幽门螺杆菌（Hp）与慢性胃炎的发病有着密切的联系。改善Hp致胃黏膜炎性损伤是治疗这类疾病的主要途径，因而成为近年来研究的热点。前期基础实验发现艾灸通过抑制炎性因子的表达而发挥保护胃黏膜的作用，但艾灸如何抑制细胞炎性损伤内在机制的研究尚不明确。Nrf2/HO-1信号通路与炎症损伤密切相关，该通路的激活可抑制氧化应激损伤的发生，减少组织的炎性损伤。据此，我们提出艾灸改善胃黏膜的炎性损伤可能是通过激活该信号通路而起保护作用，以揭示艾灸保护胃黏膜的作用机制。本课题拟应用Nrf2(-/-) 转基因小鼠建立Hp胃黏膜损伤模型，探讨Nrf2/HO-1信号通路阻断前后，艾灸对Hp胃黏膜细胞凋亡、炎性因子的表达的调控作用。本项目的研究将深化艾灸治疗慢性胃炎机理的认识，为艾灸应用于慢性胃炎的防治提供新的理论依据。

Helicobacter pylori (Hp) is closely related to the patients with chronic gastritis.It is the main way of the treatment for this kind of disease to improve gastric mucosa inflammatory damage by Hp infection, and thus it become a research hotspot in recent years.It is show that moxibustion protect gastric mucosa by inhibiting the expression of inflammatory cytokines during the early stage of the basic experiment. But it is unclear of the inner mechanism how moxibustion inhibit inflammatory cell damage.Nrf2/HO-1 signaling pathway is closely related to inflammatory lesions, the activation of which can inhibit oxidative stress injuries, and reduce the inflammatory damage of tissue.On this basis, We hypothesized that moxibustion improve inflammatory injury of gastric mucosa by activating this signal pathway, in order to reveal the mechanism of moxibustion protecting gastric mucosa.Base on the mice model of Hp gastric mucosal damage by Nrf2(-/-) transgenic mice, this study discusses the regulation of moxibustion for Hp gastric mucosa of the occurrence of apoptosis and inflammatory factor expression,whether the blocking of Nrf2/HO-1 signaling pathway.This study will deepen the understanding of the mechanism of therapy of chronic gastritis by moxibustion, which providing new theoretical basis for prevention and control of chronic gastritis for application of moxibustion.