The analysis of physical stimulation to proliferative gastric cells.

胃粘膜细胞在体外的创伤修复(即培养细胞填充人工构建的无细胞区域的能力)需要激活细胞迁移和增殖。但在这个模型中，细胞迁移的作用比增殖作用重要得多，因为超过四分之三的伤口修复发生在BrdU阳性细胞检测之前。大多数过程，特别是修复的初始阶段，仅由细胞迁移完成，只有后期可能包括细胞增殖。可能调节愈合过程的因素已经被研究。在一系列实验中，我们考察了各种可用的生长因子的影响。肝细胞生长因子等生长因子诱导单层胃上皮细胞片损伤修复。在本项目中，我们利用上述创面修复模型评估了温度、自由基和幽门螺杆菌水提物对修复过程的影响。胆汁酸、乙醇和幽门螺杆菌提取物等自由基诱导剂通过诱导细胞凋亡，延缓了细胞的增殖和迁移等修复过程。尤其是幽门螺杆菌水提物中的毒素不同于VacA基因产物和cagA基因产物。必须做进一步的研究来鉴定这种新毒素的性质。

The wound repair of gastric mucosal cells in vitro (i.e.the ability of cultured cells to fill the artificially made cell-free area) requires activation of both cell migration and proliferation.However, in this model, the role of cell migration is much more important than that of proliferation because more than three-fourths of wound repair occurred before detection of BrdU-positive cells. Most of the process, especially the initial stage of repair, is completed by only cell migration, and only the late stage might include cell proliferation. Factors which might modulate the healing process have been investigated. In a series of experiments, we examined the effects of a variety of available growth factors. Addition of growth factors such as hepatocyte growth factor induced wound repair in the monolayr gastric epithelial cell sheet. In this project, we assessed the effects of temperature, free radicals and Helicobacter pylori water extract on the process of restoration using above wound repair model. Free radical inducer such as bile acids, ethanol and H.pylori extract retarded the restoration process including cell proliferation and migration with the induction of apoptosis. Especially, toxin in H.pylori water extract used in this experiment is different from vacA gene products and cagA gene products. Further study must be done to identify the character of this new toxin.