我们前期研究表明，Hp感染可诱导ROS生成，促进胃上皮细胞凋亡，同时也可激活Akt信号通路促细胞增殖，ROS和Akt信号通路相互影响，在Hp诱导胃上皮细胞凋亡增殖的调控中起关键作用。新近研究提示激活的ROS/Akt信号可抑制肿瘤生长，表明ROS/Akt信号通路是肿瘤进展的双刃剑。那么在Hp诱导胃上皮间质转化过程中，ROS/Akt信号通路是否有双向调控作用？CD44（CD44V9）分子可以调节胃上皮细胞氧化还原状态，可克服ROS积聚导致的细胞凋亡，因此我们推测其可能是促进ROS/Akt信号通路调控Hp诱导胃胃上皮间质转化的关键因素。本课题结合巨噬细胞微环境的影响，从分子、细胞、动物和临床不同层面研究CD44（CD44V9）分子介导ROS/Akt信号通路调控Hp诱导胃上皮细胞间质转化的作用，以期更好理解Hp致病机制，为阻断Hp感染诱导胃上皮细胞恶性转化提供新思路。

Our previous project funded by the National Natural Science Fund showed that Hp infection could induce the generation of ROS, causing DNA injury, promoting the apotisis of gastric epithelial cells. At the same time, Hp infection could promote cell proliferation via activating Akt pathway. ROS and Akt pathway interacted, playing a key role in the modulation of H.pylori( Hp) induced apotisis and proliferation of gastric epithelial cells. Meanwhile, different from traditional opinions that ROS/Akt pathway has the cancer-promoting activity, recently researchers found that the activation of ROS/Akt pathway could inhibit tumor growth, indicating that ROS/Akt pathway is a double-edged sword for tumor development. Therefore, during the process of Hp inducing epithelial-mesenchymal transition of gastric epithelial cells, what affects the bidirectional regulationof ROS/Akt pathway? With a character as tumor stem cell marker, CD44(CD44V9) could regulate the redox state of gastric epithelial cells and overcome the apotisis caused by ROS. Thereby, we speculate that it could be the key point for promoting ROS/Akt pathway, inducing epithelial-mesenchymal transition of gastric epithelial cells. Combined with the influence of macrophage microenvironment,our project will study CD44(CD44V9) mediating ROS/Akt pathway on regulating epithelial-mesenchymal transition of gastric epithelial cells induced by Hp, for a better understanding of the mechanisms of Hp related diseases and providing a new thought for blocking epithelial-mesenchymal transition of gastric epithelial cells induced by Hp infection.