viability. The dual labeling propidium iodide Hoechst 33342 distinguished between death, respectively, allowed total viable cells be determined. All decreased after 72 Neither necrosis apoptosis was observed. Counting revealed proliferation all when compared controls, again reaching significance at In conclusion, both counting technique demonstrated that induced cytostatic but not cytotoxic MVECs. suggests microcirculatory observed vivo damage. However, inhibition angiogenesis explain why ulcer healing is delayed pylori-infected patients.